PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
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	MDM2 proto-oncogene	Homo sapiens	58-62
9548451-0	1998	Role of MDM2 overexpression in doxorubicin resistance of breast carcinoma.	Doxorubicin	31-42	MDM2 proto-oncogene	Homo sapiens	8-12
11244964-3	1998	MDM2 and p53 genes were detected by digoxigenin labeling in situ hybridization-technique.	Digoxigenin	36-47	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	46-50
9548451-4	1998	An in vitro experimental model using stable mdm2-transfected MCF-7 cells carrying wild-type p53 confirmed that the cells become approximately 3-fold more resistant to doxorubicin as a result of MDM2 overexpression, and the wild-type p53 function, such as the induction of p21Waf1 following DNA damage, was significantly suppressed.	Doxorubicin	167-178	MDM2 proto-oncogene	Homo sapiens	44-48
9548451-5	1998	MDM2 overexpression is suggested to be a novel marker for predicting lack of response to doxorubicin treatment in breast cancer patients.	Doxorubicin	89-100	MDM2 proto-oncogene	Homo sapiens	0-4
9419352-3	1998	An MDM2 antisense phosphorothioate oligodeoxynucleotide has been identified that effectively inhibits MDM2 expression in tumor cells containing MDM2 gene amplifications.	phosphorothioate oligodeoxynucleotide	18-55	MDM2 proto-oncogene	Homo sapiens	3-7
9419352-3	1998	An MDM2 antisense phosphorothioate oligodeoxynucleotide has been identified that effectively inhibits MDM2 expression in tumor cells containing MDM2 gene amplifications.	phosphorothioate oligodeoxynucleotide	18-55	MDM2 proto-oncogene	Homo sapiens	102-106
9419352-3	1998	An MDM2 antisense phosphorothioate oligodeoxynucleotide has been identified that effectively inhibits MDM2 expression in tumor cells containing MDM2 gene amplifications.	phosphorothioate oligodeoxynucleotide	18-55	MDM2 proto-oncogene	Homo sapiens	102-106
9419352-7	1998	MDM2 antisense oligonucleotides may be useful as antitumor agents alone or as enhancers of other conventional DNA-damaging drugs.	Oligonucleotides	15-31	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	162-166
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	MDM2 proto-oncogene	Homo sapiens	162-166
9438391-4	1998	Increases in mdm2 protein levels by MG132 was accompanied by increases in polyubiquitinated forms of the proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	114-119
9700726-3	1998	Northern analysis showed an induction of mdm-2 mRNA upon cisplatin treatment.	Cisplatin	57-66	MDM2 proto-oncogene	Homo sapiens	41-46
9700726-4	1998	It was further demonstrated, using an RNase protection assay, that the p53-responsive, mdm-2 promoter (P2) was activated in cisplatin-treated A2780 cells.	Cisplatin	124-133	MDM2 proto-oncogene	Homo sapiens	71-92
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	MDM2 proto-oncogene	Homo sapiens	80-85
9450543-4	1997	The cysteine residue in the carboxyl terminus of MDM2 was essential for the activity.	Cysteine	4-12	MDM2 proto-oncogene	Homo sapiens	49-53
9292533-4	1997	Treatment of MM cells with MDM2 antisense, but not sense, nonsense, or scrambled, oligodeoxyribonucleotides (ODNs) decreased DNA synthesis and cell viability; it also induced G1 growth arrest, as evidenced by propidium iodide (PI) staining and induction of retinoblastoma protein (pRB) to E2F-1 binding.	Oligodeoxyribonucleotides	82-107	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	167-183
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	MDM2 proto-oncogene	Homo sapiens	154-158
10374333-2	1997	METHODS: Digoxigenin labeling in situ hybridization technique was used to investigate the expression of MDM2 and p53 in 38 cases of bone tumors, including 12 osteosarcomas, 10 chondrosarcomas, 14 giant cell tumors of bone and 2 chondroblastomas.	Digoxigenin	9-20	MDM2 proto-oncogene	Homo sapiens	104-108
9326321-5	1997	However, delta24-25 ablated interaction of pRB with MDM2.	delta24-25	9-19	MDM2 proto-oncogene	Homo sapiens	52-56
9292533-4	1997	Treatment of MM cells with MDM2 antisense, but not sense, nonsense, or scrambled, oligodeoxyribonucleotides (ODNs) decreased DNA synthesis and cell viability; it also induced G1 growth arrest, as evidenced by propidium iodide (PI) staining and induction of retinoblastoma protein (pRB) to E2F-1 binding.	Propidium	209-225	MDM2 proto-oncogene	Homo sapiens	27-31
9292533-5	1997	Moreover, inhibition of MDM2 using antisense ODNs also triggered MM cell apoptosis as evidenced by acridine orange-ethidium bromide staining.	Acridine Orange	99-114	MDM2 proto-oncogene	Homo sapiens	24-28
9292533-5	1997	Moreover, inhibition of MDM2 using antisense ODNs also triggered MM cell apoptosis as evidenced by acridine orange-ethidium bromide staining.	Ethidium	115-131	MDM2 proto-oncogene	Homo sapiens	24-28
9291435-2	1997	mdm-2 mRNA expression was an independent prognostic factor for patients with primary ovarian cancer, FIGO (International Federation of Gynecology and Obstetrics) stages III and IV (n = 57), who all received chemotherapy with carboplatin or cisplatin and cyclophosphamide.	Carboplatin	225-236	MDM2 proto-oncogene	Homo sapiens	0-5
9291435-2	1997	mdm-2 mRNA expression was an independent prognostic factor for patients with primary ovarian cancer, FIGO (International Federation of Gynecology and Obstetrics) stages III and IV (n = 57), who all received chemotherapy with carboplatin or cisplatin and cyclophosphamide.	Cisplatin	240-249	MDM2 proto-oncogene	Homo sapiens	0-5
9291435-2	1997	mdm-2 mRNA expression was an independent prognostic factor for patients with primary ovarian cancer, FIGO (International Federation of Gynecology and Obstetrics) stages III and IV (n = 57), who all received chemotherapy with carboplatin or cisplatin and cyclophosphamide.	Cyclophosphamide	254-270	MDM2 proto-oncogene	Homo sapiens	0-5
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	MDM2 proto-oncogene	Homo sapiens	25-30
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	MDM2 proto-oncogene	Homo sapiens	25-30
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	MDM2 proto-oncogene	Homo sapiens	109-114
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	MDM2 proto-oncogene	Homo sapiens	249-254
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	MDM2 proto-oncogene	Homo sapiens	109-114
9226370-4	1997	The homology between Mdmx and Mdm2 is most prominent in the p53-binding domain and the putative metal-binding domains.	Metals	96-101	MDM2 proto-oncogene	Homo sapiens	30-34
9178766-0	1997	The carboxy terminus of p53 mimics the polylysine effect of protein kinase CK2-catalyzed MDM2 phosphorylation.	Polylysine	39-49	MDM2 proto-oncogene	Homo sapiens	89-93
9178766-1	1997	The oncogene product MDM2 can be phosphorylated by protein kinase CK2 in vitro 0.5-1 mol of phosphate were incorporated per mol MDM2 protein.	Phosphates	92-101	MDM2 proto-oncogene	Homo sapiens	21-25
9178766-1	1997	The oncogene product MDM2 can be phosphorylated by protein kinase CK2 in vitro 0.5-1 mol of phosphate were incorporated per mol MDM2 protein.	Phosphates	92-101	MDM2 proto-oncogene	Homo sapiens	128-132
9178766-2	1997	The catalytic subunit of protein kinase CK2 (alpha-subunit) catalyzed the incorporation of twice as much phosphate into the MDM2 protein as it was obtained with the holoenzyme.	Phosphates	105-114	MDM2 proto-oncogene	Homo sapiens	124-128
9178766-3	1997	Polylysine stimulated MDM2 phosphorylation by CK2 holoenzyme threefold in contrast to the alpha-subunit-catalyzed MDM2 phosphorylation which was reduced by about 66% when polylysine was added.	Polylysine	0-10	MDM2 proto-oncogene	Homo sapiens	22-26
9178766-3	1997	Polylysine stimulated MDM2 phosphorylation by CK2 holoenzyme threefold in contrast to the alpha-subunit-catalyzed MDM2 phosphorylation which was reduced by about 66% when polylysine was added.	Polylysine	171-181	MDM2 proto-oncogene	Homo sapiens	114-118
9178766-7	1997	Phosphorylation of MDM2 by CK2 holoenzyme in the presence of the p21(WAF1/CIP1), known to be a potent inhibitor of cyclin-dependent protein kinases, also led to a significant reduction of phosphate incorporation into MDM2 indicating that p21(WAF1/CIP1) does not exclusively inhibit cell cycle kinases.	Phosphates	188-197	MDM2 proto-oncogene	Homo sapiens	19-23
9178766-7	1997	Phosphorylation of MDM2 by CK2 holoenzyme in the presence of the p21(WAF1/CIP1), known to be a potent inhibitor of cyclin-dependent protein kinases, also led to a significant reduction of phosphate incorporation into MDM2 indicating that p21(WAF1/CIP1) does not exclusively inhibit cell cycle kinases.	Phosphates	188-197	MDM2 proto-oncogene	Homo sapiens	217-221
10374529-0	1997	[Detection of p53 and MDM2 gene expression in osteosarcoma with biotin-labelled in situ].	Biotin	64-70	MDM2 proto-oncogene	Homo sapiens	22-26
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	MDM2 proto-oncogene	Homo sapiens	45-49
8827714-5	1996	RESULTS: The MDM2 protein binds efficiently to the homopolyribonucleotide poly(G) but not to other homopolyribonucleotides.	homopolyribonucleotide	51-73	MDM2 proto-oncogene	Homo sapiens	13-17
9260591-4	1997	The expression of the proteins p53 and mdm2 was determined immunohistochemically using formalin-fixed, paraffin-embedded material.	Formaldehyde	87-95	MDM2 proto-oncogene	Homo sapiens	39-43
9260591-4	1997	The expression of the proteins p53 and mdm2 was determined immunohistochemically using formalin-fixed, paraffin-embedded material.	Paraffin	103-111	MDM2 proto-oncogene	Homo sapiens	39-43
8895579-3	1996	In addition, the putative metal binding domains in the C-terminal part of MDM2 are completely conserved in MDMX.	Metals	26-31	MDM2 proto-oncogene	Homo sapiens	74-78
8883415-4	1996	The mdm2 gene, in addition, conferred the resistance of U87-MG cells to the apoptotic cell death induced by etoposide (VP-16) or doxorubicin.	Etoposide	108-117	MDM2 proto-oncogene	Homo sapiens	4-8
8883415-4	1996	The mdm2 gene, in addition, conferred the resistance of U87-MG cells to the apoptotic cell death induced by etoposide (VP-16) or doxorubicin.	Etoposide	119-124	MDM2 proto-oncogene	Homo sapiens	4-8
8883415-4	1996	The mdm2 gene, in addition, conferred the resistance of U87-MG cells to the apoptotic cell death induced by etoposide (VP-16) or doxorubicin.	Doxorubicin	129-140	MDM2 proto-oncogene	Homo sapiens	4-8
8883415-5	1996	Furthermore, treatment with mdm2 antisense oligonucleotides inhibited the expression of P-gp in MDM2-expressing U87-MG cells.	Oligonucleotides	43-59	MDM2 proto-oncogene	Homo sapiens	28-32
8883415-5	1996	Furthermore, treatment with mdm2 antisense oligonucleotides inhibited the expression of P-gp in MDM2-expressing U87-MG cells.	Oligonucleotides	43-59	MDM2 proto-oncogene	Homo sapiens	96-100
8827714-5	1996	RESULTS: The MDM2 protein binds efficiently to the homopolyribonucleotide poly(G) but not to other homopolyribonucleotides.	Poly G	74-81	MDM2 proto-oncogene	Homo sapiens	13-17
33771522-0	2021	MiR-221-3p-mediated downregulation of MDM2 reverses the paclitaxel resistance of non-small cell lung cancer in vitro and in vivo.	mir-221-3p	0-10	MDM2 proto-oncogene	Homo sapiens	38-42
8666362-4	1996	Paraffin-embedded tissue sections were immunostained with monoclonal antibody to p53 and MDM2 proteins.	Paraffin	0-8	MDM2 proto-oncogene	Homo sapiens	89-93
21544443-6	1996	Expression of both was reduced in the presence of increasing concentrations of estradiol (10(-10)-10(-8) M) thus, estrogen may be involved in regulation of MDM2 expression in proliferative breast lesions.	Estradiol	79-88	MDM2 proto-oncogene	Homo sapiens	156-160
7654034-4	1995	In this study the immunohistochemical detection of the MDM2 protein in 186 paraffin embedded tissue sections of normal mucosa, premalignant, malignant and metastatic lesions of the oropharyngeal mucosa is reported for the first time.	Paraffin	75-83	MDM2 proto-oncogene	Homo sapiens	55-59
7663443-0	1995	Expression of the protooncogene mdm2 markedly increases in response to carbon tetrachloride but not after partial hepatectomy in contrast to p53.	Carbon Tetrachloride	71-91	MDM2 proto-oncogene	Homo sapiens	32-36
7761100-0	1995	MDM2 protein confers the resistance of a human glioblastoma cell line to cisplatin-induced apoptosis.	Cisplatin	73-82	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	261-265
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	MDM2 proto-oncogene	Homo sapiens	261-265
7761100-5	1995	Overexpression of MDM2 in U87-MG cells transfected with human mdm2 expression vector conferred the resistance of tumor cell to cisplatin-induced apoptosis.	Cisplatin	127-136	MDM2 proto-oncogene	Homo sapiens	18-22
7761100-5	1995	Overexpression of MDM2 in U87-MG cells transfected with human mdm2 expression vector conferred the resistance of tumor cell to cisplatin-induced apoptosis.	Cisplatin	127-136	MDM2 proto-oncogene	Homo sapiens	62-66
7761100-6	1995	In contrast, the treatment with mdm2 antisense oligonucleotide targeted against mdm2 mRNA increased the susceptibility of tumor cells to apoptosis.	Oligonucleotides	47-62	MDM2 proto-oncogene	Homo sapiens	32-36
7761100-6	1995	In contrast, the treatment with mdm2 antisense oligonucleotide targeted against mdm2 mRNA increased the susceptibility of tumor cells to apoptosis.	Oligonucleotides	47-62	MDM2 proto-oncogene	Homo sapiens	80-84
7761100-8	1995	These findings suggest that MDM2 protein may act as a negative regulator of cisplatin-induced apoptosis, and moreover, may play an important role in the development of resistance to cisplatin in human tumors.	Cisplatin	76-85	MDM2 proto-oncogene	Homo sapiens	28-32
7761100-8	1995	These findings suggest that MDM2 protein may act as a negative regulator of cisplatin-induced apoptosis, and moreover, may play an important role in the development of resistance to cisplatin in human tumors.	Cisplatin	182-191	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	4-9
7923211-5	1994	We found only one mutation, an A-T to T-A transversion involving the second base of codon 285 and resulting in the substitution of valine for glutamic acid, amplification of the mdm2 gene could be detected in zero of eight of these tumors.	Valine	131-137	MDM2 proto-oncogene	Homo sapiens	178-182
7923211-5	1994	We found only one mutation, an A-T to T-A transversion involving the second base of codon 285 and resulting in the substitution of valine for glutamic acid, amplification of the mdm2 gene could be detected in zero of eight of these tumors.	Glutamic Acid	142-155	MDM2 proto-oncogene	Homo sapiens	178-182
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	MDM2 proto-oncogene	Homo sapiens	104-109
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	MDM2 proto-oncogene	Homo sapiens	83-88
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	MDM2 proto-oncogene	Homo sapiens	143-148
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	MDM2 proto-oncogene	Homo sapiens	82-86
8058315-5	1994	Several p53 synthetic peptides libraries, and an alanine substitution series at the optimal binding site, were used to establish the MDM2 binding site, in fine detail, to the sequence TFSGLW (aa 18-23) in mouse and TFSDLW in man (aa 18-23).	Alanine	49-56	MDM2 proto-oncogene	Homo sapiens	133-137
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	MDM2 proto-oncogene	Homo sapiens	182-187
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	MDM2 proto-oncogene	Homo sapiens	182-187
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	MDM2 proto-oncogene	Homo sapiens	107-112
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	MDM2 proto-oncogene	Homo sapiens	114-119
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	MDM2 proto-oncogene	Homo sapiens	107-112
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	MDM2 proto-oncogene	Homo sapiens	114-119
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	MDM2 proto-oncogene	Homo sapiens	79-83
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	MDM2 proto-oncogene	Homo sapiens	137-141
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	MDM2 proto-oncogene	Homo sapiens	48-53
8415687-4	1993	Similarly, p53her induces expression of an endogenous MDM-2 transcript only in the presence of estradiol.	Estradiol	95-104	MDM2 proto-oncogene	Homo sapiens	54-59
9431695-0	1996	Immunoreactivity of new antibodies anti-p53 and anti-MDM-2 in paraffin embedded tissue samples.	Paraffin	62-70	MDM2 proto-oncogene	Homo sapiens	53-58
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	MDM2 proto-oncogene	Homo sapiens	45-50
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	MDM2 proto-oncogene	Homo sapiens	45-50
8751388-4	1996	Fluorescene in situ hybridization to tumor metaphases with probes specific for this region indicated that the double minutes contained the MDM2 gene but not the CDK4 gene.	fluorescene	0-11	MDM2 proto-oncogene	Homo sapiens	139-143
7734324-4	1995	Immunohistochemical analysis of the formalin-fixed, paraffin-embedded tumours demonstrated that 7/97 (7%) had nuclear expression for MDM2 in 10-50% of the tumour cells (type 2 staining) and were denoted MDM2+.	Formaldehyde	36-44	MDM2 proto-oncogene	Homo sapiens	133-137
8288680-0	1994	Detection of MDM2-proto-oncogene in paraffin embedded human bronchial epithelium.	Paraffin	36-44	MDM2 proto-oncogene	Homo sapiens	13-17
8288680-6	1994	Here we describe the successful use of a monoclonal antibody (IF2) for the detection of MDM2 protein in paraffin-embedded tissue from human lung biopsies.	Paraffin	104-112	MDM2 proto-oncogene	Homo sapiens	88-92
33771522-0	2021	MiR-221-3p-mediated downregulation of MDM2 reverses the paclitaxel resistance of non-small cell lung cancer in vitro and in vivo.	Paclitaxel	56-66	MDM2 proto-oncogene	Homo sapiens	38-42
33771522-5	2021	PTX increased miR-221-3p expression and regulated MDM2/P53 expression in the PTX-sensitive NSCLC strain (A549).	Paclitaxel	0-3	MDM2 proto-oncogene	Homo sapiens	50-54
33771522-5	2021	PTX increased miR-221-3p expression and regulated MDM2/P53 expression in the PTX-sensitive NSCLC strain (A549).	Paclitaxel	77-80	MDM2 proto-oncogene	Homo sapiens	50-54
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	MDM2 proto-oncogene	Homo sapiens	56-60
33941774-0	2021	MDM2 inhibitor APG-115 exerts potent antitumor activity and synergizes with standard-of-care agents in preclinical acute myeloid leukemia models.	AA-115	15-22	MDM2 proto-oncogene	Homo sapiens	0-4
33941774-6	2021	APG-115 is a potent MDM2 inhibitor under clinical development for patients with solid tumors.	AA-115	0-7	MDM2 proto-oncogene	Homo sapiens	20-24
33034426-0	2020	The MDM2 inhibitor CGM097 combined with the BET inhibitor OTX015 induces cell death and inhibits tumor growth in models of neuroblastoma.	NVP-CGM097	19-25	MDM2 proto-oncogene	Homo sapiens	4-8
33773191-0	2021	Bibenzyl analogue DS-1 inhibits MDM2-mediated p53 degradation and sensitizes apoptosis in lung cancer cells.	Bibenzyls	0-8	MDM2 proto-oncogene	Homo sapiens	32-36
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	MDM2 proto-oncogene	Homo sapiens	119-123
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	72-76
33034426-7	2020	Our study focuses on the combined treatment of a MDM2 inhibitor (CGM097) with a BET inhibitor (OTX015) in neuroblastoma.	NVP-CGM097	65-71	MDM2 proto-oncogene	Homo sapiens	49-53
23266121-0	2013	Lead optimization of novel p53-MDM2 interaction inhibitors possessing dihydroimidazothiazole scaffold.	dihydroimidazothiazole	70-92	MDM2 proto-oncogene	Homo sapiens	31-35
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	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	293-297
23266121-4	2013	The incorporation of the pyrrolidine moiety at the C-2 position raised another hydrophobic interaction site with MDM2 protein, which was generated by the induced-fitting observed by co-crystal structure analysis.	pyrrolidine	25-36	MDM2 proto-oncogene	Homo sapiens	113-117
19477214-8	2009	MDM2, a negative regulator of p21(WAF1), was ubiquitinated and degraded after hispolon treatment.	hispolon	78-86	MDM2 proto-oncogene	Homo sapiens	0-4
34802714-7	2022	Our analysis showed that the anti-angiogenic activity of CDDO-Im is mediated by its inhibition of the expression of PLAT, ETS1, A2M, SPAG9, RASGRP3, FBXO32, GCNT1 and HDGFRP3 and its direct interactions with EGFR, mTOR, NOS2, HSP90AA1, MDM2, SYK, IRF3, ATR and KIF14.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	57-64	MDM2 proto-oncogene	Homo sapiens	236-240
34899944-11	2021	Conclusion: The possible mechanisms of the components of the Zhishi-Baizhu herb pair in treating gastric cancer might be related to luteolin and naringenin, which intervened with the targets AKT1, MMP9, IL-6, CCND1, BCL2, MTOR, and MDM2, and are linked with the PI3K-Akt and IL-17 signaling pathways.	naringenin	145-155	MDM2 proto-oncogene	Homo sapiens	232-236
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	MDM2 proto-oncogene	Homo sapiens	74-78
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	MDM2 proto-oncogene	Homo sapiens	148-152
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	MDM2 proto-oncogene	Homo sapiens	98-102
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	MDM2 proto-oncogene	Homo sapiens	169-173
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	MDM2 proto-oncogene	Homo sapiens	169-173
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	MDM2 proto-oncogene	Homo sapiens	45-49
34933330-0	2022	MDM2 antagonist idasanutlin in patients with polycythemia vera: results from a single-arm phase 2 study.	RG7388	16-27	MDM2 proto-oncogene	Homo sapiens	0-4
34933330-1	2022	Idasanutlin, an MDM2 antagonist, showed clinical activity and rapid reduction in JAK2 V617F allele burden in patients with polycythemia vera (PV) in a phase 1 study.	RG7388	0-11	MDM2 proto-oncogene	Homo sapiens	16-20
34927257-9	2022	Moreover, mdm2 can potentially be utilized as a therapeutic target in the Luminal subtype.	Phenobarbital	74-81	MDM2 proto-oncogene	Homo sapiens	10-14
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	MDM2 proto-oncogene	Homo sapiens	174-178
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	MDM2 proto-oncogene	Homo sapiens	136-140
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	MDM2 proto-oncogene	Homo sapiens	95-99
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	MDM2 proto-oncogene	Homo sapiens	106-110
34956872-6	2021	Western blot analysis showed that levels of two USP2a target proteins, FAS and Mdm2, were dose-dependently decreased in A253 submaxillary carcinoma cells treated with 6-TG or 6-MP.	Thioguanine	167-171	MDM2 proto-oncogene	Homo sapiens	79-83
34956872-6	2021	Western blot analysis showed that levels of two USP2a target proteins, FAS and Mdm2, were dose-dependently decreased in A253 submaxillary carcinoma cells treated with 6-TG or 6-MP.	Mercaptopurine	175-179	MDM2 proto-oncogene	Homo sapiens	79-83
34956872-14	2021	In summary, these findings suggest 6-TG and 6-MP reduce the stability of some USP2a targets, including FAS and Mdm2, by inhibiting USP2a-catalyzed deubiquitination in some cancer cells.	Thioguanine	35-39	MDM2 proto-oncogene	Homo sapiens	111-115
34956872-14	2021	In summary, these findings suggest 6-TG and 6-MP reduce the stability of some USP2a targets, including FAS and Mdm2, by inhibiting USP2a-catalyzed deubiquitination in some cancer cells.	Mercaptopurine	44-48	MDM2 proto-oncogene	Homo sapiens	111-115
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	MDM2 proto-oncogene	Homo sapiens	74-78
34747636-8	2021	Administration of apolipoprotein E-deficient (ApoE-/-) mice with CK2-specific inhibitor tetrabromocinnamic acid or atorvastatin inhibits atherosclerosis formation through down-regulations of EC phospho-YY1S118 and HDM2.	tetrabromocinnamic acid	88-111	MDM2 proto-oncogene	Homo sapiens	214-218
34747636-8	2021	Administration of apolipoprotein E-deficient (ApoE-/-) mice with CK2-specific inhibitor tetrabromocinnamic acid or atorvastatin inhibits atherosclerosis formation through down-regulations of EC phospho-YY1S118 and HDM2.	Atorvastatin	115-127	MDM2 proto-oncogene	Homo sapiens	214-218
34794098-3	2021	Herein, we employed a rapid combinatorial approach to generate a novel series of hybrid spirooxindole-based MDM2 inhibitors (5a-s) endowed with BCL2 signaling attenuation.	Spirooxindole	88-101	MDM2 proto-oncogene	Homo sapiens	108-112
34794098-3	2021	Herein, we employed a rapid combinatorial approach to generate a novel series of hybrid spirooxindole-based MDM2 inhibitors (5a-s) endowed with BCL2 signaling attenuation.	5a-s	125-129	MDM2 proto-oncogene	Homo sapiens	108-112
34794098-4	2021	The adducts were designed to mimic the thematic features of the chemically stable potent spiro(3H-indole-3,2"-pyrrolidin)-2(1H)-ones MDM2 inhibitors while installing a pyrrole ring on the core via a carbonyl spacer inspired by the natural product marinopyrrole A that efficiently inhibits BCL2 family functions by various mechanisms.	3h-indole-3,2"-pyrrolidin)-2(1h)	95-127	MDM2 proto-oncogene	Homo sapiens	133-137
34794098-4	2021	The adducts were designed to mimic the thematic features of the chemically stable potent spiro(3H-indole-3,2"-pyrrolidin)-2(1H)-ones MDM2 inhibitors while installing a pyrrole ring on the core via a carbonyl spacer inspired by the natural product marinopyrrole A that efficiently inhibits BCL2 family functions by various mechanisms.	marinopyrrole A	247-262	MDM2 proto-oncogene	Homo sapiens	133-137
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	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	88-92
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	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	119-123
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	MDM2 proto-oncogene	Homo sapiens	38-42
34827693-11	2021	Combination treatment resulted in a 14-fold and 1.6-fold induction of MDM2 in LU-NB-2 and IMR-32 spheroids, respectively.	Niobium	80-83	MDM2 proto-oncogene	Homo sapiens	70-74
34732238-6	2021	In this study, we performed a comprehensive validation of MDM2 inhibitor RG7388 in patient-derived DIPG cell lines established from both TP53 wild-type/PPM1D-mutant and TP53 mutant/PPM1D wild-type tumors, as well in TP53 knockout isogenic DIPG cell line models.	RG7388	73-79	MDM2 proto-oncogene	Homo sapiens	58-62
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	MDM2 proto-oncogene	Homo sapiens	118-122
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	MDM2 proto-oncogene	Homo sapiens	118-122
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	MDM2 proto-oncogene	Homo sapiens	118-122
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	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	105-109
34180037-0	2021	Phase I study of daily and weekly regimens of the orally administered MDM2 antagonist idasanutlin in patients with advanced tumors.	RG7388	86-97	MDM2 proto-oncogene	Homo sapiens	70-74
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	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	58-62
34866036-0	2022	Effects of the MDM2 inhibitor Nutlin-3a on sensitivity of pancreatic cancer cells to berberine and modified berberines in the presence and absence of WT-TP53.	nutlin 3	30-39	MDM2 proto-oncogene	Homo sapiens	15-19
34866036-0	2022	Effects of the MDM2 inhibitor Nutlin-3a on sensitivity of pancreatic cancer cells to berberine and modified berberines in the presence and absence of WT-TP53.	Berberine	108-118	MDM2 proto-oncogene	Homo sapiens	15-19
34806333-3	2022	Among them, WY-5 is the most active MDM2 inhibitor with an IC50 value of 14.1 +- 2.8 nM.	wy-5	12-16	MDM2 proto-oncogene	Homo sapiens	36-40
34799910-0	2021	P1-39: Paclitaxel induces growth inhibition in gefitinib-resistant PC9-MET cells by downregulating MDM2 and activating p53.	Paclitaxel	7-17	MDM2 proto-oncogene	Homo sapiens	99-103
34799910-0	2021	P1-39: Paclitaxel induces growth inhibition in gefitinib-resistant PC9-MET cells by downregulating MDM2 and activating p53.	Gefitinib	47-56	MDM2 proto-oncogene	Homo sapiens	99-103
34684885-8	2021	To explore the plausible mechanism of anticancer activity of di-spirooxindole analogs, molecular docking studies were investigated which suggested that spirooxindole analogs potentially inhibit the activity of MDM2.	di-spirooxindole	61-77	MDM2 proto-oncogene	Homo sapiens	210-214
34684885-8	2021	To explore the plausible mechanism of anticancer activity of di-spirooxindole analogs, molecular docking studies were investigated which suggested that spirooxindole analogs potentially inhibit the activity of MDM2.	Spirooxindole	152-165	MDM2 proto-oncogene	Homo sapiens	210-214
34426149-0	2021	Design, synthesis and biological evaluation of novel pyrrolidone-based derivatives as potent p53-MDM2 inhibitors.	Pyrrolidinones	53-64	MDM2 proto-oncogene	Homo sapiens	97-101
34170069-1	2021	In silico studies of a library of diarylpentanoids led us to the identification of potential new MDM2/X ligands.	diarylpentanoids	34-50	MDM2 proto-oncogene	Homo sapiens	97-101
34426149-2	2021	The natural product chalcone exhibited moderate inhibitory activity against MDM2, thus based on the binding mode between chalcone and MDM2, a hit unsaturated pyrrolidone scaffold was obtained through virtual screening.	Chalcone	20-28	MDM2 proto-oncogene	Homo sapiens	76-80
34426149-2	2021	The natural product chalcone exhibited moderate inhibitory activity against MDM2, thus based on the binding mode between chalcone and MDM2, a hit unsaturated pyrrolidone scaffold was obtained through virtual screening.	Chalcone	20-28	MDM2 proto-oncogene	Homo sapiens	134-138
34426149-2	2021	The natural product chalcone exhibited moderate inhibitory activity against MDM2, thus based on the binding mode between chalcone and MDM2, a hit unsaturated pyrrolidone scaffold was obtained through virtual screening.	Chalcone	121-129	MDM2 proto-oncogene	Homo sapiens	76-80
34426149-2	2021	The natural product chalcone exhibited moderate inhibitory activity against MDM2, thus based on the binding mode between chalcone and MDM2, a hit unsaturated pyrrolidone scaffold was obtained through virtual screening.	Chalcone	121-129	MDM2 proto-oncogene	Homo sapiens	134-138
34426149-2	2021	The natural product chalcone exhibited moderate inhibitory activity against MDM2, thus based on the binding mode between chalcone and MDM2, a hit unsaturated pyrrolidone scaffold was obtained through virtual screening.	unsaturated pyrrolidone	146-169	MDM2 proto-oncogene	Homo sapiens	76-80
34426149-2	2021	The natural product chalcone exhibited moderate inhibitory activity against MDM2, thus based on the binding mode between chalcone and MDM2, a hit unsaturated pyrrolidone scaffold was obtained through virtual screening.	unsaturated pyrrolidone	146-169	MDM2 proto-oncogene	Homo sapiens	134-138
34426149-4	2021	As a result, because the three critical hydrophobic pockets of MDM2 were occupied by the substituted-phenyl linked at the pyrrolidone fragment, compound 4 h demonstrated good binding affinity with the MDM2.	Pyrrolidinones	122-133	MDM2 proto-oncogene	Homo sapiens	63-67
34426149-4	2021	As a result, because the three critical hydrophobic pockets of MDM2 were occupied by the substituted-phenyl linked at the pyrrolidone fragment, compound 4 h demonstrated good binding affinity with the MDM2.	Pyrrolidinones	122-133	MDM2 proto-oncogene	Homo sapiens	201-205
34426149-7	2021	Thus, the novel unsaturated pyrrolidone p53-MDM2 inhibitors could be developed as novel antitumor agents.	unsaturated pyrrolidone	16-39	MDM2 proto-oncogene	Homo sapiens	44-48
34803431-0	2021	Ginsenoside Rg3 attenuates skin disorders via down-regulation of MDM2/HIF1alpha signaling pathway.	ginsenoside Rg3	0-15	MDM2 proto-oncogene	Homo sapiens	65-69
34572735-2	2021	Inhibition of MDM2 expression in the SKBR3 cell line (HER2 subtype) diminished the survival of cancer cells treated with doxorubicin, etoposide, and camptothecin.	Doxorubicin	121-132	MDM2 proto-oncogene	Homo sapiens	14-18
34572735-2	2021	Inhibition of MDM2 expression in the SKBR3 cell line (HER2 subtype) diminished the survival of cancer cells treated with doxorubicin, etoposide, and camptothecin.	Etoposide	134-143	MDM2 proto-oncogene	Homo sapiens	14-18
34572735-2	2021	Inhibition of MDM2 expression in the SKBR3 cell line (HER2 subtype) diminished the survival of cancer cells treated with doxorubicin, etoposide, and camptothecin.	Camptothecin	149-161	MDM2 proto-oncogene	Homo sapiens	14-18
34572735-3	2021	Moreover, we demonstrated that inhibition of MDM2 expression diminished DNA repair by homologous recombination (HR) and sensitized SKBR3 cells to a PARP inhibitor, olaparib.	olaparib	164-172	MDM2 proto-oncogene	Homo sapiens	45-49
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	MDM2 proto-oncogene	Homo sapiens	190-194
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	MDM2 proto-oncogene	Homo sapiens	190-194
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	MDM2 proto-oncogene	Homo sapiens	190-194
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	MDM2 proto-oncogene	Homo sapiens	137-141
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	MDM2 proto-oncogene	Homo sapiens	222-226
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	MDM2 proto-oncogene	Homo sapiens	70-74
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	MDM2 proto-oncogene	Homo sapiens	70-74
34697748-0	2021	Andrographolide Induces Apoptosis in Gastric Cancer Cells through Reactivation of p53 and Inhibition of Mdm-2.	andrographolide	0-15	MDM2 proto-oncogene	Homo sapiens	104-109
34697748-4	2021	This study evaluated the effect of andrographolide on proliferation of human gastric carcinoma cells in relevance to p53 and Mdm-2 pathways.	andrographolide	35-50	MDM2 proto-oncogene	Homo sapiens	125-130
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	MDM2 proto-oncogene	Homo sapiens	97-102
34803431-8	2021	Rg3 down-regulated the MDM2 expression level increased by PMACI stimulation.	ginsenoside Rg3	0-3	MDM2 proto-oncogene	Homo sapiens	23-27
34471176-0	2021	Retraction Note: Activation of PERK-Nrf2 oncogenic signaling promotes Mdm2-mediated Rb degradation in persistently infected HCV culture.	Rubidium	84-86	MDM2 proto-oncogene	Homo sapiens	70-74
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	MDM2 proto-oncogene	Homo sapiens	109-113
34977581-2	2021	Using a mRNA based display technique to screen a library of >1012 in vitro-translated cyclic peptides, we have identified a macrocyclic ligand that shows picomolar potency on MDM2.	Peptides, Cyclic	86-101	MDM2 proto-oncogene	Homo sapiens	175-179
34977581-3	2021	X-Ray crystallography reveals a novel binding mode utilizing a unique pharmacophore to occupy the Phe/Trp/Leu pockets on MDM2.	Phenylalanine	98-101	MDM2 proto-oncogene	Homo sapiens	121-125
34977581-3	2021	X-Ray crystallography reveals a novel binding mode utilizing a unique pharmacophore to occupy the Phe/Trp/Leu pockets on MDM2.	Tryptophan	102-105	MDM2 proto-oncogene	Homo sapiens	121-125
34977581-3	2021	X-Ray crystallography reveals a novel binding mode utilizing a unique pharmacophore to occupy the Phe/Trp/Leu pockets on MDM2.	Leucine	106-109	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	92-96
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	MDM2 proto-oncogene	Homo sapiens	92-96
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	MDM2 proto-oncogene	Homo sapiens	74-78
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	MDM2 proto-oncogene	Homo sapiens	74-78
34445495-8	2021	Subsequent analysis revealed that, under the combined inhibition of gefitinib and JNJ-26854165, the cytonuclear trafficking of EGFR and MDM2 was disrupted.	Gefitinib	68-77	MDM2 proto-oncogene	Homo sapiens	136-140
34286973-3	2021	Recent studies of the experimental drug ALRN-6924, a dual MDM4 and MDM2 inhibitor, suggest that concurrent inhibition of MDM4 and MDM2 might be beneficial over only MDM2 inhibition.	alrn-6924	40-49	MDM2 proto-oncogene	Homo sapiens	67-71
34286973-3	2021	Recent studies of the experimental drug ALRN-6924, a dual MDM4 and MDM2 inhibitor, suggest that concurrent inhibition of MDM4 and MDM2 might be beneficial over only MDM2 inhibition.	alrn-6924	40-49	MDM2 proto-oncogene	Homo sapiens	130-134
34286973-3	2021	Recent studies of the experimental drug ALRN-6924, a dual MDM4 and MDM2 inhibitor, suggest that concurrent inhibition of MDM4 and MDM2 might be beneficial over only MDM2 inhibition.	alrn-6924	40-49	MDM2 proto-oncogene	Homo sapiens	165-169
34413896-5	2021	Compound AO-022/43452814 could be used as a scaffold for the development of anticancer agents targeting MDM2.	ao-022	9-15	MDM2 proto-oncogene	Homo sapiens	104-108
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	MDM2 proto-oncogene	Homo sapiens	153-157
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	MDM2 proto-oncogene	Homo sapiens	153-157
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	MDM2 proto-oncogene	Homo sapiens	153-157
34140638-0	2021	Pharmacokinetic-pharmacodynamic guided optimisation of dose and schedule of CGM097, an HDM2 inhibitor, in preclinical and clinical studies.	NVP-CGM097	76-82	MDM2 proto-oncogene	Homo sapiens	87-91
34140638-1	2021	BACKGROUND: CGM097 inhibits the p53-HDM2 interaction leading to downstream p53 activation.	NVP-CGM097	12-18	MDM2 proto-oncogene	Homo sapiens	36-40
34258531-0	2021	Editorial Comment to Prominent response to platinum-based chemotherapy in a patient with BRCA2 mutant-neuroendocrine prostate cancer and MDM2 amplification.	Platinum	43-51	MDM2 proto-oncogene	Homo sapiens	137-141
34230007-5	2021	Furthermore, MDM2 inhibitor ALRN-6924 induced a viral mimicry pathway and tumor inflammation signature genes in melanoma patients.	alrn-6924	28-37	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	134-138
34130704-0	2021	Retraction Note to: Differential modulatory effects of GSK-3b and HDM2 on sorafenib-induced AIF nuclear translocation (programmed necrosis) in melanoma.	Sorafenib	74-83	MDM2 proto-oncogene	Homo sapiens	66-70
34116693-0	2021	Retraction Note to: Effects of HDM2 antagonism on sunitinib resistance, p53 activation, SDF-1 induction, and tumor infiltration by CD11b+/Gr-1+ myeloid derived suppressor cells.	Sunitinib	50-59	MDM2 proto-oncogene	Homo sapiens	31-35
34185411-12	2021	Although reduction of FOLRalpha brought about vulnerability for oxaliplatin by diminishing MDM2 expression, farletuzumab did not suppress the MDM2-mediated chemoresistance and cell proliferation in GC cells.	Oxaliplatin	64-75	MDM2 proto-oncogene	Homo sapiens	91-95
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	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	147-151
34272277-9	2021	MK2 degradation is mediated by the E3 ubiquitin ligase MDM2, and we identify four lysine residues in MK2 that are directly ubiquitinated by MDM2.	Lysine	82-88	MDM2 proto-oncogene	Homo sapiens	55-59
34272277-9	2021	MK2 degradation is mediated by the E3 ubiquitin ligase MDM2, and we identify four lysine residues in MK2 that are directly ubiquitinated by MDM2.	Lysine	82-88	MDM2 proto-oncogene	Homo sapiens	140-144
34287267-3	2021	The purpose of the current study was to investigate the ability of ibrutinib plus the MDM2-inhibitor nutlin-3 to counteract the tumor microenvironment protective effect.	nutlin 3	101-109	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	82-86
34230221-10	2021	The rescue assays showed that miR-579-3p reversed cell behaviors caused by HCG11, and MDM2 reversed cell properties induced by miR-579-3p.	mir-579-3p	127-137	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	120-125
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	MDM2 proto-oncogene	Homo sapiens	120-125
34258530-0	2021	Prominent response to platinum-based chemotherapy in a patient with BRCA2 mutant-neuroendocrine prostate cancer and MDM2 amplification.	Platinum	22-30	MDM2 proto-oncogene	Homo sapiens	116-120
35628480-0	2022	Epigenetic Silencing of PTEN and Epi-Transcriptional Silencing of MDM2 Underlied Progression to Secondary Acute Myeloid Leukemia in Myelodysplastic Syndrome Treated with Hypomethylating Agents.	hypomethylating agents	170-192	MDM2 proto-oncogene	Homo sapiens	66-70
34063233-0	2021	The Impact of Chlorambucil and Valproic Acid on Cell Viability, Apoptosis and Expression of p21, HDM2, BCL2 and MCL1 Genes in Chronic Lymphocytic Leukemia.	Valproic Acid	31-44	MDM2 proto-oncogene	Homo sapiens	97-101
34085012-9	2020	RESULTS: This meta-analysis found that MDM2 309T>G polymorphism was significantly associated with Rb risk in the dominant model, TG+GG versus TT (OR = 1.43, 95% CI = 1.11-1.84, P = 0.006).	Thioguanine	129-131	MDM2 proto-oncogene	Homo sapiens	39-43
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	MDM2 proto-oncogene	Homo sapiens	65-69
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	MDM2 proto-oncogene	Homo sapiens	167-171
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	MDM2 proto-oncogene	Homo sapiens	148-152
35628480-5	2022	DNA hypomethylation of MDM2 was detected with downregulation of MDM2 in HMA resistant cell lines.	5-(N,N-hexamethylene)amiloride	72-75	MDM2 proto-oncogene	Homo sapiens	23-27
35628480-5	2022	DNA hypomethylation of MDM2 was detected with downregulation of MDM2 in HMA resistant cell lines.	5-(N,N-hexamethylene)amiloride	72-75	MDM2 proto-oncogene	Homo sapiens	64-68
35628480-6	2022	Long-read sequencing revealed significant RNA hypomethylation of MDM2 resulting in alternative splicing and production of a truncated MDM2 transcript in azacitidine-resistant P39 cells.	Azacitidine	153-164	MDM2 proto-oncogene	Homo sapiens	65-69
35628480-6	2022	Long-read sequencing revealed significant RNA hypomethylation of MDM2 resulting in alternative splicing and production of a truncated MDM2 transcript in azacitidine-resistant P39 cells.	Azacitidine	153-164	MDM2 proto-oncogene	Homo sapiens	134-138
35628480-7	2022	The expression of this MDM2 truncated transcript was also significantly increased in HMA-resistant patients compared with HMA-responsive patients.	5-(N,N-hexamethylene)amiloride	85-88	MDM2 proto-oncogene	Homo sapiens	23-27
35628480-8	2022	In conclusion, epigenetic and epi-transcriptomic dysregulation of PTEN and MDM2 were associated with resistance to hypomethylating agents.	hypomethylating agents	115-137	MDM2 proto-oncogene	Homo sapiens	75-79
35574675-6	2022	Following this, both inhibitor (MDM2) and activator (p19-ARF) protein levels in response to low oxygen stress were studied.	Oxygen	96-102	MDM2 proto-oncogene	Homo sapiens	32-36
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	MDM2 proto-oncogene	Homo sapiens	156-160
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	MDM2 proto-oncogene	Homo sapiens	156-160
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	MDM2 proto-oncogene	Homo sapiens	4-8
35266324-0	2022	Peptide-Conjugated Silver Nanoparticles for the Colorimetric Detection of the Oncoprotein Mdm2 in Human Serum.	Silver	19-25	MDM2 proto-oncogene	Homo sapiens	78-94
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	MDM2 proto-oncogene	Homo sapiens	48-52
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.	nutlin 3	74-83	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	229-233
35455441-0	2022	Synthetic Design and Biological Evaluation of New p53-MDM2 Interaction Inhibitors Based on Imidazoline Core.	Imidazolines	91-102	MDM2 proto-oncogene	Homo sapiens	54-58
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	MDM2 proto-oncogene	Homo sapiens	156-160
35044106-0	2022	Peptide-Conjugated Silver Nanoparticles for the Colorimetric Detection of the Oncoprotein Mdm2 in Human Serum.	Silver	19-25	MDM2 proto-oncogene	Homo sapiens	78-94
35044106-2	2022	Herein, we report a biosensor based on silver nanoparticles functionalized by peptide aptamers for the detection of a cancer biomarker, i. e. the Mdm2 protein.	Silver	39-45	MDM2 proto-oncogene	Homo sapiens	146-150
35044106-5	2022	Our results showed that replacing AuNPs by AgNPs improves the detection limit by nearly one order of magnitude, down to 5 nM, while the high selectivity of the system and the stability of the particles provided by the calixarene coating allow the detection of Mdm2 in human serum.	Calixarenes	218-228	MDM2 proto-oncogene	Homo sapiens	260-264
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	MDM2 proto-oncogene	Homo sapiens	147-151
35625571-0	2022	Hinokiflavone Inhibits MDM2 Activity by Targeting the MDM2-MDMX RING Domain.	hinokiflavone	0-13	MDM2 proto-oncogene	Homo sapiens	23-27
35625571-0	2022	Hinokiflavone Inhibits MDM2 Activity by Targeting the MDM2-MDMX RING Domain.	hinokiflavone	0-13	MDM2 proto-oncogene	Homo sapiens	54-58
35625571-4	2022	Virtual screening was performed using the crystal structure of the MDM2-MDMX RING domain dimer against a natural product library and identified a biflavonoid Hinokiflavone as a promising candidate compound targeting MDM2.	Biflavonoids	146-157	MDM2 proto-oncogene	Homo sapiens	67-71
35625571-4	2022	Virtual screening was performed using the crystal structure of the MDM2-MDMX RING domain dimer against a natural product library and identified a biflavonoid Hinokiflavone as a promising candidate compound targeting MDM2.	Biflavonoids	146-157	MDM2 proto-oncogene	Homo sapiens	216-220
35625571-4	2022	Virtual screening was performed using the crystal structure of the MDM2-MDMX RING domain dimer against a natural product library and identified a biflavonoid Hinokiflavone as a promising candidate compound targeting MDM2.	hinokiflavone	158-171	MDM2 proto-oncogene	Homo sapiens	67-71
35625571-4	2022	Virtual screening was performed using the crystal structure of the MDM2-MDMX RING domain dimer against a natural product library and identified a biflavonoid Hinokiflavone as a promising candidate compound targeting MDM2.	hinokiflavone	158-171	MDM2 proto-oncogene	Homo sapiens	216-220
35625571-5	2022	Hinokiflavone was shown to bind the MDM2-MDMX RING domain and inhibit MDM2-mediated ubiquitination in vitro.	hinokiflavone	0-13	MDM2 proto-oncogene	Homo sapiens	36-40
35625571-5	2022	Hinokiflavone was shown to bind the MDM2-MDMX RING domain and inhibit MDM2-mediated ubiquitination in vitro.	hinokiflavone	0-13	MDM2 proto-oncogene	Homo sapiens	70-74
35625571-6	2022	Hinokiflavone treatment resulted in the downregulation of MDM2 and MDMX and induction of apoptosis in various cancer cell lines.	hinokiflavone	0-13	MDM2 proto-oncogene	Homo sapiens	58-62
35625571-8	2022	This report provides biochemical and cellular evidence demonstrating the anti-cancer effects of Hinokiflavone through targeting the MDM2-MDMX RING domain.	hinokiflavone	96-109	MDM2 proto-oncogene	Homo sapiens	132-136
35468881-0	2022	JMJD2C mediates the MDM2/p53/IL5RA axis to promote CDDP resistance in uveal melanoma.	Cisplatin	51-55	MDM2 proto-oncogene	Homo sapiens	20-24
35410638-0	2022	AURKB, in concert with REST, acts as an oxygen-sensitive epigenetic regulator of the hypoxic induction of MDM2.	Oxygen	40-46	MDM2 proto-oncogene	Homo sapiens	106-110
35410638-6	2022	Under normoxia, phosphorylated AURKB, in concert with the repressor element-1 silencing transcription factor (REST), phosphorylates H3S10, which allows the AURKB-REST complex to access the MDM2 proto-oncogene.	h3s10	132-137	MDM2 proto-oncogene	Homo sapiens	189-193
35413116-1	2022	The phase III MIRROS trial (NCT02545283) evaluated the efficacy and safety of the small-molecule MDM2 antagonist idasanutlin plus cytarabine in patients with relapsed/refractory acute myeloid leukemia (R/R AML).	RG7388	113-124	MDM2 proto-oncogene	Homo sapiens	97-101
35413116-1	2022	The phase III MIRROS trial (NCT02545283) evaluated the efficacy and safety of the small-molecule MDM2 antagonist idasanutlin plus cytarabine in patients with relapsed/refractory acute myeloid leukemia (R/R AML).	Cytarabine	130-140	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	532-536
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	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	28-32
35384151-0	2022	2-Methoxy-5((3,4,5-trimethosyphenyl) seleninyl) phenol causes G2/M cell cycle arrest and apoptosis in NSCLC cells through mitochondrial apoptotic pathway and MDM2 inhibition.	2-methoxy-5-((3,4,5-trimethosyphenyl)seleninyl)phenol	0-54	MDM2 proto-oncogene	Homo sapiens	158-162
35156778-0	2022	Design, Synthesis and Molecular Modeling of Coumarin Derivatives as MDM2 Inhibitors Targeting Breast Cancer.	coumarin	44-52	MDM2 proto-oncogene	Homo sapiens	68-72
35156778-1	2022	The coumarin ring was used as a central scaffold that was substituted with a variety of bioactive functional groups, for designing and synthesizing novel MDM2 inhibitors targeting breast cancer.	coumarin	4-12	MDM2 proto-oncogene	Homo sapiens	154-158
35266324-2	2022	The cover picture shows the principle of a colorimetric sensor, based on peptide-conjugated silver nanoparticles, for the detection of the cancer biomarker Mdm2.	Silver	92-98	MDM2 proto-oncogene	Homo sapiens	156-160
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	MDM2 proto-oncogene	Homo sapiens	74-78
34992144-0	2022	Small-molecule NSC59984 induces mutant p53 degradation through a ROS-ERK2-MDM2 axis in cancer cells.	Reactive Oxygen Species	65-68	MDM2 proto-oncogene	Homo sapiens	74-78
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	MDM2 proto-oncogene	Homo sapiens	125-129
34992144-6	2022	The NSC59984-sustained ERK2 activation is required for MDM2 phosphorylation at serine-166.	Serine	79-85	MDM2 proto-oncogene	Homo sapiens	55-59
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	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	217-221
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	MDM2 proto-oncogene	Homo sapiens	36-40
35408798-9	2022	Indeed, EAPB0503 selectively downregulates HDM2 expression and activates the p53 pathway in NPM1c expressing cells, resulting in apoptosis.	EAPB0503	8-16	MDM2 proto-oncogene	Homo sapiens	43-47
35440992-6	2022	Notably, the synthetic utility of a reversed 1,3-DC/(H/D-Ex) protocol has been demonstrated by catalytic asymmetric synthesis of deuterium-labelled MDM2 antagonist idasanutlin (RG7388) with high deuterium incorporation.	Deuterium	129-138	MDM2 proto-oncogene	Homo sapiens	148-152
35326742-8	2022	Inhibition of MDM2 by RNAi, or by the MDM2/XIAP dual inhibitor MX69, significantly enhanced the sensitivity of resistant HMCLs and primary MM samples to bortezomib and other anti-myeloma drugs, demonstrating that MDM2 can modulate drug response.	MX69	63-67	MDM2 proto-oncogene	Homo sapiens	14-18
35326742-8	2022	Inhibition of MDM2 by RNAi, or by the MDM2/XIAP dual inhibitor MX69, significantly enhanced the sensitivity of resistant HMCLs and primary MM samples to bortezomib and other anti-myeloma drugs, demonstrating that MDM2 can modulate drug response.	MX69	63-67	MDM2 proto-oncogene	Homo sapiens	38-42
35326742-8	2022	Inhibition of MDM2 by RNAi, or by the MDM2/XIAP dual inhibitor MX69, significantly enhanced the sensitivity of resistant HMCLs and primary MM samples to bortezomib and other anti-myeloma drugs, demonstrating that MDM2 can modulate drug response.	MX69	63-67	MDM2 proto-oncogene	Homo sapiens	213-217
35326742-8	2022	Inhibition of MDM2 by RNAi, or by the MDM2/XIAP dual inhibitor MX69, significantly enhanced the sensitivity of resistant HMCLs and primary MM samples to bortezomib and other anti-myeloma drugs, demonstrating that MDM2 can modulate drug response.	Bortezomib	153-163	MDM2 proto-oncogene	Homo sapiens	14-18
35326742-8	2022	Inhibition of MDM2 by RNAi, or by the MDM2/XIAP dual inhibitor MX69, significantly enhanced the sensitivity of resistant HMCLs and primary MM samples to bortezomib and other anti-myeloma drugs, demonstrating that MDM2 can modulate drug response.	Bortezomib	153-163	MDM2 proto-oncogene	Homo sapiens	38-42
35326742-8	2022	Inhibition of MDM2 by RNAi, or by the MDM2/XIAP dual inhibitor MX69, significantly enhanced the sensitivity of resistant HMCLs and primary MM samples to bortezomib and other anti-myeloma drugs, demonstrating that MDM2 can modulate drug response.	Bortezomib	153-163	MDM2 proto-oncogene	Homo sapiens	213-217
35440992-6	2022	Notably, the synthetic utility of a reversed 1,3-DC/(H/D-Ex) protocol has been demonstrated by catalytic asymmetric synthesis of deuterium-labelled MDM2 antagonist idasanutlin (RG7388) with high deuterium incorporation.	RG7388	164-175	MDM2 proto-oncogene	Homo sapiens	148-152
35440992-6	2022	Notably, the synthetic utility of a reversed 1,3-DC/(H/D-Ex) protocol has been demonstrated by catalytic asymmetric synthesis of deuterium-labelled MDM2 antagonist idasanutlin (RG7388) with high deuterium incorporation.	RG7388	177-183	MDM2 proto-oncogene	Homo sapiens	148-152
35440992-6	2022	Notably, the synthetic utility of a reversed 1,3-DC/(H/D-Ex) protocol has been demonstrated by catalytic asymmetric synthesis of deuterium-labelled MDM2 antagonist idasanutlin (RG7388) with high deuterium incorporation.	Deuterium	195-204	MDM2 proto-oncogene	Homo sapiens	148-152
35620326-8	2022	When HCT-116 cells were treated with different concentrations of apatinibin combination with piperine, the synergistic effects were observed (combination index < 1).In HCT-116 cells treated with apatinib and piperine at the concentrations of 0.5xIC50 and0.2xIC50, the MDM-2 gene expression was downregulated and NO levels increased comparedto the untreated control cells and related single treatments.	apatinib	195-203	MDM2 proto-oncogene	Homo sapiens	268-273
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	MDM2 proto-oncogene	Homo sapiens	28-34
35620326-0	2022	Regulatory Effects of Apatinib in Combination with Piperine on MDM-2 Gene Expression, Glutathione Peroxidase Activity and Nitric Oxide level as Mechanisms of Cytotoxicity in Colorectal Cancer Cells.	apatinib	22-30	MDM2 proto-oncogene	Homo sapiens	63-68
35620326-0	2022	Regulatory Effects of Apatinib in Combination with Piperine on MDM-2 Gene Expression, Glutathione Peroxidase Activity and Nitric Oxide level as Mechanisms of Cytotoxicity in Colorectal Cancer Cells.	piperine	51-59	MDM2 proto-oncogene	Homo sapiens	63-68
35620326-5	2022	The potential cytotoxic mechanisms of apatinib andpiperine were investigated by evaluating MDM-2 gene expression ratio using real-time PCRassay.	apatinib andpiperine	38-58	MDM2 proto-oncogene	Homo sapiens	91-96
35620326-8	2022	When HCT-116 cells were treated with different concentrations of apatinibin combination with piperine, the synergistic effects were observed (combination index < 1).In HCT-116 cells treated with apatinib and piperine at the concentrations of 0.5xIC50 and0.2xIC50, the MDM-2 gene expression was downregulated and NO levels increased comparedto the untreated control cells and related single treatments.	apatinibin	65-75	MDM2 proto-oncogene	Homo sapiens	268-273
35620326-8	2022	When HCT-116 cells were treated with different concentrations of apatinibin combination with piperine, the synergistic effects were observed (combination index < 1).In HCT-116 cells treated with apatinib and piperine at the concentrations of 0.5xIC50 and0.2xIC50, the MDM-2 gene expression was downregulated and NO levels increased comparedto the untreated control cells and related single treatments.	piperine	93-101	MDM2 proto-oncogene	Homo sapiens	268-273
35179215-6	2022	Using cell viability, colony formation and methylcellulose assays it was found that genetic MDM2 inhibition with short hairpin RNA or chemical MDM2 inhibition with small molecule inhibitors, Nutlin3 and idasanutlin (RG7388) decreased the growth of ATRT cell lines.	nutlin 3	191-198	MDM2 proto-oncogene	Homo sapiens	92-96
35179215-6	2022	Using cell viability, colony formation and methylcellulose assays it was found that genetic MDM2 inhibition with short hairpin RNA or chemical MDM2 inhibition with small molecule inhibitors, Nutlin3 and idasanutlin (RG7388) decreased the growth of ATRT cell lines.	nutlin 3	191-198	MDM2 proto-oncogene	Homo sapiens	143-147
35179215-6	2022	Using cell viability, colony formation and methylcellulose assays it was found that genetic MDM2 inhibition with short hairpin RNA or chemical MDM2 inhibition with small molecule inhibitors, Nutlin3 and idasanutlin (RG7388) decreased the growth of ATRT cell lines.	RG7388	203-214	MDM2 proto-oncogene	Homo sapiens	92-96
35179215-6	2022	Using cell viability, colony formation and methylcellulose assays it was found that genetic MDM2 inhibition with short hairpin RNA or chemical MDM2 inhibition with small molecule inhibitors, Nutlin3 and idasanutlin (RG7388) decreased the growth of ATRT cell lines.	RG7388	203-214	MDM2 proto-oncogene	Homo sapiens	143-147
35179215-6	2022	Using cell viability, colony formation and methylcellulose assays it was found that genetic MDM2 inhibition with short hairpin RNA or chemical MDM2 inhibition with small molecule inhibitors, Nutlin3 and idasanutlin (RG7388) decreased the growth of ATRT cell lines.	RG7388	216-222	MDM2 proto-oncogene	Homo sapiens	92-96
35179215-6	2022	Using cell viability, colony formation and methylcellulose assays it was found that genetic MDM2 inhibition with short hairpin RNA or chemical MDM2 inhibition with small molecule inhibitors, Nutlin3 and idasanutlin (RG7388) decreased the growth of ATRT cell lines.	RG7388	216-222	MDM2 proto-oncogene	Homo sapiens	143-147
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	MDM2 proto-oncogene	Homo sapiens	69-73
35045964-0	2022	Correction: SAR405838: A Novel and Potent Inhibitor of the MDM2:p53 Axis for the Treatment of Dedifferentiated Liposarcoma.	SAR405838	12-21	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	46-50
35154467-6	2022	Importantly, the m6A level of mdm2 mRNA was significant lower after knock-down of METTL3 and METTL14 examined by m6A-RIP and mdm2 qPCR assay, and the half-life of mdm2 under actinomycin-D treatment became shorter.	Dactinomycin	174-185	MDM2 proto-oncogene	Homo sapiens	30-34
35154467-6	2022	Importantly, the m6A level of mdm2 mRNA was significant lower after knock-down of METTL3 and METTL14 examined by m6A-RIP and mdm2 qPCR assay, and the half-life of mdm2 under actinomycin-D treatment became shorter.	Dactinomycin	174-185	MDM2 proto-oncogene	Homo sapiens	163-167
34176458-1	2022	BACKGROUND: Spirooxindoles are privileged scaffolds in medicinal chemistry and were identified through Wang"s pioneering work as inhibitors of MDM2-p53 interactions.	spirooxindoles	12-26	MDM2 proto-oncogene	Homo sapiens	143-147
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	MDM2 proto-oncogene	Homo sapiens	119-123
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	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	50-54
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	MDM2 proto-oncogene	Homo sapiens	153-157
35205710-7	2022	Indeed, miR-101-3p regulates RPL11 localization and its interaction with MDM2 by inhibiting the USP47-induced deubiquitination of RPL11.	mir-101-3p	8-18	MDM2 proto-oncogene	Homo sapiens	73-77
34861697-2	2022	Here we report that MDM2 inhibitors (MDM2i) navtemadlin and idasanutlin have potent in vivo activity in EBV+ B-cell lymphoma established in immunocompromised mice.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(1-(isopropylsulfonyl)-3-methylbutan-2-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	44-55	MDM2 proto-oncogene	Homo sapiens	20-24
34861697-2	2022	Here we report that MDM2 inhibitors (MDM2i) navtemadlin and idasanutlin have potent in vivo activity in EBV+ B-cell lymphoma established in immunocompromised mice.	RG7388	60-71	MDM2 proto-oncogene	Homo sapiens	20-24
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	MDM2 proto-oncogene	Homo sapiens	84-88
33862513-7	2021	WB214 and its related analogues did not bind to MDM2 in the p53 binding region and MDM2 was discovered as a novel neo-substrate of the E3 ligase cereblon.	wb214	0-5	MDM2 proto-oncogene	Homo sapiens	83-87
33955525-8	2021	Since EMT contributes to increased drug resistance in tumor cells, the present study also explored the relationship between MDM2 and drug sensitivity using an MTT assay, and identified that MDM2 promoted cell insensitivity to silibinin treatment in an EMT-dependent manner.	monooxyethylene trimethylolpropane tristearate	159-162	MDM2 proto-oncogene	Homo sapiens	190-194
33955525-8	2021	Since EMT contributes to increased drug resistance in tumor cells, the present study also explored the relationship between MDM2 and drug sensitivity using an MTT assay, and identified that MDM2 promoted cell insensitivity to silibinin treatment in an EMT-dependent manner.	Silybin	226-235	MDM2 proto-oncogene	Homo sapiens	190-194
33880579-0	2021	Germacrone induces lung cancer cell apoptosis and cell cycle arrest via the Akt/MDM2/p53 signaling pathway.	germacrone	0-10	MDM2 proto-oncogene	Homo sapiens	80-84
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	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	134-138
34032749-0	2021	The important role of MDM2, RPL5, and TP53 in mycophenolic acid-induced cleft lip and palate.	Mycophenolic Acid	46-63	MDM2 proto-oncogene	Homo sapiens	22-26
34044759-0	2021	miR-29a sensitizes the response of glioma cells to temozolomide by modulating the P53/MDM2 feedback loop.	Temozolomide	51-63	MDM2 proto-oncogene	Homo sapiens	86-90
34044759-8	2021	Moreover, miR-29a regulating p53/MDM2 signaling sensitized the response of glioma cells to temozolomide treatment.	Temozolomide	91-103	MDM2 proto-oncogene	Homo sapiens	33-37
33985974-0	2021	Alteration of MDM2 by the small molecule YF438 exerts anti-tumor effects in triple-negative breast cancer.	yf438	41-46	MDM2 proto-oncogene	Homo sapiens	14-18
33985974-3	2021	Proteomic and biochemical studies revealed that YF438 significantly downregulated MDM2 expression.	yf438	48-53	MDM2 proto-oncogene	Homo sapiens	82-86
33985974-4	2021	In parallel, loss of MDM2 expression or blocking MDM2 E3 ligase activity rendered TNBC cells less sensitive to YF438 treatment, revealing an essential role of MDM2 E3 ligase activity in YF438-induced inhibition of TNBC.	yf438	111-116	MDM2 proto-oncogene	Homo sapiens	49-53
33985974-4	2021	In parallel, loss of MDM2 expression or blocking MDM2 E3 ligase activity rendered TNBC cells less sensitive to YF438 treatment, revealing an essential role of MDM2 E3 ligase activity in YF438-induced inhibition of TNBC.	yf438	111-116	MDM2 proto-oncogene	Homo sapiens	49-53
33985974-4	2021	In parallel, loss of MDM2 expression or blocking MDM2 E3 ligase activity rendered TNBC cells less sensitive to YF438 treatment, revealing an essential role of MDM2 E3 ligase activity in YF438-induced inhibition of TNBC.	yf438	186-191	MDM2 proto-oncogene	Homo sapiens	21-25
33985974-4	2021	In parallel, loss of MDM2 expression or blocking MDM2 E3 ligase activity rendered TNBC cells less sensitive to YF438 treatment, revealing an essential role of MDM2 E3 ligase activity in YF438-induced inhibition of TNBC.	yf438	186-191	MDM2 proto-oncogene	Homo sapiens	49-53
33985974-4	2021	In parallel, loss of MDM2 expression or blocking MDM2 E3 ligase activity rendered TNBC cells less sensitive to YF438 treatment, revealing an essential role of MDM2 E3 ligase activity in YF438-induced inhibition of TNBC.	yf438	186-191	MDM2 proto-oncogene	Homo sapiens	49-53
33985974-5	2021	Mechanistically, YF438 disturbed the interaction between HDAC1 and MDM2, induced the dissociation of MDM2-MDMX, and subsequently increased MDM2 self-ubiquitination to accelerate its degradation, which ultimately inhibited growth and metastasis of TNBC cells.	yf438	17-22	MDM2 proto-oncogene	Homo sapiens	67-71
33985974-5	2021	Mechanistically, YF438 disturbed the interaction between HDAC1 and MDM2, induced the dissociation of MDM2-MDMX, and subsequently increased MDM2 self-ubiquitination to accelerate its degradation, which ultimately inhibited growth and metastasis of TNBC cells.	yf438	17-22	MDM2 proto-oncogene	Homo sapiens	101-105
33985974-5	2021	Mechanistically, YF438 disturbed the interaction between HDAC1 and MDM2, induced the dissociation of MDM2-MDMX, and subsequently increased MDM2 self-ubiquitination to accelerate its degradation, which ultimately inhibited growth and metastasis of TNBC cells.	yf438	17-22	MDM2 proto-oncogene	Homo sapiens	101-105
33985974-7	2021	Collectively, these findings show that MDM2 plays an essential role in TNBC progression and targeting the HDAC1-MDM2-MDMX signaling axis with YF438 may provide a promising therapeutic option for TNBC.	yf438	142-147	MDM2 proto-oncogene	Homo sapiens	39-43
33985974-7	2021	Collectively, these findings show that MDM2 plays an essential role in TNBC progression and targeting the HDAC1-MDM2-MDMX signaling axis with YF438 may provide a promising therapeutic option for TNBC.	yf438	142-147	MDM2 proto-oncogene	Homo sapiens	112-116
33985974-8	2021	Furthermore, this novel underlying mechanism of a hydroxamate-based HDACi in inducing MDM2 highlights the need for further development of HDACi for TNBC treatment.	hydroxamate	50-61	MDM2 proto-oncogene	Homo sapiens	86-90
33904383-11	2021	Collectively, our results uncovered the regenerative role of miR-140-3p in IDD via regulation of the KLF5/N-cadherin/MDM2/Slug axis, which could be a potential therapeutic target for IDD.	mir-140-3p	61-71	MDM2 proto-oncogene	Homo sapiens	117-121
33581134-0	2021	CXCR4 antagonism sensitizes cancer cells to novel indole-based MDM2/4 inhibitors in glioblastoma multiforme.	indole	50-56	MDM2 proto-oncogene	Homo sapiens	63-69
33952867-0	2021	Elaboration of non-naturally occurring helical tripeptides as p53-MDM2/MDMX interaction inhibitors.	tripeptides	47-58	MDM2 proto-oncogene	Homo sapiens	66-70
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	194-198
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	MDM2 proto-oncogene	Homo sapiens	194-198
33581134-8	2021	The dual MDM2/4 inhibitor RS3594 and the CXCR4 antagonist AMD3100 reduced GBM cell invasiveness and migration in single-agent treatment and mainly in combination.	rs3594	26-32	MDM2 proto-oncogene	Homo sapiens	9-15
33924734-0	2021	Feasibility of Developing Radiotracers for MDM2: Synthesis and Preliminary Evaluation of an 18F-Labeled Analogue of the MDM2 Inhibitor SP-141.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	135-141	MDM2 proto-oncogene	Homo sapiens	43-47
33850004-7	2021	Overall, high-throughput drug screening identified the MDM2 inhibitor idasanutlin as a promising resensitizing agent for venetoclax-resistant neuroblastoma cell lines.	RG7388	70-81	MDM2 proto-oncogene	Homo sapiens	55-59
33917342-0	2021	Pharmacological Inhibition of WIP1 Sensitizes Acute Myeloid Leukemia Cells to the MDM2 Inhibitor Nutlin-3a.	nutlin 3	97-106	MDM2 proto-oncogene	Homo sapiens	82-86
33924734-0	2021	Feasibility of Developing Radiotracers for MDM2: Synthesis and Preliminary Evaluation of an 18F-Labeled Analogue of the MDM2 Inhibitor SP-141.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	135-141	MDM2 proto-oncogene	Homo sapiens	120-124
33924734-2	2021	Herein we investigate the feasibility of developing 18F-labeled compounds based on the small molecule inhibitor SP-141 for imaging tumor MDM2 expression levels with positron emission tomography (PET).	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	112-118	MDM2 proto-oncogene	Homo sapiens	137-141
33924734-3	2021	Three nonradioactive fluorinated SP-141 analogues, 1-3, were synthesized, and their binding to the MDM2 protein was analyzed by surface plasmon resonance (SPR).	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	33-39	MDM2 proto-oncogene	Homo sapiens	99-103
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	72-78	MDM2 proto-oncogene	Homo sapiens	114-118
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	72-76
33733756-4	2021	Mass-based analysis successfully revealed the kinetics of covalent inhibition and the modification sites on HDM2 to be the N-terminal alpha-amine and Tyr67, both rarely seen in traditional covalent inhibitors.	n-terminal	123-133	MDM2 proto-oncogene	Homo sapiens	108-112
33733756-4	2021	Mass-based analysis successfully revealed the kinetics of covalent inhibition and the modification sites on HDM2 to be the N-terminal alpha-amine and Tyr67, both rarely seen in traditional covalent inhibitors.	alpha-amine	134-145	MDM2 proto-oncogene	Homo sapiens	108-112
33734108-3	2021	In this study, formalin fixed paraffin embedded clinical specimens (16 liposarcomas and 19 benign lipomatous tumors) were used to detect MDM2 amplification and other chromosomal alterations in WDLS/ALT and DDLS by single nucleotide polymorphism-based chromosome microarray (CMA).	Formaldehyde	15-23	MDM2 proto-oncogene	Homo sapiens	137-141
33734108-3	2021	In this study, formalin fixed paraffin embedded clinical specimens (16 liposarcomas and 19 benign lipomatous tumors) were used to detect MDM2 amplification and other chromosomal alterations in WDLS/ALT and DDLS by single nucleotide polymorphism-based chromosome microarray (CMA).	Paraffin	30-38	MDM2 proto-oncogene	Homo sapiens	137-141
33734108-12	2021	In conclusion, this study demonstrated that CMA on routine formalin fixed paraffin embedded tissue is a sensitive and specific clinical test for detection of MDM2 gene amplification.	Formaldehyde	59-67	MDM2 proto-oncogene	Homo sapiens	158-162
33734108-12	2021	In conclusion, this study demonstrated that CMA on routine formalin fixed paraffin embedded tissue is a sensitive and specific clinical test for detection of MDM2 gene amplification.	Paraffin	74-82	MDM2 proto-oncogene	Homo sapiens	158-162
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	MDM2 proto-oncogene	Homo sapiens	24-28
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	MDM2 proto-oncogene	Homo sapiens	24-28
33686772-0	2021	Safety and pharmacokinetics of milademetan, a MDM2 inhibitor, in Japanese patients with solid tumors: A phase I study.	Milademetan	31-42	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	81-85
33668835-4	2021	In this study, we used the MDM2 antagonist idasanutlin (RG7388) to investigate the responses of primary human macrophages to pharmacological p53 activation.	RG7388	43-54	MDM2 proto-oncogene	Homo sapiens	27-31
33668835-4	2021	In this study, we used the MDM2 antagonist idasanutlin (RG7388) to investigate the responses of primary human macrophages to pharmacological p53 activation.	RG7388	56-62	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	11-15
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	MDM2 proto-oncogene	Homo sapiens	174-178
33663585-2	2021	We sought to determine the antitumor efficacy of the combination of ALRN-6924, a dual inhibitor of MDM2/MDMX, with chemotherapy in ER+ breast cancer models.	alrn-6924	68-77	MDM2 proto-oncogene	Homo sapiens	99-103
33676897-9	2021	Additionally, beta-TrCP1 impedes MDM2 accumulation via abrogation of its lysine 63-linked polyubiquitination by beta-TrCP2.	Lysine	73-79	MDM2 proto-oncogene	Homo sapiens	33-37
33103305-7	2021	Furthermore, addition of the MDM2 inhibitor Nutiln-3 drastically reduced the FRET signal, indicating that the FRET probe competes with Nutiln-3 for MDM2 binding.	nutiln-3	44-52	MDM2 proto-oncogene	Homo sapiens	29-33
33103305-7	2021	Furthermore, addition of the MDM2 inhibitor Nutiln-3 drastically reduced the FRET signal, indicating that the FRET probe competes with Nutiln-3 for MDM2 binding.	nutiln-3	44-52	MDM2 proto-oncogene	Homo sapiens	148-152
33103305-7	2021	Furthermore, addition of the MDM2 inhibitor Nutiln-3 drastically reduced the FRET signal, indicating that the FRET probe competes with Nutiln-3 for MDM2 binding.	nutiln-3	135-143	MDM2 proto-oncogene	Homo sapiens	29-33
33103305-7	2021	Furthermore, addition of the MDM2 inhibitor Nutiln-3 drastically reduced the FRET signal, indicating that the FRET probe competes with Nutiln-3 for MDM2 binding.	nutiln-3	135-143	MDM2 proto-oncogene	Homo sapiens	148-152
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	MDM2 proto-oncogene	Homo sapiens	26-32
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	MDM2 proto-oncogene	Homo sapiens	80-86
33648535-14	2021	CONCLUSIONS: Selinexor showed a moderate antitumor activity in three DDLPS PDXs, which was, however, consistently higher than doxorubicin across all different models regardless the extent of MDM2 amplification and the histological differentiation.	selinexor	13-22	MDM2 proto-oncogene	Homo sapiens	191-195
33460527-0	2021	Phase 1 Concentration-QTc and Cardiac Safety Analysis of the MDM2 Antagonist KRT-232 in Patients With Advanced Solid Tumors, Multiple Myeloma, or Acute Myeloid Leukemia.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(1-(isopropylsulfonyl)-3-methylbutan-2-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	77-84	MDM2 proto-oncogene	Homo sapiens	61-65
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	MDM2 proto-oncogene	Homo sapiens	135-139
33433933-7	2021	Treatment with the MDM-2 antagonist Nutlin-3a also induced mitochondrial elongation through the PKA-Drp1 pathway in IMR90 normal human cells.	nutlin 3	36-45	MDM2 proto-oncogene	Homo sapiens	19-24
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	MDM2 proto-oncogene	Homo sapiens	28-32
33283357-4	2021	Mechanistically, defactinib dose and time-dependently induced the dissociation of phosphoinositide-3-kinase (PI3K) from FAK, resultantly led to blockade of protein kinase B (AKT) signaling, and the expression of several oncogenes, such as SOX2, MYC, EGFR, MET, MDM2, or TGFBR2, identified by microarray and real-time polymerase chain reaction assay.	defactinib	17-27	MDM2 proto-oncogene	Homo sapiens	261-265
33579943-0	2021	EGCG binds intrinsically disordered N-terminal domain of p53 and disrupts p53-MDM2 interaction.	epigallocatechin gallate	0-4	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	80-84
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	MDM2 proto-oncogene	Homo sapiens	123-127
32737944-3	2021	Binding studies with MDM2 showed that the antiproliferative activity of tryptophanol-derived isoindolinones does not involve the inhibition of the main negative regulator of the p53 protein.	tryptophanol	72-84	MDM2 proto-oncogene	Homo sapiens	21-25
32737944-3	2021	Binding studies with MDM2 showed that the antiproliferative activity of tryptophanol-derived isoindolinones does not involve the inhibition of the main negative regulator of the p53 protein.	phthalimidine	93-107	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	111-115
33262524-5	2021	Furthermore, miR-10a inhibition induced synergy between MDM2 inhibitor Nutlin-3a and cytarabine in both in vitro and in vivo AML models.	nutlin 3	71-80	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	139-143
33723162-0	2021	Hypericin induces apoptosis in K562 cells via downregulation of Myc and Mdm2.	hypericin	0-9	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	161-165
33723162-10	2021	Conclusion: The results showed that hypericin exerts its cytotoxicity on K562 cancer cells by downregulating Mdm2 and Myc.	hypericin	36-45	MDM2 proto-oncogene	Homo sapiens	109-113
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	MDM2 proto-oncogene	Homo sapiens	122-126
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	MDM2 proto-oncogene	Homo sapiens	124-128
33425912-0	2020	EGCG Enhanced the Anti-tumor Effect of Doxorubicine in Bladder Cancer via NF-kappaB/MDM2/p53 Pathway.	epigallocatechin gallate	0-4	MDM2 proto-oncogene	Homo sapiens	84-88
33425912-0	2020	EGCG Enhanced the Anti-tumor Effect of Doxorubicine in Bladder Cancer via NF-kappaB/MDM2/p53 Pathway.	Doxorubicin	39-51	MDM2 proto-oncogene	Homo sapiens	84-88
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	MDM2 proto-oncogene	Homo sapiens	115-119
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	MDM2 proto-oncogene	Homo sapiens	115-119
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	MDM2 proto-oncogene	Homo sapiens	218-222
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	MDM2 proto-oncogene	Homo sapiens	218-222
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	MDM2 proto-oncogene	Homo sapiens	75-79
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	MDM2 proto-oncogene	Homo sapiens	75-79
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	MDM2 proto-oncogene	Homo sapiens	35-39
33012506-6	2020	These results support that CYZ2017 might be a promising p53-MDM2 interaction inhibitor with good anti-tumor activity.	cyz2017	27-34	MDM2 proto-oncogene	Homo sapiens	60-64
33202864-6	2020	A possible synergism was observed with SNP309 in promoter P2 of MDM2.	snp309	39-45	MDM2 proto-oncogene	Homo sapiens	64-68
33039292-6	2020	RESULTS: Treatment of gemcitabine (nucleoside analogue anticancer agent) to pancreatic cancer (Panc-1, MiaPaca-2) and breast cancer (MDA-MB-231) cells amplified MDM-2 expression along with increase in EMT properties.	gemcitabine	22-33	MDM2 proto-oncogene	Homo sapiens	161-166
33039292-6	2020	RESULTS: Treatment of gemcitabine (nucleoside analogue anticancer agent) to pancreatic cancer (Panc-1, MiaPaca-2) and breast cancer (MDA-MB-231) cells amplified MDM-2 expression along with increase in EMT properties.	Nucleosides	35-45	MDM2 proto-oncogene	Homo sapiens	161-166
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	MDM2 proto-oncogene	Homo sapiens	169-173
33140956-3	2020	The most potent helical heterogeneous 1:1 alpha/Sulfono-gamma-AA peptides were shown to bind tightly to MDM2 and MDMX, with Kd of 19.3 and 66.8 nM, respectively.	alpha/sulfono-gamma-aa	42-64	MDM2 proto-oncogene	Homo sapiens	104-108
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	MDM2 proto-oncogene	Homo sapiens	198-202
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	MDM2 proto-oncogene	Homo sapiens	201-205
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	MDM2 proto-oncogene	Homo sapiens	167-171
33144587-9	2020	MDM2 and mTORC1/2 targeted drugs showed efficacy in the cisplatin sensitive PDX models.	Cisplatin	56-65	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	160-164
32827690-4	2020	In this study, we are reporting the differential mechanism of cell death induced by the two small-molecule inhibitors, named RG-7388 and Nutlin-3, that are specific for MDM2 in SJSA-1 Osteosarcoma cells (OS).	RG7388	125-132	MDM2 proto-oncogene	Homo sapiens	169-173
32561413-3	2020	Although phosphorylation at serine (S) 166 site by AKT increases Mdm2 activity, phosphatases of Mdm2 have been still elusive.	Serine	28-34	MDM2 proto-oncogene	Homo sapiens	65-69
33092134-6	2020	Combining erdafitinib with the MDM2 antagonist RG7388 exerted a synergistic effect on viability, apoptosis, and clonogenicity in one WDLPS and two DDLPS cell lines.	RG7388	47-53	MDM2 proto-oncogene	Homo sapiens	31-35
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	MDM2 proto-oncogene	Homo sapiens	92-96
32945383-12	2020	RSV elevated the p53 levels and decreased the phosphorylated (p-)Mdm2 and p-Akt levels.	Resveratrol	0-3	MDM2 proto-oncogene	Homo sapiens	65-69
32020437-0	2020	Phase 1 study of the MDM2 antagonist RO6839921 in patients with acute myeloid leukemia.	ro6839921	37-46	MDM2 proto-oncogene	Homo sapiens	21-25
32020437-2	2020	RO6839921 is an inactive pegylated prodrug of the oral MDM2 antagonist idasanutlin (active principle [AP]) that allows for IV administration.	RG7388	71-82	MDM2 proto-oncogene	Homo sapiens	55-59
33061618-5	2020	Luciferase reporter assays were performed to determine the effect of miR-758-3p on MDM2.	mir-758-3p	69-79	MDM2 proto-oncogene	Homo sapiens	83-87
33061618-11	2020	Moreover, miR-758-3p was a modulator of MDM2 in ccRCC.	mir-758-3p	10-20	MDM2 proto-oncogene	Homo sapiens	40-44
32583936-7	2020	Towards the development of new anticancer drugs, we herein describe a polypharmacology approach for the dual inhibition of Mcl-1 and HDM2 by employing three densely functionalized isoxazoles, pyrazoles, and thiazoles as mimetics of key alpha-helical domains of their partner proteins.	Isoxazoles	180-190	MDM2 proto-oncogene	Homo sapiens	133-137
32583936-7	2020	Towards the development of new anticancer drugs, we herein describe a polypharmacology approach for the dual inhibition of Mcl-1 and HDM2 by employing three densely functionalized isoxazoles, pyrazoles, and thiazoles as mimetics of key alpha-helical domains of their partner proteins.	Pyrazoles	192-201	MDM2 proto-oncogene	Homo sapiens	133-137
32583936-7	2020	Towards the development of new anticancer drugs, we herein describe a polypharmacology approach for the dual inhibition of Mcl-1 and HDM2 by employing three densely functionalized isoxazoles, pyrazoles, and thiazoles as mimetics of key alpha-helical domains of their partner proteins.	Thiazoles	207-216	MDM2 proto-oncogene	Homo sapiens	133-137
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	MDM2 proto-oncogene	Homo sapiens	114-118
32828283-5	2020	Our study showed that constitutive ubiquitination of beta-arrestin, accompanied by nuclear to cytoplasmic translocation of Mdm2, was observed in cells expressing desensitizing GPCRs (dopamine D3 receptor, K149C-dopamine D2 receptor, beta2 adrenoceptor, and lysophosphatidic acid receptor 1).	Dopamine	211-219	MDM2 proto-oncogene	Homo sapiens	123-127
32828283-6	2020	In contrast, Mdm2 was observed in the nucleus in cells expressing non-desensitizing GPCRs (dopamine D2 receptor, C147K-dopamine D3 receptor, and dopamine D4 receptor).	Dopamine	91-99	MDM2 proto-oncogene	Homo sapiens	13-17
32561413-3	2020	Although phosphorylation at serine (S) 166 site by AKT increases Mdm2 activity, phosphatases of Mdm2 have been still elusive.	Serine	36-37	MDM2 proto-oncogene	Homo sapiens	65-69
32705219-0	2020	MDM2 as a target for ellagic acid-mediated suppression of prostate cancer cells in vitro.	Ellagic Acid	21-33	MDM2 proto-oncogene	Homo sapiens	0-4
32826336-0	2020	Withdrawal: Mdm2 directs the ubiquitination of beta-arrestin-sequestered cAMP phosphodiesterase-4D5.	Cyclic AMP	73-77	MDM2 proto-oncogene	Homo sapiens	12-16
32874188-11	2020	The ATM inhibitor KU55993 reduced the levels of PD-L1 under conditions where Nutlin-3 induces PD-L1, indicating that MDM2 and ATM have opposing effects on PD-L1 steady-state levels.	ku55993	18-25	MDM2 proto-oncogene	Homo sapiens	117-121
32874188-14	2020	Conclusion: Genetic inactivation of TP53, or the use of the MDM2 ligand Nutlin-3, alters the expression of the immune blockade receptors PD-L1 and CD276.	nutlin 3	72-80	MDM2 proto-oncogene	Homo sapiens	60-64
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	MDM2 proto-oncogene	Homo sapiens	94-98
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	MDM2 proto-oncogene	Homo sapiens	100-104
32793900-6	2020	Computational alanine scanning mutagenesis was performed to predict changes in Gibbs free energy that are associated with mutating residues at the positive control (PMI/MDM2) or SARS RBD/ACE2 binding interface to alanine.	Alanine	213-220	MDM2 proto-oncogene	Homo sapiens	169-173
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	MDM2 proto-oncogene	Homo sapiens	109-113
32759684-5	2020	Comparing metabolomic profiles between MDM2 higher and lower amplification cells yielded a total of 17 differentially abundant metabolites across both panels (FDR < 0.05, log2 fold change < 0.75), including ceramides, glycosylated ceramides, and sphingomyelins.	Ceramides	207-216	MDM2 proto-oncogene	Homo sapiens	39-43
32593915-8	2020	Several pre-clinical approaches have proven successful in overcoming cisplatin resistance, including specific targeting of PARP, MDM2 or AKT/mTOR combined with cisplatin.	Cisplatin	69-78	MDM2 proto-oncogene	Homo sapiens	129-133
32611363-10	2020	In vitro experiments suggested that MDM2 amplification induces primary resistance to erlotinib.	Erlotinib Hydrochloride	85-94	MDM2 proto-oncogene	Homo sapiens	36-40
31734832-0	2020	A phase 1 study of the MDM2 antagonist RO6839921, a pegylated prodrug of idasanutlin, in patients with advanced solid tumors.	RG7388	73-84	MDM2 proto-oncogene	Homo sapiens	23-27
31734832-2	2020	RO6839921 is an inactive pegylated prodrug of idasanutlin, an MDM2 antagonist, developed for intravenous administration.	RG7388	46-57	MDM2 proto-oncogene	Homo sapiens	62-66
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	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	86-90
32471716-0	2020	MDM2 phosphorylation mediates H2O2-induced lens epithelial cells apoptosis and age-related cataract.	Hydrogen Peroxide	30-34	MDM2 proto-oncogene	Homo sapiens	0-4
32471716-2	2020	This study aimed to investigate the effects of MDM2 phosphorylation in ARC and H2O2-induced lens epithelial cells apoptosis.	Hydrogen Peroxide	79-83	MDM2 proto-oncogene	Homo sapiens	47-51
32471716-6	2020	It was confirmed that MDM2 could regulate lens epithelial cell apoptosis, and MDM2 inhibitors could partly inhibited AKT"s role in suppressing apoptosis induced by H2O2.	Hydrogen Peroxide	164-168	MDM2 proto-oncogene	Homo sapiens	78-82
32471716-8	2020	Our study revealed that MDM2 phosphorylation mediated H2O2-induced lens epithelial cells apoptosis and ARC, which could provide new ideas for the clinical treatment of ARC.	Hydrogen Peroxide	54-58	MDM2 proto-oncogene	Homo sapiens	24-28
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	MDM2 proto-oncogene	Homo sapiens	24-28
32793491-0	2020	NVP-CGM097, an HDM2 Inhibitor, Antagonizes ATP-Binding Cassette Subfamily B Member 1-Mediated Drug Resistance.	NVP-CGM097	0-10	MDM2 proto-oncogene	Homo sapiens	15-19
32390036-0	2020	Diarylethene moiety as an enthalpy-entropy switch: photoisomerizable stapled peptides for modulating p53/MDM2 interaction.	diarylethene	0-12	MDM2 proto-oncogene	Homo sapiens	105-109
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	MDM2 proto-oncogene	Homo sapiens	56-60
32615946-12	2020	The combination Nutlin-3 (inhibition of MDM2) and PX-478 (inhibition of HIF-1alpha) could be confirmed for all three cell lines.	nutlin 3	16-24	MDM2 proto-oncogene	Homo sapiens	40-44
32630235-3	2020	The present study was designed to evaluate the in vitro and in vivo antitumor activity of a novel brain-penetrating small molecule MDM2 degrader, termed SP-141.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	153-159	MDM2 proto-oncogene	Homo sapiens	131-135
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	MDM2 proto-oncogene	Homo sapiens	45-49
32611363-11	2020	Over-expressed MDM2 elevated the IC50 value of erlotinib in HCC2279 line and reduced the inhibition rate.	Erlotinib Hydrochloride	47-56	MDM2 proto-oncogene	Homo sapiens	15-19
32448094-4	2021	Here, we used global peptide docking, normal molecular dynamics, Gaussian accelerated molecular dynamics (GaMD), two-dimensional (2D) potential of mean force (PMF) profiles, and solvated interaction energy (SIE) techniques to investigate the interactions of MDM2/MDMX with three N-to-C-terminal cyclic peptide-based inhibitors.	Peptides, Cyclic	295-309	MDM2 proto-oncogene	Homo sapiens	258-262
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	MDM2 proto-oncogene	Homo sapiens	38-42
32636834-8	2020	We have also found lysine residues in FOXP3 required for MDM2-mediated ubiquitination.	Lysine	19-25	MDM2 proto-oncogene	Homo sapiens	57-61
32459661-7	2020	These findings suggest resveratrol may alleviate osteoporosis at least in part by modulating the MDM2/p53 signaling pathway.	Resveratrol	23-34	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	237-241
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	MDM2 proto-oncogene	Homo sapiens	237-241
32453417-5	2020	The MDM2 serine 166 regulates the interaction with the E2F1 mRNA and deletion of MDM2 C-terminal RING domain results in a constitutive E2F1 mRNA binding.	Serine	9-15	MDM2 proto-oncogene	Homo sapiens	4-8
32453417-5	2020	The MDM2 serine 166 regulates the interaction with the E2F1 mRNA and deletion of MDM2 C-terminal RING domain results in a constitutive E2F1 mRNA binding.	Serine	9-15	MDM2 proto-oncogene	Homo sapiens	81-85
32522803-0	2020	Targeting MDM2-dependent serine metabolism as a therapeutic strategy for liposarcoma.	Serine	25-31	MDM2 proto-oncogene	Homo sapiens	10-14
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	MDM2 proto-oncogene	Homo sapiens	78-82
32522803-4	2020	Treatment of LPS cells with Nutlin-3A, a pharmacological inhibitor of the MDM2-p53 interaction, stabilized p53 but unexpectedly enhanced MDM2-mediated control of serine metabolism by increasing its recruitment to chromatin, likely explaining the poor clinical efficacy of this class of MDM2 inhibitors.	Serine	162-168	MDM2 proto-oncogene	Homo sapiens	137-141
32522803-4	2020	Treatment of LPS cells with Nutlin-3A, a pharmacological inhibitor of the MDM2-p53 interaction, stabilized p53 but unexpectedly enhanced MDM2-mediated control of serine metabolism by increasing its recruitment to chromatin, likely explaining the poor clinical efficacy of this class of MDM2 inhibitors.	Serine	162-168	MDM2 proto-oncogene	Homo sapiens	137-141
32522803-6	2020	Our data indicate that targeting MDM2 functions in serine metabolism represents a potential therapeutic strategy for LPS.	Serine	51-57	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	295-299
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	MDM2 proto-oncogene	Homo sapiens	227-231
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	MDM2 proto-oncogene	Homo sapiens	76-80
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	MDM2 proto-oncogene	Homo sapiens	143-147
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	MDM2 proto-oncogene	Homo sapiens	55-59
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	MDM2 proto-oncogene	Homo sapiens	74-78
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	MDM2 proto-oncogene	Homo sapiens	41-45
32448094-5	2021	We determined the possible cyclic peptide-MDM2/MDMX complex structures via 2D PMF profiles and SIE calculations.	Peptides, Cyclic	27-41	MDM2 proto-oncogene	Homo sapiens	42-46
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	MDM2 proto-oncogene	Homo sapiens	65-69
32392664-7	2020	RESULTS: In multivariate logistic regression, significantly increased risk of lung cancer was observed for MDM2 SNP309 in the dominant model (TG + GG vs. TT: OR, 2.13; 95% CI, 1.29 to 3.53).	snp309	112-118	MDM2 proto-oncogene	Homo sapiens	107-111
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	MDM2 proto-oncogene	Homo sapiens	80-84
32167393-2	2020	Idasanutlin is a small-molecule inhibitor of MDM2, a negative regulator of tumor suppressor p53.	RG7388	0-11	MDM2 proto-oncogene	Homo sapiens	45-49
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	MDM2 proto-oncogene	Homo sapiens	22-26
32392664-7	2020	RESULTS: In multivariate logistic regression, significantly increased risk of lung cancer was observed for MDM2 SNP309 in the dominant model (TG + GG vs. TT: OR, 2.13; 95% CI, 1.29 to 3.53).	Thioguanine	142-144	MDM2 proto-oncogene	Homo sapiens	107-111
32392664-8	2020	Stratification analysis revealed that age, sex, obesity, and smoking also increases the risk of lung cancer when carrying the MDM2 SNP309.	snp309	131-137	MDM2 proto-oncogene	Homo sapiens	126-130
32211658-0	2020	Cisplatin binds to the MDM2 RING finger domain and inhibits the ubiquitination activity.	Cisplatin	0-9	MDM2 proto-oncogene	Homo sapiens	23-27
32350255-4	2020	A crystal structure of phospho-Ser429 (pS429)-MDM2 bound to E2-ubiquitin reveals a unique 310-helical feature present in MDM2 homodimer that allows pS429 to stabilize the closed E2-ubiquitin conformation and thereby enhancing ubiquitin transfer.	phospho-ser429	23-37	MDM2 proto-oncogene	Homo sapiens	46-50
32350255-4	2020	A crystal structure of phospho-Ser429 (pS429)-MDM2 bound to E2-ubiquitin reveals a unique 310-helical feature present in MDM2 homodimer that allows pS429 to stabilize the closed E2-ubiquitin conformation and thereby enhancing ubiquitin transfer.	phospho-ser429	23-37	MDM2 proto-oncogene	Homo sapiens	121-125
32350255-4	2020	A crystal structure of phospho-Ser429 (pS429)-MDM2 bound to E2-ubiquitin reveals a unique 310-helical feature present in MDM2 homodimer that allows pS429 to stabilize the closed E2-ubiquitin conformation and thereby enhancing ubiquitin transfer.	ps429	39-44	MDM2 proto-oncogene	Homo sapiens	46-50
32350255-4	2020	A crystal structure of phospho-Ser429 (pS429)-MDM2 bound to E2-ubiquitin reveals a unique 310-helical feature present in MDM2 homodimer that allows pS429 to stabilize the closed E2-ubiquitin conformation and thereby enhancing ubiquitin transfer.	ps429	39-44	MDM2 proto-oncogene	Homo sapiens	121-125
32350255-4	2020	A crystal structure of phospho-Ser429 (pS429)-MDM2 bound to E2-ubiquitin reveals a unique 310-helical feature present in MDM2 homodimer that allows pS429 to stabilize the closed E2-ubiquitin conformation and thereby enhancing ubiquitin transfer.	Estradiol	60-62	MDM2 proto-oncogene	Homo sapiens	46-50
32350255-4	2020	A crystal structure of phospho-Ser429 (pS429)-MDM2 bound to E2-ubiquitin reveals a unique 310-helical feature present in MDM2 homodimer that allows pS429 to stabilize the closed E2-ubiquitin conformation and thereby enhancing ubiquitin transfer.	Estradiol	60-62	MDM2 proto-oncogene	Homo sapiens	121-125
32211658-1	2020	Cisplatin can directly bind to the RING finger domain of MDM2, leading to the zinc-release and protein unfolding.	Cisplatin	0-9	MDM2 proto-oncogene	Homo sapiens	57-61
32211658-2	2020	Consequently, cisplatin inhibits the MDM2-mediated ubiquitination, which is the molecular basis of p53 activation.	Cisplatin	14-23	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	252-256
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	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	107-111
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	MDM2 proto-oncogene	Homo sapiens	62-66
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	MDM2 proto-oncogene	Homo sapiens	156-160
31812766-7	2020	Additionally, reactive oxygen species, Ca2+ levels, DNA damage, and phosphorylated MDM2 were all synergistically induced by aldehyde mixtures, while total p53, phosphorylated p53 and phosphorylated AKT (serine/threonine kinase) were inhibited.	Aldehydes	124-132	MDM2 proto-oncogene	Homo sapiens	83-87
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	MDM2 proto-oncogene	Homo sapiens	252-256
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	MDM2 proto-oncogene	Homo sapiens	153-157
32156076-6	2020	Like mammalian p53, the affinity of Scp53BSF for the SCS oligonucleotide was higher than for the MDM2 oligonucleotide.	Oligonucleotides	102-117	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	132-136
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	MDM2 proto-oncogene	Homo sapiens	79-83
31201607-14	2020	CONCLUSION: BI-907828 showed significant anti-tumor activity in DDLPS PDX harboring MDM2 amplifications, providing a strong rationale for early clinical testing of BI-907828 in a DDLPS patient population.	bi-907828	12-21	MDM2 proto-oncogene	Homo sapiens	84-88
32321249-6	2020	The MDM2 antagonist and the proteasome inhibitor promote 13a-triggered apoptosis by preventing p53 degradation.	13a	57-60	MDM2 proto-oncogene	Homo sapiens	4-8
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	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	141-145
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	MDM2 proto-oncogene	Homo sapiens	98-102
32257953-8	2019	MTHFR rs1801131 and MDM2 rs1690924 were significantly correlated with platinum-induced GI toxicity (P = 0.04 and P = 0.02, respectively).	Platinum	70-78	MDM2 proto-oncogene	Homo sapiens	20-24
32001262-7	2020	The developed pDIm and mainly pDIdm peptides showed stable conformations over the simulation time with conserved secondary structure and effective interaction with MDM2/X by physical binding such as hydrogen bonding.	Hydrogen	199-207	MDM2 proto-oncogene	Homo sapiens	164-168
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	MDM2 proto-oncogene	Homo sapiens	35-39
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	MDM2 proto-oncogene	Homo sapiens	105-109
32271428-0	2020	MiR-548b-3p inhibits proliferation and migration of breast cancer cells by targeting MDM2.	mir-548b-3p	0-11	MDM2 proto-oncogene	Homo sapiens	85-89
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	MDM2 proto-oncogene	Homo sapiens	20-24
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	MDM2 proto-oncogene	Homo sapiens	207-211
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	MDM2 proto-oncogene	Homo sapiens	20-24
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	MDM2 proto-oncogene	Homo sapiens	207-211
31923941-6	2020	In summary, selective regulation of MDM2 in cancer cells is a promising strategy to overcome DOX resistance, and may provide a perspective on the management of malignant tumors.	Doxorubicin	93-96	MDM2 proto-oncogene	Homo sapiens	36-40
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	MDM2 proto-oncogene	Homo sapiens	35-39
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	MDM2 proto-oncogene	Homo sapiens	35-39
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	MDM2 proto-oncogene	Homo sapiens	122-126
32062612-2	2020	BBR can induce apoptosis of acute lymphoblastic leukemia (ALL) cells through the MDM2/p53 pathway.	Berberine	0-3	MDM2 proto-oncogene	Homo sapiens	81-85
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	MDM2 proto-oncogene	Homo sapiens	100-104
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	MDM2 proto-oncogene	Homo sapiens	110-114
31825612-3	2020	Herein we report the first example of the use of alkenyl cyclopropane building blocks to constrain MDM2-targeting helical peptides.	cyclopropane	49-69	MDM2 proto-oncogene	Homo sapiens	99-103
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	MDM2 proto-oncogene	Homo sapiens	192-196
31907996-3	2020	However, the role of Mdm2 in iron homeostasis is not certain.	Iron	29-33	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	340-344
31971801-0	2020	alpha-Helix-Mimicking Sulfono-gamma-AApeptide Inhibitors for p53-MDM2/MDMX Protein-Protein Interactions.	sulfoquinovosylacylglycerol	22-35	MDM2 proto-oncogene	Homo sapiens	65-69
31907996-4	2020	Here, we showed that Mdm2 expression was increased by iron depletion but decreased by iron repletion.	Iron	54-58	MDM2 proto-oncogene	Homo sapiens	21-25
31907996-4	2020	Here, we showed that Mdm2 expression was increased by iron depletion but decreased by iron repletion.	Iron	86-90	MDM2 proto-oncogene	Homo sapiens	21-25
31907996-5	2020	We also showed that Iron Regulatory Protein 2 (IRP2) mediated iron-regulated Mdm2 expression.	Iron	62-66	MDM2 proto-oncogene	Homo sapiens	77-81
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	MDM2 proto-oncogene	Homo sapiens	224-228
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	MDM2 proto-oncogene	Homo sapiens	232-236
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	MDM2 proto-oncogene	Homo sapiens	288-292
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	MDM2 proto-oncogene	Homo sapiens	112-116
31753697-0	2020	Upregulation of p53 through induction of MDM2 degradation: Amino acid prodrugs of anthraquinone analogs.	Anthraquinones	82-95	MDM2 proto-oncogene	Homo sapiens	41-45
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	MDM2 proto-oncogene	Homo sapiens	224-228
31573955-11	2020	FES depletion promoted radiation-induced reactive oxygen species formation, which resulted in phosphorylation of S6K and MDM2.	Oxygen	50-56	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	340-344
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	MDM2 proto-oncogene	Homo sapiens	18-22
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	MDM2 proto-oncogene	Homo sapiens	24-28
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	MDM2 proto-oncogene	Homo sapiens	14-18
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	MDM2 proto-oncogene	Homo sapiens	112-116
31781989-4	2020	Here we demonstrate the important role of the flexible N-terminal region of the MDM2 protein in the binding with small molecule compounds, which contributes to the transition from three point binding to four point binding during the development of new anticancer agents.	Nitrogen	55-56	MDM2 proto-oncogene	Homo sapiens	80-84
31892970-4	2020	The ability of the dual-target MDM2/MDMX inhibitor in reversing doxorubicin resistance was subsequently verified, (9.15 and 13.92 - fold reversal indexes) respectively.	Doxorubicin	64-75	MDM2 proto-oncogene	Homo sapiens	31-35
31892970-5	2020	We observed that the MDM2/MDMX inhibitor in combination with DOX could suppress proliferation, promote cell cycle arrest and induce apoptosis.	Doxorubicin	61-64	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	39-43
31146672-0	2020	Novel p-Functionalized Chromen-4-on-3-yl Chalcones Bearing Astonishing Boronic Acid Moiety as MDM2 Inhibitor: Synthesis, Cytotoxic Evaluation and Simulation Studies.	chromen-4-on-3-yl chalcones	23-50	MDM2 proto-oncogene	Homo sapiens	94-98
31146672-0	2020	Novel p-Functionalized Chromen-4-on-3-yl Chalcones Bearing Astonishing Boronic Acid Moiety as MDM2 Inhibitor: Synthesis, Cytotoxic Evaluation and Simulation Studies.	Boronic Acids	71-83	MDM2 proto-oncogene	Homo sapiens	94-98
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	MDM2 proto-oncogene	Homo sapiens	44-48
31146672-3	2020	In addition, docking studies were performed on these chromeno-chalcones in order to have an insight into their interaction possibilities with MDM2 protein.	chromeno-chalcones	53-71	MDM2 proto-oncogene	Homo sapiens	142-146
31146672-10	2020	The molecular docking study proposed good activity as a MDM-2 inhibitor suggesting hydrophobic as well as hydrogen bonding interactions with MDM2.	Hydrogen	106-114	MDM2 proto-oncogene	Homo sapiens	56-61
31146672-10	2020	The molecular docking study proposed good activity as a MDM-2 inhibitor suggesting hydrophobic as well as hydrogen bonding interactions with MDM2.	Hydrogen	106-114	MDM2 proto-oncogene	Homo sapiens	141-145
31477836-8	2020	Mechanistically, ROS inducers promote TXNDC9 to dissociate from PRDX1, but enhance a protein association with MDM2.	Reactive Oxygen Species	17-20	MDM2 proto-oncogene	Homo sapiens	110-114
30976094-5	2019	Finally, we used the champion inhibitor (NH-23-C2) in reversine-treated HCT-116 colon cancer cells to selectively block caspase-2 activity and caspase-2-mediated MDM-2 cleavage.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	54-63	MDM2 proto-oncogene	Homo sapiens	162-167
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	MDM2 proto-oncogene	Homo sapiens	72-76
31568878-0	2019	Co-delivery of p53 and MDM2 inhibitor RG7388 using a hydroxyl terminal PAMAM dendrimer derivative for synergistic cancer therapy.	RG7388	38-44	MDM2 proto-oncogene	Homo sapiens	23-27
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	MDM2 proto-oncogene	Homo sapiens	23-27
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	MDM2 proto-oncogene	Homo sapiens	23-27
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	MDM2 proto-oncogene	Homo sapiens	94-98
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	MDM2 proto-oncogene	Homo sapiens	14-18
31634457-4	2019	Here, we show that in response to stimulation of the Gq-coupled angiotensin II type 1 receptor or treatment with phorbol ester, Mdm2, E3 ubiquitin ligase, interacted with PKCbetaII isotype in the nucleus, resulting in ubiquitination of PKCbetaII at the C-terminal K668 and K672 residues and its subsequent downregulation.	Phorbol Esters	113-126	MDM2 proto-oncogene	Homo sapiens	128-132
30976094-0	2019	Potent and selective caspase-2 inhibitor prevents MDM-2 cleavage in reversine-treated colon cancer cells.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	68-77	MDM2 proto-oncogene	Homo sapiens	50-55
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	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	198-202
31628385-9	2019	A major lignan, phyllanthin was isolated from the chloroform fraction and showed strong irreversible affinities for viral E6 and MDM2 in in silico analysis.	Lignans	8-14	MDM2 proto-oncogene	Homo sapiens	129-133
31536651-4	2020	Patients with MDM2-positive InS who were treated with anthracycline-based regimens, gemcitabine-based regimens, or pazopanib between October 2001 and January 2018 were selected.	pazopanib	115-124	MDM2 proto-oncogene	Homo sapiens	14-18
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	MDM2 proto-oncogene	Homo sapiens	23-27
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	MDM2 proto-oncogene	Homo sapiens	198-202
31779710-0	2019	MDM2 inhibitor APG-115 synergizes with PD-1 blockade through enhancing antitumor immunity in the tumor microenvironment.	AA-115	15-22	MDM2 proto-oncogene	Homo sapiens	0-4
31779710-6	2019	METHOD: Using APG-115 that is a MDM2 antagonist in clinical development as a pharmacological p53 activator, we investigated the role of p53 in immune modulation and combination therapy with PD-1 blockade.	AA-115	14-21	MDM2 proto-oncogene	Homo sapiens	32-36
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	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	65-69
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	MDM2 proto-oncogene	Homo sapiens	142-146
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	MDM2 proto-oncogene	Homo sapiens	65-69
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	MDM2 proto-oncogene	Homo sapiens	142-146
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	MDM2 proto-oncogene	Homo sapiens	65-69
31652301-0	2019	Allosteric changes in HDM2 by the ATM phospho-mimetic S395D mutation: Implications on HDM2 function.	phosphorylleucylphenylalanine	38-45	MDM2 proto-oncogene	Homo sapiens	22-26
31652301-0	2019	Allosteric changes in HDM2 by the ATM phospho-mimetic S395D mutation: Implications on HDM2 function.	phosphorylleucylphenylalanine	38-45	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	106-110
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	MDM2 proto-oncogene	Homo sapiens	138-142
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	MDM2 proto-oncogene	Homo sapiens	138-142
31689961-10	2019	A clinical phase III trial using MDM2/X inhibitors, idasanutlin (RG7388) combined with cytarabine, is being performed involving relapse/refractory acute myeloid leukemia patients.	RG7388	65-71	MDM2 proto-oncogene	Homo sapiens	33-37
31693454-7	2019	MDM2 expression was correlated with the exposure to aristolochic acids (p = 0.020), better preoperative renal function (p = 0.016), ureter location (p = 0.002), higher pathological T stage (p = 0.006), high tumor grade (p &lt; 0.001), presence of glandular differentiation (p = 0.036), and sarcoma differentiation (p = 0.020).	Aristolochic Acids	52-70	MDM2 proto-oncogene	Homo sapiens	0-4
31628385-9	2019	A major lignan, phyllanthin was isolated from the chloroform fraction and showed strong irreversible affinities for viral E6 and MDM2 in in silico analysis.	phyllanthin	16-27	MDM2 proto-oncogene	Homo sapiens	129-133
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	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	97-101
31451549-3	2019	This function is in turn controlled by the cell fate determinant NUMB, which binds to and inhibits MDM2 via a short stretch of 11 amino acids, contained in its phosphotyrosine-binding (PTB) domain, encoded by exon 3 of the NUMB gene.	Phosphotyrosine	160-175	MDM2 proto-oncogene	Homo sapiens	99-103
31632968-0	2019	Novel Function of lncRNA ADAMTS9-AS2 in Promoting Temozolomide Resistance in Glioblastoma via Upregulating the FUS/MDM2 Ubiquitination Axis.	temozolomide	50-62	MDM2 proto-oncogene	Homo sapiens	115-119
31632968-15	2019	Conclusion: ADAMTS9-AS2 possessed a novel function that promotes TMZ resistance via upregulating the FUS/MDM2 axis in GBM cells.	temozolomide	65-68	MDM2 proto-oncogene	Homo sapiens	105-109
31632968-16	2019	The RRM or Znf_RanBP2 domains of FUS facilitate the combination of ADAMTS9-AS2 and FUS, competitively inhibiting MDM2-dependent FUS K48 ubiquitination and resulting in enhanced FUS stability and TMZ resistance.	temozolomide	195-198	MDM2 proto-oncogene	Homo sapiens	113-117
31632968-17	2019	Our results suggest that the ADAMTS9-AS2/FUS/MDM2 axis may represent a suitable prognostic biomarker and a potential target in TMZ-resistant GBM therapy.	temozolomide	127-130	MDM2 proto-oncogene	Homo sapiens	45-49
31428819-16	2019	In contrast, in FKBP12-transfected MDA-MB-468 cells, MDM2 was more greatly inhibited by doxorubicin, resulting in greater cytotoxic and apoptotic effect.	Doxorubicin	88-99	MDM2 proto-oncogene	Homo sapiens	53-57
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	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	161-165
31181320-0	2019	MDM2-NFAT1 dual inhibitor, MA242: Effective against hepatocellular carcinoma, independent of p53.	MA242	27-32	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	124-128
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	MDM2 proto-oncogene	Homo sapiens	124-128
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	MDM2 proto-oncogene	Homo sapiens	124-128
31425749-3	2019	We found that CPHSP, a novel spirooxindole-pyrrolizidine derivative, can target the MDM2/p53 signaling that is essential for the tumorigenesis of hepatocellular carcinoma (HCC).	Spirooxindole	29-42	MDM2 proto-oncogene	Homo sapiens	84-88
31425749-3	2019	We found that CPHSP, a novel spirooxindole-pyrrolizidine derivative, can target the MDM2/p53 signaling that is essential for the tumorigenesis of hepatocellular carcinoma (HCC).	PYRROLIZIDINE	43-56	MDM2 proto-oncogene	Homo sapiens	84-88
31607289-8	2019	At Flu concentration of 10 mmol/L, mRNA levels PTEN and BAD in miR-214-ASO group significantly increased (P<0.05), but mRNA levels of MDM2 and NF-kappaB significantly decreased (P<0.05).	fludarabine	3-6	MDM2 proto-oncogene	Homo sapiens	134-138
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	MDM2 proto-oncogene	Homo sapiens	151-155
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	MDM2 proto-oncogene	Homo sapiens	151-155
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	MDM2 proto-oncogene	Homo sapiens	151-155
31181320-6	2019	We have also identified a MDM2 and NFAT1 dual inhibitor (termed MA242) that induces MDM2 auto-ubiquitination and degradation and represses NFAT1-mediated MDM2 transcription.	MA242	64-69	MDM2 proto-oncogene	Homo sapiens	26-30
31181320-6	2019	We have also identified a MDM2 and NFAT1 dual inhibitor (termed MA242) that induces MDM2 auto-ubiquitination and degradation and represses NFAT1-mediated MDM2 transcription.	MA242	64-69	MDM2 proto-oncogene	Homo sapiens	84-88
31181320-6	2019	We have also identified a MDM2 and NFAT1 dual inhibitor (termed MA242) that induces MDM2 auto-ubiquitination and degradation and represses NFAT1-mediated MDM2 transcription.	MA242	64-69	MDM2 proto-oncogene	Homo sapiens	84-88
30985989-3	2019	ATP and GTP are the most active nucleoside triphosphates and show specificity for STAT5b over STAT5a, STAT3, STAT6 and the p53-binding protein HDM2.	Adenosine Triphosphate	0-3	MDM2 proto-oncogene	Homo sapiens	143-147
30985989-3	2019	ATP and GTP are the most active nucleoside triphosphates and show specificity for STAT5b over STAT5a, STAT3, STAT6 and the p53-binding protein HDM2.	Guanosine Triphosphate	8-11	MDM2 proto-oncogene	Homo sapiens	143-147
30985989-3	2019	ATP and GTP are the most active nucleoside triphosphates and show specificity for STAT5b over STAT5a, STAT3, STAT6 and the p53-binding protein HDM2.	nucleoside triphosphates	32-56	MDM2 proto-oncogene	Homo sapiens	143-147
30538285-9	2019	Pertinently, 2DG downregulated two other short-lived oncoproteins, MYC and MDM2.	Deoxyglucose	13-16	MDM2 proto-oncogene	Homo sapiens	75-79
30809951-8	2019	In AGS and MGC803 cells with melatonin exposure, cleaved Caspase 9 was upregulated and Caspase 3 was activated; moreover, MDM2 and AKT expression and phosphorylation were downregulated.	Melatonin	29-38	MDM2 proto-oncogene	Homo sapiens	122-126
30809951-9	2019	Melatonin promoted apoptosis of AGS and MGC803 cells by the downregulation of AKT and MDM2.	Melatonin	0-9	MDM2 proto-oncogene	Homo sapiens	86-90
31324563-0	2019	Upregulation of p53 through induction of MDM2 degradation: Anthraquinone analogs.	Anthraquinones	59-72	MDM2 proto-oncogene	Homo sapiens	41-45
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	MDM2 proto-oncogene	Homo sapiens	98-102
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	MDM2 proto-oncogene	Homo sapiens	98-102
31339234-0	2019	Oridonin induces Mdm2-p60 to promote p53-mediated apoptosis and cell cycle arrest in neuroblastoma.	oridonin	0-8	MDM2 proto-oncogene	Homo sapiens	17-21
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	MDM2 proto-oncogene	Homo sapiens	84-88
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	MDM2 proto-oncogene	Homo sapiens	118-122
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	MDM2 proto-oncogene	Homo sapiens	118-122
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	MDM2 proto-oncogene	Homo sapiens	111-115
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	MDM2 proto-oncogene	Homo sapiens	212-216
31282659-7	2019	In the MDM2 case, the higher affinity of MIP is ascribed to a larger gain of translational, configurational entropy of water upon binding.	Water	119-124	MDM2 proto-oncogene	Homo sapiens	7-11
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	MDM2 proto-oncogene	Homo sapiens	79-83
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	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	145-149
31167802-5	2019	Therefore, we performed an investigator-initiated phase 1 trial of the oral MDM2 antagonist idasanutlin (RG7388; Roche) in patients with high-risk PV/ET for whom at least 1 prior therapy had failed.	RG7388	92-103	MDM2 proto-oncogene	Homo sapiens	76-80
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	MDM2 proto-oncogene	Homo sapiens	200-204
31036564-8	2019	Further experiments suggested that MDM2 amplification increases histone methylation in Nutlin-treated cells by causing depletion of the histone demethylase Jumonji domain-containing protein 2B (JMJD2B).	nutlin	87-93	MDM2 proto-oncogene	Homo sapiens	35-39
31066983-5	2019	We also reveal the key additive 18-crown-ether, which we discovered to enable HdmX crystallization and show its stabilization of various Lys residues.	18-crown-ether	32-46	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	85-89
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	MDM2 proto-oncogene	Homo sapiens	123-127
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	MDM2 proto-oncogene	Homo sapiens	8-12
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	MDM2 proto-oncogene	Homo sapiens	8-12
30896089-8	2019	Alterations within the TP53-MDM2 signal transduction pathway appear to be enriched among patients with platinum-resistant disease.	Platinum	103-111	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	181-185
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	MDM2 proto-oncogene	Homo sapiens	87-91
31019022-10	2019	Doxorubicin treatment of DDLPS cells in vitro demonstrated variable sensitivity based on baseline MDM2 levels, and doxorubicin treatment elevated MDM2 expression.	Doxorubicin	0-11	MDM2 proto-oncogene	Homo sapiens	98-102
31019022-10	2019	Doxorubicin treatment of DDLPS cells in vitro demonstrated variable sensitivity based on baseline MDM2 levels, and doxorubicin treatment elevated MDM2 expression.	Doxorubicin	115-126	MDM2 proto-oncogene	Homo sapiens	146-150
31019022-11	2019	In vivo, treatment with doxorubicin followed by an MDM2 inhibitor improved doxorubicin sensitivity.	Doxorubicin	75-86	MDM2 proto-oncogene	Homo sapiens	51-55
31056264-0	2019	A novel mechanism of irinotecan targeting MDM2 and Bcl-xL.	Irinotecan	21-31	MDM2 proto-oncogene	Homo sapiens	42-46
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	MDM2 proto-oncogene	Homo sapiens	89-93
31056264-3	2019	In our structure modelling study, Irinotecan could fit to the binding sites of MDM2 and Bcl-xL for their known drugs, Nutlin-3 and ABT-737, with a better binding affinity than to Topo I.	Irinotecan	34-44	MDM2 proto-oncogene	Homo sapiens	79-83
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	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	96-100
31089613-3	2019	A hexahistidine-tag on MDM2 allows the binding of the protein complex to the Ni-NTA affinity resin, while the fluorescent protein fused to p53 enables the direct visualization of the interaction of p53 with MDM2.	His-His-His-His-His-His	2-15	MDM2 proto-oncogene	Homo sapiens	23-27
31089613-3	2019	A hexahistidine-tag on MDM2 allows the binding of the protein complex to the Ni-NTA affinity resin, while the fluorescent protein fused to p53 enables the direct visualization of the interaction of p53 with MDM2.	ni-nta	77-83	MDM2 proto-oncogene	Homo sapiens	23-27
31089613-9	2019	Interestingly, two types of novel inhibitors of MDM2, including cyclohexyl-triphenylamine derivatives and platinum complexes, were identified and their binding affinities were obtained.	cyclohexyl-triphenylamine	64-89	MDM2 proto-oncogene	Homo sapiens	48-52
31089613-9	2019	Interestingly, two types of novel inhibitors of MDM2, including cyclohexyl-triphenylamine derivatives and platinum complexes, were identified and their binding affinities were obtained.	Platinum	106-114	MDM2 proto-oncogene	Homo sapiens	48-52
31226791-10	2019	The resultant analog sequence Ac-Leu-Thr-Phe-Aib-Glu-Tyr-Trp-Gln-Leu-Cba-Aib-Ser-Ala-Ala-NH2 exhibited high-affinity target binding (Mdm2 Kd = 43 nM) and significant alpha-helicity in circular dichroism studies.	ac-leu-thr	30-40	MDM2 proto-oncogene	Homo sapiens	133-137
31226791-10	2019	The resultant analog sequence Ac-Leu-Thr-Phe-Aib-Glu-Tyr-Trp-Gln-Leu-Cba-Aib-Ser-Ala-Ala-NH2 exhibited high-affinity target binding (Mdm2 Kd = 43 nM) and significant alpha-helicity in circular dichroism studies.	Phenylalanine	41-44	MDM2 proto-oncogene	Homo sapiens	133-137
31226791-10	2019	The resultant analog sequence Ac-Leu-Thr-Phe-Aib-Glu-Tyr-Trp-Gln-Leu-Cba-Aib-Ser-Ala-Ala-NH2 exhibited high-affinity target binding (Mdm2 Kd = 43 nM) and significant alpha-helicity in circular dichroism studies.	Glutamic Acid	49-52	MDM2 proto-oncogene	Homo sapiens	133-137
31226791-10	2019	The resultant analog sequence Ac-Leu-Thr-Phe-Aib-Glu-Tyr-Trp-Gln-Leu-Cba-Aib-Ser-Ala-Ala-NH2 exhibited high-affinity target binding (Mdm2 Kd = 43 nM) and significant alpha-helicity in circular dichroism studies.	Tyrosine	53-56	MDM2 proto-oncogene	Homo sapiens	133-137
31226791-10	2019	The resultant analog sequence Ac-Leu-Thr-Phe-Aib-Glu-Tyr-Trp-Gln-Leu-Cba-Aib-Ser-Ala-Ala-NH2 exhibited high-affinity target binding (Mdm2 Kd = 43 nM) and significant alpha-helicity in circular dichroism studies.	Tryptophan	57-60	MDM2 proto-oncogene	Homo sapiens	133-137
31226791-10	2019	The resultant analog sequence Ac-Leu-Thr-Phe-Aib-Glu-Tyr-Trp-Gln-Leu-Cba-Aib-Ser-Ala-Ala-NH2 exhibited high-affinity target binding (Mdm2 Kd = 43 nM) and significant alpha-helicity in circular dichroism studies.	Glutamine	61-64	MDM2 proto-oncogene	Homo sapiens	133-137
31226791-10	2019	The resultant analog sequence Ac-Leu-Thr-Phe-Aib-Glu-Tyr-Trp-Gln-Leu-Cba-Aib-Ser-Ala-Ala-NH2 exhibited high-affinity target binding (Mdm2 Kd = 43 nM) and significant alpha-helicity in circular dichroism studies.	Leucine	33-36	MDM2 proto-oncogene	Homo sapiens	133-137
31226791-10	2019	The resultant analog sequence Ac-Leu-Thr-Phe-Aib-Glu-Tyr-Trp-Gln-Leu-Cba-Aib-Ser-Ala-Ala-NH2 exhibited high-affinity target binding (Mdm2 Kd = 43 nM) and significant alpha-helicity in circular dichroism studies.	Serine	77-80	MDM2 proto-oncogene	Homo sapiens	133-137
31226791-10	2019	The resultant analog sequence Ac-Leu-Thr-Phe-Aib-Glu-Tyr-Trp-Gln-Leu-Cba-Aib-Ser-Ala-Ala-NH2 exhibited high-affinity target binding (Mdm2 Kd = 43 nM) and significant alpha-helicity in circular dichroism studies.	Alanine	81-84	MDM2 proto-oncogene	Homo sapiens	133-137
31226791-10	2019	The resultant analog sequence Ac-Leu-Thr-Phe-Aib-Glu-Tyr-Trp-Gln-Leu-Cba-Aib-Ser-Ala-Ala-NH2 exhibited high-affinity target binding (Mdm2 Kd = 43 nM) and significant alpha-helicity in circular dichroism studies.	Alanine	85-88	MDM2 proto-oncogene	Homo sapiens	133-137
31226791-11	2019	Relative to this linear ATSP-7041 analog, several d-amino acid substitutions at Mdm2(X) non-binding residues (e.g., d-Glu5, d-Gln8, and d-Leu9) demonstrated decreased binding and alpha-helicity.	d-glu5	116-122	MDM2 proto-oncogene	Homo sapiens	80-84
31226791-11	2019	Relative to this linear ATSP-7041 analog, several d-amino acid substitutions at Mdm2(X) non-binding residues (e.g., d-Glu5, d-Gln8, and d-Leu9) demonstrated decreased binding and alpha-helicity.	d-gln8	124-130	MDM2 proto-oncogene	Homo sapiens	80-84
31226791-14	2019	Overall, macrocyclization by hydrocarbon stapling appears to overcome the destabilization of alpha-helicity by helix breaking residues and, in the specific case of d-Trp7-modification, a highly potent ATSP-7041 analog (Mdm2 Kd = 30 nM; cellular EC50 = 600 nM) was identified.	Hydrocarbons	29-40	MDM2 proto-oncogene	Homo sapiens	219-223
31181622-0	2019	Benzimidazoles Downregulate Mdm2 and MdmX and Activate p53 in MdmX Overexpressing Tumor Cells.	Benzimidazoles	0-14	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	164-168
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	MDM2 proto-oncogene	Homo sapiens	142-146
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	MDM2 proto-oncogene	Homo sapiens	147-151
31832522-7	2019	The inhibition of MDM2 by SP141 also increases the sensitivity of HCC cells to sorafenib.	sorafenib	79-88	MDM2 proto-oncogene	Homo sapiens	18-22
30802707-0	2019	Design and synthesis of new substituted spirooxindoles as potential inhibitors of the MDM2-p53 interaction.	spirooxindoles	40-54	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	216-220
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	MDM2 proto-oncogene	Homo sapiens	212-216
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	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	62-66
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	MDM2 proto-oncogene	Homo sapiens	147-151
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	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	108-112
31024344-8	2019	When we introduced the cysteine residue into the corresponding site in MdmX, the RING domain became capable of forming dimers with other MdmX molecules in vivo, suggesting that one conserved amino acid residue in the RINGs of Mdm2 and MdmX could serve as the determinant of the differential ability of these domains to form dimers and their E3 activity.	Cysteine	23-31	MDM2 proto-oncogene	Homo sapiens	226-230
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	MDM2 proto-oncogene	Homo sapiens	91-95
31022952-6	2019	Notably, puromycin upregulated the expression of RPL5 and RPL11 to directly bind to MDM2 in HCT116 cells.	Puromycin	9-18	MDM2 proto-oncogene	Homo sapiens	84-88
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	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	75-79
30628640-0	2019	CP-31398 attenuates endometrial cancer cell invasion, metastasis and resistance to apoptosis by downregulating MDM2 expression.	CP 31398	0-8	MDM2 proto-oncogene	Homo sapiens	111-115
30715803-0	2019	A fluorinated indole-based MDM2 antagonist selectively inhibits the growth of p53wt osteosarcoma cells.	indole	14-20	MDM2 proto-oncogene	Homo sapiens	27-31
30715803-5	2019	Previously, we have reported the discovery of a panel of fluoro-substituted indole-based antagonists of MDM2.	indole	76-82	MDM2 proto-oncogene	Homo sapiens	104-108
30715803-9	2019	The analysis of the crystal structure of human MDM2 in complex with the compound (R)-6a (carboxylic acid of the active (R)-5a compound) revealed the classical three-finger binding mode.	(r)-6a	81-87	MDM2 proto-oncogene	Homo sapiens	47-51
30715803-9	2019	The analysis of the crystal structure of human MDM2 in complex with the compound (R)-6a (carboxylic acid of the active (R)-5a compound) revealed the classical three-finger binding mode.	Carboxylic Acids	89-104	MDM2 proto-oncogene	Homo sapiens	47-51
30896891-0	2019	Nitroxoline induces cell apoptosis by inducing MDM2 degradation in small-cell lung cancer.	nitroxoline	0-11	MDM2 proto-oncogene	Homo sapiens	47-51
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)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid	26-29	MDM2 proto-oncogene	Homo sapiens	56-60
30896891-3	2019	In the mechanistic study, NXQ was found to downregulate MDM2 expression by inducing its proteasomal degradation, and thus upregulated p53 expression, which was a substrate protein of MDM2.	2-[5-fluoranyl-2-[[3-[methyl(oxidanyl)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid	26-29	MDM2 proto-oncogene	Homo sapiens	183-187
30896891-4	2019	Moreover, overexpression of MDM2 decreased the cytotoxicity of NXQ on SCLC cells.	2-[5-fluoranyl-2-[[3-[methyl(oxidanyl)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid	63-66	MDM2 proto-oncogene	Homo sapiens	28-32
30896891-5	2019	These results demonstrated that NXQ displayed anti-SCLC activity by suppressing MDM2 expression, which suggested that anti-infective NXQ had potential for SCLC treatment by targeting the MDM2/p53 axis.	2-[5-fluoranyl-2-[[3-[methyl(oxidanyl)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid	32-35	MDM2 proto-oncogene	Homo sapiens	80-84
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)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid	32-35	MDM2 proto-oncogene	Homo sapiens	187-191
30896891-5	2019	These results demonstrated that NXQ displayed anti-SCLC activity by suppressing MDM2 expression, which suggested that anti-infective NXQ had potential for SCLC treatment by targeting the MDM2/p53 axis.	2-[5-fluoranyl-2-[[3-[methyl(oxidanyl)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid	133-136	MDM2 proto-oncogene	Homo sapiens	80-84
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	MDM2 proto-oncogene	Homo sapiens	187-191
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	MDM2 proto-oncogene	Homo sapiens	161-165
30794402-6	2019	We extracted the binding pocket of Nutlin from the crystal structure of Nutlin bound MDM2.	nutlin	35-41	MDM2 proto-oncogene	Homo sapiens	85-89
30532073-9	2019	Moreover, the senescent phenotype induced by DNA damage reagents, such as Etoposide, is at least in part mediated by MDM2-dependent WRN degradation as it can be significantly attenuated by ectopic expression of WRN.	Etoposide	74-83	MDM2 proto-oncogene	Homo sapiens	117-121
29662106-3	2019	ERCC1, ERCC2, XRCC1, MDM2, MTHFR, MTR, and SLC19A1 gene polymorphisms may contribute to individual variation in response and survival to platinum-based chemotherapy.	Platinum	137-145	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	52-56
30628640-11	2019	Moreover, treatment with CP-31398 and siRNA against MDM2 further enhanced these effects.	CP 31398	25-33	MDM2 proto-oncogene	Homo sapiens	52-56
30628640-12	2019	Taken together, the findings of this study indicate that the CP-31398-mediated downregulation of MDM2 may suppress EC progression via its inhibitory role in EC cell migration, invasion and resistance to apoptosis.	CP 31398	61-69	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	151-155
30873235-0	2019	Design of indole- and MCR-based macrocycles as p53-MDM2 antagonists.	indole	10-16	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	33-37
30488540-0	2019	Augmented antitumor activity of 5-fluorouracil by double knockdown of MDM4 and MDM2 in colon and gastric cancer cells.	Fluorouracil	32-46	MDM2 proto-oncogene	Homo sapiens	79-83
29992578-7	2019	MDM2 was found to be stabilized mainly by activated EGFR signaling as targeting EGFR by Erlotinib or sh-RNA repressed MDM2 in a transcription-independent manner.	Erlotinib Hydrochloride	88-97	MDM2 proto-oncogene	Homo sapiens	0-4
30455251-6	2019	The mutant p53-MDM2 complex is deficient in catalyzing ubiquitin release from the activated E2 conjugating enzyme.	Estradiol	92-94	MDM2 proto-oncogene	Homo sapiens	15-19
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	MDM2 proto-oncogene	Homo sapiens	45-49
30886745-5	2019	PpIX induces p53-dependent and TAp73-dependent apoptosis and inhibits TAp73/MDM2 and TAp73/MDM4 interactions.	protoporphyrin IX	0-4	MDM2 proto-oncogene	Homo sapiens	76-80
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	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	27-31
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	197-201	MDM2 proto-oncogene	Homo sapiens	27-31
30488540-6	2019	Exposure to 5-FU alone induced MDM2 as well as p21 and PUMA by p53 activation.	Fluorouracil	12-16	MDM2 proto-oncogene	Homo sapiens	31-35
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	MDM2 proto-oncogene	Homo sapiens	7-11
30647052-1	2019	The BCL2 inhibitor venetoclax plus the MDM2 inhibitor idasanutlin may be effective in treating relapsed/refractory acute myeloid leukemia.	RG7388	54-65	MDM2 proto-oncogene	Homo sapiens	39-43
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	MDM2 proto-oncogene	Homo sapiens	96-100
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	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	131-135
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	MDM2 proto-oncogene	Homo sapiens	29-33
30840303-0	2019	Metformin inhibits proliferation and migration of endometrial cancer cells through regulating PI3K/AKT/MDM2 pathway.	Metformin	0-9	MDM2 proto-oncogene	Homo sapiens	103-107
30840303-10	2019	Western blotting results manifested that the activation of PI3K/AKT/MDM2 signaling pathway was inhibited by metformin (p&lt;0.05).	Metformin	108-117	MDM2 proto-oncogene	Homo sapiens	68-72
30840303-11	2019	CONCLUSIONS: Metformin can inhibit the proliferation and migration of EC cells by inhibiting the activation of PI3K/AKT/MDM2 signaling pathway.	Metformin	13-22	MDM2 proto-oncogene	Homo sapiens	120-124
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	MDM2 proto-oncogene	Homo sapiens	182-186
30447641-15	2019	In addition, we observed that bortezomib suppressed MDM2 expression in a dose-dependent manner.	Bortezomib	30-40	MDM2 proto-oncogene	Homo sapiens	52-56
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	MDM2 proto-oncogene	Homo sapiens	124-128
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	MDM2 proto-oncogene	Homo sapiens	107-111
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	MDM2 proto-oncogene	Homo sapiens	160-164
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.	Serine	115-121	MDM2 proto-oncogene	Homo sapiens	107-111
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	MDM2 proto-oncogene	Homo sapiens	107-111
30447641-8	2019	Among the different candidate anticancer drugs, we tested the effect of bortezomib, which was expected to inhibit MDM2 amplification.	Bortezomib	72-82	MDM2 proto-oncogene	Homo sapiens	114-118
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	MDM2 proto-oncogene	Homo sapiens	179-183
30774764-0	2019	Downregulation of miR-194-5p induces paclitaxel resistance in ovarian cancer cells by altering MDM2 expression.	mir-194-5p	18-28	MDM2 proto-oncogene	Homo sapiens	95-99
30774764-0	2019	Downregulation of miR-194-5p induces paclitaxel resistance in ovarian cancer cells by altering MDM2 expression.	Paclitaxel	37-47	MDM2 proto-oncogene	Homo sapiens	95-99
30774764-10	2019	MDM2 was upregulated in paclitaxel resistant cells compared with parental cells.	Paclitaxel	24-34	MDM2 proto-oncogene	Homo sapiens	0-4
30774764-11	2019	MDM2 inhibition also resensitized resistant cells to paclitaxel and forced MDM2 induced paclitaxel resistance in parental cells.	Paclitaxel	53-63	MDM2 proto-oncogene	Homo sapiens	0-4
30774764-11	2019	MDM2 inhibition also resensitized resistant cells to paclitaxel and forced MDM2 induced paclitaxel resistance in parental cells.	Paclitaxel	88-98	MDM2 proto-oncogene	Homo sapiens	0-4
30774764-11	2019	MDM2 inhibition also resensitized resistant cells to paclitaxel and forced MDM2 induced paclitaxel resistance in parental cells.	Paclitaxel	88-98	MDM2 proto-oncogene	Homo sapiens	75-79
30774764-12	2019	miR-194-5p induced p21 upregulation and G1 phase arrest in resistant cells by downregulating MDM2.	mir-194-5p	0-10	MDM2 proto-oncogene	Homo sapiens	93-97
30774764-13	2019	Furthermore, a public database showed that high MDM2 expression was associated with a shorter progression-free survival in EOC patients treated with paclitaxel.	Paclitaxel	149-159	MDM2 proto-oncogene	Homo sapiens	48-52
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	MDM2 proto-oncogene	Homo sapiens	140-144
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	MDM2 proto-oncogene	Homo sapiens	140-144
30398270-6	2019	We also identified that the mean translocation time of MDM2 through the polyurea nanopore was 26.1 +- 3.7 mus while that of the SiN nanopore was 14.2 +- 2.0 mus, hence suggesting that the enhanced electrostatic interaction between positively charged MDM2 and the negatively charged pore surface affects the translocation speed.	polyurea	72-80	MDM2 proto-oncogene	Homo sapiens	55-59
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	MDM2 proto-oncogene	Homo sapiens	16-20
30585255-0	2019	A phase I study of the HDM2 antagonist SAR405838 combined with the MEK inhibitor pimasertib in patients with advanced solid tumours.	SAR405838	39-48	MDM2 proto-oncogene	Homo sapiens	23-27
30700046-3	2019	The small molecule RG7388 (idasanutlin, R05503781) is a newly developed inhibitor that is specific for an oncogene-derived protein called MDM2, which is also in clinical trials for the treatment of various types of cancers.	RG7388	27-38	MDM2 proto-oncogene	Homo sapiens	138-142
30666091-8	2019	Next-generation sequencing of formalin-fixed paraffin-embedded RC tissues showed MDM2 amplification without MDM4 amplification, EGFR aberrations, or DNMT3A alterations.	Formaldehyde	30-38	MDM2 proto-oncogene	Homo sapiens	81-85
30666091-8	2019	Next-generation sequencing of formalin-fixed paraffin-embedded RC tissues showed MDM2 amplification without MDM4 amplification, EGFR aberrations, or DNMT3A alterations.	Paraffin	45-53	MDM2 proto-oncogene	Homo sapiens	81-85
31474710-10	2019	Other data further showed that cinobufagin increased p73 expression and decreased Mdm2 expression, whereas p53 expression was not significantly changed.	cinobufagin	31-42	MDM2 proto-oncogene	Homo sapiens	82-86
30393117-7	2019	p53 stability was enhanced by miR-944s targeting E3 ligases COP1 and MDM2.	mir-944s	30-38	MDM2 proto-oncogene	Homo sapiens	69-73
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	MDM2 proto-oncogene	Homo sapiens	87-91
30462562-8	2019	These findings indicate that dual-target MDM2/MDMX inhibitor could increase the sensitization of doxorubicin and inhibit migration and invasion abilities in TNBC cells through p38 MAPK pathway activation caused EMT suppression and hence could be useful in TNBC treatments in future.	Doxorubicin	97-108	MDM2 proto-oncogene	Homo sapiens	41-45
30511219-1	2019	PURPOSE: Idasanutlin is a selective small-molecule MDM2 antagonist.	RG7388	9-20	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	83-87
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	MDM2 proto-oncogene	Homo sapiens	142-146
30177839-2	2019	Arsenite exposure induces ribosomal stress responses mediated by the ribosomal protein S7, which can block MDM2 activity and result in GADD45alpha accumulation and cell apoptosis.	arsenite	0-8	MDM2 proto-oncogene	Homo sapiens	107-111
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	MDM2 proto-oncogene	Homo sapiens	177-181
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	MDM2 proto-oncogene	Homo sapiens	241-245
30564368-0	2019	MDM2 inhibitor ameliorates cisplatin-induced nephropathy via NFkappaBeta signal inhibition.	Cisplatin	27-36	MDM2 proto-oncogene	Homo sapiens	0-4
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.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	286-293	MDM2 proto-oncogene	Homo sapiens	156-160
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	MDM2 proto-oncogene	Homo sapiens	136-140
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	MDM2 proto-oncogene	Homo sapiens	72-76
30564368-4	2019	However, independent of p53, MDM2 acts as a co-transcription factor for nuclear factor-kappaB (NFkappaB), whose signaling can be involved in cisplatin-induced tubular injury.	Cisplatin	141-150	MDM2 proto-oncogene	Homo sapiens	29-33
30564368-5	2019	We therefore examined the effects of MDM2 inhibitor on cisplatin cytotoxicity.	Cisplatin	55-64	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	271-275
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	MDM2 proto-oncogene	Homo sapiens	179-183
30524726-6	2018	R248W, but not R175H, can engage p21 and MDM2, which both function to limit oxidative stress and facilitate the switch to de novo serine synthesis.	Serine	130-136	MDM2 proto-oncogene	Homo sapiens	41-45
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	MDM2 proto-oncogene	Homo sapiens	90-94
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	MDM2 proto-oncogene	Homo sapiens	122-126
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	MDM2 proto-oncogene	Homo sapiens	198-202
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	MDM2 proto-oncogene	Homo sapiens	198-202
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	MDM2 proto-oncogene	Homo sapiens	198-202
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	MDM2 proto-oncogene	Homo sapiens	84-88
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	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	156-160
30809370-5	2019	Crystallographic studies of peptide-MDM2/MDMX complexes structurally validated the chemoselectivity of the dithiocarbamate staple bridging Lys and Cys at (i, i + 4) positions.	Dithiocarbamate	107-122	MDM2 proto-oncogene	Homo sapiens	36-40
30809370-5	2019	Crystallographic studies of peptide-MDM2/MDMX complexes structurally validated the chemoselectivity of the dithiocarbamate staple bridging Lys and Cys at (i, i + 4) positions.	Lysine	139-142	MDM2 proto-oncogene	Homo sapiens	36-40
30809370-5	2019	Crystallographic studies of peptide-MDM2/MDMX complexes structurally validated the chemoselectivity of the dithiocarbamate staple bridging Lys and Cys at (i, i + 4) positions.	Cysteine	147-150	MDM2 proto-oncogene	Homo sapiens	36-40
30809370-6	2019	One dithiocarbamate-stapled PMI derivative, DTCPMI, showed a 50-fold stronger binding to MDM2 and MDMX than its linear counterpart.	Dithiocarbamate	4-19	MDM2 proto-oncogene	Homo sapiens	89-93
30809370-6	2019	One dithiocarbamate-stapled PMI derivative, DTCPMI, showed a 50-fold stronger binding to MDM2 and MDMX than its linear counterpart.	dtcpmi	44-50	MDM2 proto-oncogene	Homo sapiens	89-93
30366433-7	2018	SHS-SP protection from transformation is provided presumably by low oncogene expression maintained by tight co-regulation between thermosensitive HR drivers BRCA, ATM, ATR, and RAD51 (decreasing expression after SHS), and oncogenes mTOR, MDM2, KRAS, and EGFR.	shs-sp	0-6	MDM2 proto-oncogene	Homo sapiens	238-242
30253242-0	2018	The development of piperidinones as potent MDM2-P53 protein-protein interaction inhibitors for cancer therapy.	2-piperidone	19-32	MDM2 proto-oncogene	Homo sapiens	43-47
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	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	240-244
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	MDM2 proto-oncogene	Homo sapiens	240-244
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	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	37-41
30543590-8	2018	Early-phase clinical trials have also suggested that MDM2 inhibitors such as idasanutlin and histone deacetylase inhibitors should continue in their development.	RG7388	77-88	MDM2 proto-oncogene	Homo sapiens	53-57
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	MDM2 proto-oncogene	Homo sapiens	155-159
30284823-3	2018	Herein, the design, synthesis and biological evaluation is described of a photoactivatable MDM2 inhibitor, PPG-idasanutlin, which exerts no functional effect on cellular outgrowth, but allows for the selective, noninvasive activation of antitumor properties upon irradiation visible light, demonstrating activation with micrometer, single cell precision.	ppg-idasanutlin	107-122	MDM2 proto-oncogene	Homo sapiens	91-95
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	MDM2 proto-oncogene	Homo sapiens	72-76
29877036-4	2018	The results demonstrate that the introductions of thiazole and pyridine rings into 2TZ as well as the change in the orientation of inhibitors lead to the increase in the polar interactions of 2U0, 2U1, 2U5, 2U6, and 2U7 with MDM2 relative to 2TZ.	Thiazoles	50-58	MDM2 proto-oncogene	Homo sapiens	225-229
29877036-4	2018	The results demonstrate that the introductions of thiazole and pyridine rings into 2TZ as well as the change in the orientation of inhibitors lead to the increase in the polar interactions of 2U0, 2U1, 2U5, 2U6, and 2U7 with MDM2 relative to 2TZ.	pyridine	63-71	MDM2 proto-oncogene	Homo sapiens	225-229
30158012-1	2018	A concise asymmetric synthesis has been developed to prepare idasanutlin, a small molecule MDM2 antagonist.	RG7388	61-72	MDM2 proto-oncogene	Homo sapiens	91-95
30355102-0	2018	Single-Nucleotide Polymorphism 309T&gt;G in the MDM2 Promoter Determines Functional Outcome After Stroke.	single-nucleotide	0-17	MDM2 proto-oncogene	Homo sapiens	48-52
30355102-7	2018	The interaction of MDM2 with p53 was disrupted by neuronal treatment with nutlin-3a.	nutlin 3	74-83	MDM2 proto-oncogene	Homo sapiens	19-23
30355102-10	2018	Results- Experimental stroke and oxygen and glucose deprivation induced the expression of MDM2 in the brain and neurons, respectively.	Oxygen	33-39	MDM2 proto-oncogene	Homo sapiens	90-94
30355102-11	2018	Moreover, oxygen and glucose deprivation promoted MDM2 binding with p53 in neurons.	Oxygen	10-16	MDM2 proto-oncogene	Homo sapiens	50-54
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	MDM2 proto-oncogene	Homo sapiens	18-22
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	MDM2 proto-oncogene	Homo sapiens	58-62
30544467-7	2018	Our meta-analysis showed a significant association between RB susceptibility and MDM2 rs2279744 recessive model (OR = 1.427, 95%CI: 1.107-1.840, P = .006, I = 0%).	Rubidium	59-61	MDM2 proto-oncogene	Homo sapiens	81-85
30176902-14	2018	CONCLUSION: XWL-1-48 may be a promising orally topoII inhibitor, its mechanisms are associated with suppression of TopoII, induction of DNA damage and apoptosis, blockage of PI3K/AKT/Mdm2 pathway.	xwl-1-48	12-20	MDM2 proto-oncogene	Homo sapiens	183-187
29970480-0	2018	Efficacy of the MDM2 Inhibitor SAR405838 in Glioblastoma Is Limited by Poor Distribution Across the Blood-Brain Barrier.	SAR405838	31-40	MDM2 proto-oncogene	Homo sapiens	16-20
29970480-7	2018	MDM2-amplified PDX lines with high MDM2 expression were sensitive to SAR405838 in comparison with MDM2 control lines in both in vitro and heterotopic models.	SAR405838	69-78	MDM2 proto-oncogene	Homo sapiens	0-4
29970480-7	2018	MDM2-amplified PDX lines with high MDM2 expression were sensitive to SAR405838 in comparison with MDM2 control lines in both in vitro and heterotopic models.	SAR405838	69-78	MDM2 proto-oncogene	Homo sapiens	35-39
29970480-7	2018	MDM2-amplified PDX lines with high MDM2 expression were sensitive to SAR405838 in comparison with MDM2 control lines in both in vitro and heterotopic models.	SAR405838	69-78	MDM2 proto-oncogene	Homo sapiens	35-39
30158012-0	2018	Efficient Industrial Synthesis of the MDM2 Antagonist Idasanutlin via a Cu(I)-catalyzed [3+2] Asymmetric Cycloaddition.	RG7388	54-65	MDM2 proto-oncogene	Homo sapiens	38-42
30158012-0	2018	Efficient Industrial Synthesis of the MDM2 Antagonist Idasanutlin via a Cu(I)-catalyzed [3+2] Asymmetric Cycloaddition.	cuprous ion	72-77	MDM2 proto-oncogene	Homo sapiens	38-42
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	MDM2 proto-oncogene	Homo sapiens	123-127
29772439-6	2018	Treated with 5-azacytidine decreased the level of MDM2, DNMT1 and miR21, but increased the level of MEG3 and PTEN.	Azacitidine	13-26	MDM2 proto-oncogene	Homo sapiens	50-54
29190376-6	2018	Apoptosis in MDM2-amplified cells was associated with a reduction in glycolysis and the PPP, reduced NADPH, increased ROS, and depletion of the transcription factor SP1, which normally promotes PPP gene expression.	NADP	101-106	MDM2 proto-oncogene	Homo sapiens	13-17
29190376-6	2018	Apoptosis in MDM2-amplified cells was associated with a reduction in glycolysis and the PPP, reduced NADPH, increased ROS, and depletion of the transcription factor SP1, which normally promotes PPP gene expression.	Reactive Oxygen Species	118-121	MDM2 proto-oncogene	Homo sapiens	13-17
29190376-11	2018	These findings provide insight into how glucose metabolism reduces Nutlin-3a-induced apoptosis, and also provide a mechanism for the heightened sensitivity of MDM2-amplified cells to apoptosis in response to Nutlin-3a.	Glucose	40-47	MDM2 proto-oncogene	Homo sapiens	159-163
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	MDM2 proto-oncogene	Homo sapiens	153-157
29762656-0	2018	Prevention of prostate cancer by natural product MDM2 inhibitor GS25: In vitro and in vivo activities and molecular mechanisms.	gs25	64-68	MDM2 proto-oncogene	Homo sapiens	49-53
29851469-4	2018	Here, we describe the design, synthesis, and biological evaluation of a trans-cyclooctene tagged derivative of RG7388, RG7388-TCO, which showed high cellular potency and specificity for MDM2.	Cyclooctanes	72-89	MDM2 proto-oncogene	Homo sapiens	186-190
29768700-1	2018	Venetoclax (ABT-199) and idasanutlin (RG7388) are efficient anticancer drugs targeting two essential apoptosis markers, Bcl-2 and MDM2, respectively.	RG7388	25-36	MDM2 proto-oncogene	Homo sapiens	130-134
30022047-0	2018	Potent effect of the MDM2 inhibitor AMG232 on suppression of glioblastoma stem cells.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(1-(isopropylsulfonyl)-3-methylbutan-2-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	36-42	MDM2 proto-oncogene	Homo sapiens	21-25
30022047-3	2018	RG7112 is the first-in class inhibitor and recently discovered AMG232 is the most potent MDM2 inhibitor known to date.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(1-(isopropylsulfonyl)-3-methylbutan-2-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	63-69	MDM2 proto-oncogene	Homo sapiens	89-93
29878773-3	2018	We have used stopped flow fluorescence to investigate the binding reaction between MDM2 and TAD from p53 as well as from its paralogs p63 and p73, and in particular, focused on the salt dependence of the interaction.	Salts	181-185	MDM2 proto-oncogene	Homo sapiens	83-87
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	MDM2 proto-oncogene	Homo sapiens	289-293
29737431-2	2018	We examined the influence of Mycoplasma hyorhinis infection on sensitivity of human lung carcinoma cells NCI-H292 to MDM2 inhibitor Nutlin-3.	4-Bromophthalic anhydride	109-113	MDM2 proto-oncogene	Homo sapiens	117-121
29737431-2	2018	We examined the influence of Mycoplasma hyorhinis infection on sensitivity of human lung carcinoma cells NCI-H292 to MDM2 inhibitor Nutlin-3.	nutlin 3	132-140	MDM2 proto-oncogene	Homo sapiens	117-121
29851469-5	2018	The in-cell reaction of RG7388-TCO with a tetrazine-tagged BODIPY dye enabled fluorescence imaging of endogenous MDM2 in SJSA-1 and T778 tumor cells.	1,2,3,4-tetrazine	42-51	MDM2 proto-oncogene	Homo sapiens	113-117
29851469-6	2018	RG7388-TCO was also used to pull down MDM2 by reaction with tetrazine-tagged agarose beads in SJSA-1 lysates.	1,2,3,4-tetrazine	60-69	MDM2 proto-oncogene	Homo sapiens	38-42
29851469-6	2018	RG7388-TCO was also used to pull down MDM2 by reaction with tetrazine-tagged agarose beads in SJSA-1 lysates.	Sepharose	77-84	MDM2 proto-oncogene	Homo sapiens	38-42
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	MDM2 proto-oncogene	Homo sapiens	98-102
29394130-1	2018	MDM2 antagonists stabilize and activate wild-type p53, and histone methyltransferase (HMT) inhibitors reduce methylation on histone lysines and arginines.	Lysine	132-139	MDM2 proto-oncogene	Homo sapiens	0-4
29655550-10	2018	In conclusion, our study showed that the combined treatment with JNJ and gefitinib exerted synergistic inhibition on cell proliferation, thereby suggesting the potential application of combining MDM2 inhibitors with EGFR inhibitors for enhancing efficacy in ovarian cancer treatment.	Gefitinib	73-82	MDM2 proto-oncogene	Homo sapiens	195-199
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	MDM2 proto-oncogene	Homo sapiens	245-249
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	MDM2 proto-oncogene	Homo sapiens	245-249
29571049-4	2018	We conjugated to LONp via metal-thiolate bonds a dodecameric peptide antagonist of both MDM2 and MDMX, termed PMI, and a CD33-targeted, humanized monoclonal antibody to allow for AML-specific intracellular delivery of a stabilized PMI.	lonp	17-21	MDM2 proto-oncogene	Homo sapiens	88-92
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	MDM2 proto-oncogene	Homo sapiens	198-202
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	MDM2 proto-oncogene	Homo sapiens	198-202
29575058-5	2018	It can be explained by the presence of a flexible linker between the isoindolinone core and amino acid fragment, which provides the optimal arrangement of the molecule in the hydrophobic cavity of MDM2 for both isomers.	phthalimidine	69-82	MDM2 proto-oncogene	Homo sapiens	197-201
29490944-3	2018	The novel MDM2 inhibitor DS-3032b is 10-fold more potent than the first-generation inhibitor nutlin-3a.	DS-3032B	25-33	MDM2 proto-oncogene	Homo sapiens	10-14
29861848-4	2018	Here we report that the novel small molecule anti-androgen, galeterone targets USP12 and USP46, two highly homologous deubiquitinating enzymes that control the AR-AKT-MDM2-P53 signalling pathway.	3-hydroxy-17-(1H-benzimidazole-1-yl)androsta-5,16-diene	60-70	MDM2 proto-oncogene	Homo sapiens	167-171
29508534-1	2018	The total synthesis of siladenoserinol A, an inhibitor of the p53-Hdm2 interaction, has been achieved.	siladenoserinol a	23-40	MDM2 proto-oncogene	Homo sapiens	66-70
29484412-0	2018	Melatonin induces the apoptosis and inhibits the proliferation of human gastric cancer cells via blockade of the AKT/MDM2 pathway.	Melatonin	0-9	MDM2 proto-oncogene	Homo sapiens	117-121
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	MDM2 proto-oncogene	Homo sapiens	43-47
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	MDM2 proto-oncogene	Homo sapiens	57-61
29484412-13	2018	The present study demonstrated that the oncostatic effects of melatonin on SGC-7901 GC cells are mediated via the blockade of the AKT/MDM2 intracellular pathway.	Melatonin	62-71	MDM2 proto-oncogene	Homo sapiens	134-138
29643228-6	2018	Dual MDMX/MDM2 inhibition by ALRN-6924 inhibits cellular proliferation by inducing cell cycle arrest and apoptosis in cell lines and primary AML patient cells, including leukemic stem cell-enriched populations, and disrupts functional clonogenic and serial replating capacity.	alrn-6924	29-38	MDM2 proto-oncogene	Homo sapiens	10-14
29670376-0	2018	Butein activates p53 in hepatocellular carcinoma cells via blocking MDM2-mediated ubiquitination.	butein	0-6	MDM2 proto-oncogene	Homo sapiens	68-72
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	MDM2 proto-oncogene	Homo sapiens	60-64
29532999-5	2018	Only one compound, Nutlin-3a, an MDM2 inhibitor, was significantly sensitive in 18 cancer cells with CTNNB1 mutation.	nutlin 3	19-28	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	193-197
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	MDM2 proto-oncogene	Homo sapiens	193-197
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	MDM2 proto-oncogene	Homo sapiens	49-53
29168472-6	2018	Ursolic acid dose-dependently inhibited the proliferation of the myeloma cells with IC50 of 6.56 mumol/L, accompanied by reductions in USP7 substrates such as MDM2, UHRF1 and DNMT1.	ursolic acid	0-12	MDM2 proto-oncogene	Homo sapiens	159-163
29368050-0	2018	Effects of posaconazole (a strong CYP3A4 inhibitor), two new tablet formulations, and food on the pharmacokinetics of idasanutlin, an MDM2 antagonist, in patients with advanced solid tumors.	RG7388	118-129	MDM2 proto-oncogene	Homo sapiens	134-138
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	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	99-103
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	MDM2 proto-oncogene	Homo sapiens	215-219
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	MDM2 proto-oncogene	Homo sapiens	196-200
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	112-116
29410603-6	2018	MDM2 immunohistochemical staining was performed on archival paraffin-embedded and formalin-fixed specimens (with a threshold of nuclear positivity &gt; 10%).	Formaldehyde	82-90	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	112-116
29387014-0	2018	Inhibiting beta-Catenin by beta-Carboline-Type MDM2 Inhibitor for Pancreatic Cancer Therapy.	norharman	27-41	MDM2 proto-oncogene	Homo sapiens	47-51
29216716-0	2018	Cyclodipeptide c(Orn-Pro) Conjugate with 4-Ethylpiperic Acid Abrogates Cancer Cell Metastasis through Modulating MDM2.	cyclodipeptide c	0-16	MDM2 proto-oncogene	Homo sapiens	113-117
29216716-0	2018	Cyclodipeptide c(Orn-Pro) Conjugate with 4-Ethylpiperic Acid Abrogates Cancer Cell Metastasis through Modulating MDM2.	orn-pro	17-24	MDM2 proto-oncogene	Homo sapiens	113-117
29216716-0	2018	Cyclodipeptide c(Orn-Pro) Conjugate with 4-Ethylpiperic Acid Abrogates Cancer Cell Metastasis through Modulating MDM2.	4-ethylpiperic acid	41-60	MDM2 proto-oncogene	Homo sapiens	113-117
29387014-4	2018	We have recently identified a novel class of beta-carboline compounds as the specific and potent MDM2 inhibitors, including a lead compound SP141.	norharman	45-59	MDM2 proto-oncogene	Homo sapiens	97-101
29387014-4	2018	We have recently identified a novel class of beta-carboline compounds as the specific and potent MDM2 inhibitors, including a lead compound SP141.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	140-145	MDM2 proto-oncogene	Homo sapiens	97-101
29387014-6	2018	We found that the silencing of either beta-catenin or MDM2 largely reduced the anticancer activity of SP141 while the double silencing of both genes almost completely blocked SP141"s activity.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	102-107	MDM2 proto-oncogene	Homo sapiens	54-58
29387014-8	2018	The inhibitory effects of SP141 on beta-catenin were mediated by the ubiquitin-proteasome system in an MDM2-independent manner.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	26-31	MDM2 proto-oncogene	Homo sapiens	103-107
29387014-9	2018	In conclusion, these results suggest that SP141 exerts its anticancer activity by dually inhibiting beta-catenin and MDM2.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	42-47	MDM2 proto-oncogene	Homo sapiens	117-121
29387014-10	2018	We envision that beta-carboline derivatives can be developed as promising dual inhibitors of beta-catenin and MDM2 for the treatment of advanced pancreatic cancer.	norharman	17-31	MDM2 proto-oncogene	Homo sapiens	110-114
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	MDM2 proto-oncogene	Homo sapiens	99-103
29392451-0	2018	Phase 1 summary of plasma concentration-QTc analysis for idasanutlin, an MDM2 antagonist, in patients with advanced solid tumors and AML.	RG7388	57-68	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	4-8
28356026-3	2018	MATERIALS AND METHODS: The pharmaceutical attributes of essential oil components, specifically focusing on their affinity towards COX, 5-LOX, AKT, MDM2, PDK1 and mTOR which defines the phosphatidylinositol-3- kinase (PI3K) pathway, were assessed.	Oils, Volatile	56-69	MDM2 proto-oncogene	Homo sapiens	147-151
29866023-1	2018	BACKGROUND: Pyrrolo[2,3-d]pyrimidines have been recently reported to have anticancer activities through inhibition of different targets such as, Epidermal Growth Factor Receptor (EGFR) tyrosine kinase, Janus Kinase (JAK), mitotic checkpoint protein kinase (Mps1), carbonic anhydrase, MDM-2.	Pyrrolo(2,3-d)pyrimidine	12-37	MDM2 proto-oncogene	Homo sapiens	284-289
30109812-0	2018	Novel isatin-derived molecules activate p53 via interference with Mdm2 to promote apoptosis.	Isatin	6-12	MDM2 proto-oncogene	Homo sapiens	66-70
30393841-6	2018	In our study, we examined the effect of RA on the expression of ZEB1, MDM2, ABCB1, PTEN and TWIST1 genes in MCF-7 breast cancer cells.	rosmarinic acid	40-42	MDM2 proto-oncogene	Homo sapiens	70-74
29248726-6	2018	Differential mRNA abundance of AKT1, PTEN, PIK3CA controlling metabolism, drug efflux, nutrient transport and epigenetic control MDM2 are potentially critical in shaping DNA methylation effects of temozolomide.	Temozolomide	197-209	MDM2 proto-oncogene	Homo sapiens	129-133
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	MDM2 proto-oncogene	Homo sapiens	10-14
27871087-3	2018	The small molecule NVP-CGM097 is a novel MDM2 inhibitor.	NVP-CGM097	23-29	MDM2 proto-oncogene	Homo sapiens	41-45
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	MDM2 proto-oncogene	Homo sapiens	41-45
29416773-8	2018	CRISPR-mediated MDM2 knockout in neuroblastoma cells mimicked DS-3032b treatment.	DS-3032B	62-70	MDM2 proto-oncogene	Homo sapiens	16-20
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	MDM2 proto-oncogene	Homo sapiens	130-134
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	MDM2 proto-oncogene	Homo sapiens	4-8
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	MDM2 proto-oncogene	Homo sapiens	10-14
29311926-2	2017	The present study was designed to test a natural MDM2 inhibitor, Inulanolide A (InuA), for anti-prostate cancer activity and to determine the underlying mechanism(s) of action.	Inulanolide A	65-78	MDM2 proto-oncogene	Homo sapiens	49-53
29311926-2	2017	The present study was designed to test a natural MDM2 inhibitor, Inulanolide A (InuA), for anti-prostate cancer activity and to determine the underlying mechanism(s) of action.	inua	80-84	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	96-100
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	MDM2 proto-oncogene	Homo sapiens	165-169
29153842-5	2017	MDM2 targeting may be useful for preventing PDAC development in high-risk individuals.	pdac	44-48	MDM2 proto-oncogene	Homo sapiens	0-4
29228061-6	2017	Further analysis of linear and stapled peptides comprising 6-Me-tryptophan provides mechanistic insight into dual Mdm2/Mdm4 antagonism and confirms L98 of Mdm4 as a mutable steric gate.	6-me-tryptophan	59-74	MDM2 proto-oncogene	Homo sapiens	114-118
29153098-6	2017	Using cut point analysis and comparison of Kaplan-Meier survival curves by log rank tests, high amplification levels of MDM2 (&gt;38 copies) and CDK4 (&gt;30 copies) correlated with decreased disease free survival (DFS) (P = .0168 and 0.0169 respectively) and disease specific survival (DSS) (P = .0082 and 0.0140 respectively).	dss	287-290	MDM2 proto-oncogene	Homo sapiens	120-124
29089230-0	2017	Proapoptotic modification of substituted isoindolinones as MDM2-p53 inhibitors.	phthalimidine	41-55	MDM2 proto-oncogene	Homo sapiens	59-63
29089230-2	2017	The rationale for augmentation of the target activity of 2,3-substituted isoindolinones was based on the introduction of new fragments in the structure of the inhibitor that would provide additional binding sites in the hydrophobic cavity of MDM2.	2,3-substituted isoindolinones	57-87	MDM2 proto-oncogene	Homo sapiens	242-246
29089230-6	2017	Valine and phenylglycine ester derivatives were identified as potentially active MDM2-p53 inhibitors.	Valine	0-6	MDM2 proto-oncogene	Homo sapiens	81-85
29089230-6	2017	Valine and phenylglycine ester derivatives were identified as potentially active MDM2-p53 inhibitors.	phenylglycine ester	11-30	MDM2 proto-oncogene	Homo sapiens	81-85
28643424-0	2017	MDM2 is implicated in high-glucose-induced podocyte mitotic catastrophe via Notch1 signalling.	Glucose	27-34	MDM2 proto-oncogene	Homo sapiens	0-4
28643424-5	2017	Here, we explore whether MDM2 is involved in podocyte MC during hyperglycaemia.	Methylcholanthrene	54-56	MDM2 proto-oncogene	Homo sapiens	25-29
28643424-7	2017	In vitro, cultured podocytes treated by high glucose (HG) also showed an up-regulation of mitotic markers and abnormal mitotic status, accompanied by elevated expression of MDM2.	Glucose	45-52	MDM2 proto-oncogene	Homo sapiens	173-177
28643424-13	2017	In conclusion, high glucose up-regulates MDM2 expression and leads to podocyte MC.	Glucose	20-27	MDM2 proto-oncogene	Homo sapiens	41-45
28643424-14	2017	Notch1 signalling is an essential downstream pathway of MDM2 in mediating HG-induced MC in podocytes.	Methylcholanthrene	85-87	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	89-93
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	MDM2 proto-oncogene	Homo sapiens	72-76
28692049-3	2017	Tumor cells that overexpress Mdm2 have reduced DNA double-strand breaks in response to doxorubicin or etoposide.	Doxorubicin	87-98	MDM2 proto-oncogene	Homo sapiens	29-33
28692049-3	2017	Tumor cells that overexpress Mdm2 have reduced DNA double-strand breaks in response to doxorubicin or etoposide.	Etoposide	102-111	MDM2 proto-oncogene	Homo sapiens	29-33
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	MDM2 proto-oncogene	Homo sapiens	59-63
28928040-8	2017	Furthermore, release of RPS27a from the nucleolus into the nucleoplasm led to decrease phosphorylation of Mdm2 at serine residue 166 and inhibit Mdm2-mediated ubiquitination of P53 in (P-3F)-treated HeLa cells.	Serine	114-120	MDM2 proto-oncogene	Homo sapiens	106-110
28797774-0	2017	Design, synthesis and biological evaluation of novel antitumor spirotetrahydrothiopyran-oxindole derivatives as potent p53-MDM2 inhibitors.	spirotetrahydrothiopyran-oxindole	63-96	MDM2 proto-oncogene	Homo sapiens	123-127
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	MDM2 proto-oncogene	Homo sapiens	127-131
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	MDM2 proto-oncogene	Homo sapiens	79-83
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	MDM2 proto-oncogene	Homo sapiens	134-138
28708672-4	2017	Furthermore, artemisinin stimulated AR ubiquitination and AR receptor interactions with the E3 ubiquitin ligase MDM2 in LNCaP cells.	artemisinin	13-24	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	56-60
29057045-3	2017	Their binding affinity with MDM2 was evaluated using fluorescence polarization (FP) assay and 1H-15N two-dimensional HSQC nuclear magnetic resonance experiments.	Hydrogen	94-96	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	39-43
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	MDM2 proto-oncogene	Homo sapiens	39-43
28959361-0	2017	Effect of etoposide-induced alteration of the Mdm2-Rb signaling pathway on cellular senescence in A549 lung adenocarcinoma cells.	Etoposide	10-19	MDM2 proto-oncogene	Homo sapiens	46-50
28959361-1	2017	The present study aimed to investigate the effect of various concentrations of etoposide (VP-16) on the E3 ubiquitin-protein ligase Mdm2 (Mdm2)-retinoblastoma (Rb) signaling pathway in the cellular senescence of A549 lung adenocarcinoma cells.	Etoposide	79-88	MDM2 proto-oncogene	Homo sapiens	132-136
28959361-1	2017	The present study aimed to investigate the effect of various concentrations of etoposide (VP-16) on the E3 ubiquitin-protein ligase Mdm2 (Mdm2)-retinoblastoma (Rb) signaling pathway in the cellular senescence of A549 lung adenocarcinoma cells.	Etoposide	79-88	MDM2 proto-oncogene	Homo sapiens	138-142
29057045-3	2017	Their binding affinity with MDM2 was evaluated using fluorescence polarization (FP) assay and 1H-15N two-dimensional HSQC nuclear magnetic resonance experiments.	15n	97-100	MDM2 proto-oncogene	Homo sapiens	28-32
29116067-4	2017	Using molecular docking, it has been shown that Akt1 and MDM2 may be potential targets of the studied triterpene acids.	triterpene acids	102-118	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	149-153
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	MDM2 proto-oncogene	Homo sapiens	169-173
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	MDM2 proto-oncogene	Homo sapiens	169-173
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	MDM2 proto-oncogene	Homo sapiens	169-173
28785074-0	2017	Low dose arsenite confers resistance to UV induced apoptosis via p53-MDM2 pathway in ketatinocytes.	arsenite	9-17	MDM2 proto-oncogene	Homo sapiens	69-73
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	MDM2 proto-oncogene	Homo sapiens	69-73
28785074-6	2017	Moreover, low-dose arsenite treatment dramatically decreased the MDM2 gene promoter activity, suggesting that this effect has been mediated through transcription.	arsenite	19-27	MDM2 proto-oncogene	Homo sapiens	65-69
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	MDM2 proto-oncogene	Homo sapiens	120-124
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	MDM2 proto-oncogene	Homo sapiens	69-73
28604107-5	2017	The Neuroblastoma New Drug Development Strategy (NDDS) has: 1) established a group with expertise in drug development; 2) prioritised targets and drugs according to tumour biology (target expression, dependency, pre-clinical data; potential combinations; biomarkers), identifying as priority targets ALK, MEK, CDK4/6, MDM2, MYCN (druggable by BET bromodomain, aurora kinase, mTORC1/2) BIRC5 and checkpoint kinase 1; 3) promoted clinical trials with target-prioritised drugs.	ndds	49-53	MDM2 proto-oncogene	Homo sapiens	318-322
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	MDM2 proto-oncogene	Homo sapiens	108-112
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	MDM2 proto-oncogene	Homo sapiens	177-181
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	MDM2 proto-oncogene	Homo sapiens	177-181
28766886-8	2017	Exposure of the SCLC lines to the MDM2 inhibitor JNJ-27291199 produced enhanced killing in 80% of the SCLC lines.	TDP665759	49-61	MDM2 proto-oncogene	Homo sapiens	34-38
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	MDM2 proto-oncogene	Homo sapiens	39-43
28615518-7	2017	The knockdown of MDM2 in both cell lines decreased Rb phosphorylation and the level of E2F1 protein.	Rubidium	51-53	MDM2 proto-oncogene	Homo sapiens	17-21
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	MDM2 proto-oncogene	Homo sapiens	122-126
28615518-8	2017	This signaling was through the estrogen receptor because fulvestrant (a selective estrogen receptor degrader) decreased MDM2 protein levels and decreased phosphorylation of Rb.	Fulvestrant	57-68	MDM2 proto-oncogene	Homo sapiens	120-124
28468838-4	2017	Tat appears to stabilise Mdm2 at the post-translational level by inducing its phosphorylation at serine-166 position through AKT.	Serine	97-103	MDM2 proto-oncogene	Homo sapiens	25-29
28678832-0	2017	Association of MDM2 expression with shorter progression-free survival and overall survival in patients with advanced pancreatic cancer treated with gemcitabine-based chemotherapy.	gemcitabine	148-159	MDM2 proto-oncogene	Homo sapiens	15-19
28678832-3	2017	Immunohistochemical staining for MDM2 and p53 with formalin-fixed, paraffin-embedded tumor tissues was independently reviewed.	Formaldehyde	51-59	MDM2 proto-oncogene	Homo sapiens	33-37
28678832-7	2017	Additionally, MDM2 expression was significantly associated with progressive disease (PD) and death (P = .015) following first-line gemcitabine-based therapy.	gemcitabine	131-142	MDM2 proto-oncogene	Homo sapiens	14-18
28678832-8	2017	In advanced pancreatic cancer patients, MDM2 expression is associated with shorter OS and PFS after gemcitabine-based chemotherapy.	gemcitabine	100-111	MDM2 proto-oncogene	Homo sapiens	40-44
28760302-7	2017	In polycythemia vera, a novel interferon administered every 2 weeks is being developed for front-line therapy in high-risk individuals, and inhibitors of human double minute 2 (HDM2) have shown promise in preclinical studies, as have HDAC inhibitors such as givinostat (both in the laboratory and in the clinic).	givinostat	258-268	MDM2 proto-oncogene	Homo sapiens	177-181
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	MDM2 proto-oncogene	Homo sapiens	10-14
28418896-7	2017	Further, overexpression of wild type p65 NFkB increased MDM2 expression while the NFkB inhibitors NEMO-binding domain (NBD) and Bay11-7082 blocked the activin-induced increase in MDM2.	3-(4-methylphenylsulfonyl)-2-propenenitrile	128-138	MDM2 proto-oncogene	Homo sapiens	179-183
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	MDM2 proto-oncogene	Homo sapiens	160-164
28400230-4	2017	In this study, we investigated the inhibitory mechanism of both enantiomers of apomorphine against the MDM2-p53 interaction.	Apomorphine	79-90	MDM2 proto-oncogene	Homo sapiens	103-107
28362162-4	2017	To that end, we have identified several novel ischemia-related mRNAs that are synergistically stabilized by oxygen and glucose deprivation including VEGF, MYC, MDM2, and CYR61.	Oxygen	108-114	MDM2 proto-oncogene	Homo sapiens	160-164
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	MDM2 proto-oncogene	Homo sapiens	162-166
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	MDM2 proto-oncogene	Homo sapiens	162-166
28155209-15	2017	The gap of osteogenic differentiation potency between MSCs from normal adipose tissue and ALT/WDL was decreased as MDM2-inhibitor Nutlin-3 concentration increased.	nutlin 3	130-138	MDM2 proto-oncogene	Homo sapiens	115-119
28155209-16	2017	CONCLUSIONS: MSCs derived from ALT/WDL had higher osteogenic differentiation potency based on ALP staining, which disappeared as Nutlin-3 concentration increased, suggesting that could be caused by amplified MDM2 in ALT/WDL.	nutlin 3	129-137	MDM2 proto-oncogene	Homo sapiens	208-212
28223335-4	2017	However, in response to gemcitabine or cisplatin treatment, MSI2 silencing simultaneously down-regulated MDM2 and up-regulated Numb and wtp53 protein levels.	gemcitabine	24-35	MDM2 proto-oncogene	Homo sapiens	105-109
28223335-4	2017	However, in response to gemcitabine or cisplatin treatment, MSI2 silencing simultaneously down-regulated MDM2 and up-regulated Numb and wtp53 protein levels.	Cisplatin	39-48	MDM2 proto-oncogene	Homo sapiens	105-109
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	MDM2 proto-oncogene	Homo sapiens	41-45
28498468-9	2017	Rescue experiments showed that upregulation of MDM2 reversed the inhibitory effects of miR-379-5p on bladder cancer cell proliferation, migration and invasion.	mir-379	87-94	MDM2 proto-oncogene	Homo sapiens	47-51
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	MDM2 proto-oncogene	Homo sapiens	77-81
28425916-5	2017	We further demonstrate that concurrent inhibition of MDM2 and ALK was able to overcome ceritinib resistance conferred by MYCN upregulation in vitro and in vivo.	ceritinib	87-96	MDM2 proto-oncogene	Homo sapiens	53-57
29088763-11	2017	Furthermore, we found that overexpression of CENP-K stimulated the tyrosine phosphorylation of the AKT and MDM2 proteins, but inhibited tyrosine phosphorylation of the TP53 protein.	Tyrosine	67-75	MDM2 proto-oncogene	Homo sapiens	107-111
28667029-8	2017	CONCLUSIONS: The MDM2 Del1518 polymorphism was associated with BC susceptibility, particularly in menopausal patients with BC who reported tobacco consumption, pregnancy loss, obesity and high glucose levels in the analyzed Mexican population.	Glucose	193-200	MDM2 proto-oncogene	Homo sapiens	17-21
28400230-0	2017	Investigation of the inhibitory mechanism of apomorphine against MDM2-p53 interaction.	Apomorphine	45-56	MDM2 proto-oncogene	Homo sapiens	65-69
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	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	159-163
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	MDM2 proto-oncogene	Homo sapiens	159-163
28400230-3	2017	In addition, both enantiomers of apomorphine showed potent inhibitory activity against the native MDM2-p53 interaction.	Apomorphine	33-44	MDM2 proto-oncogene	Homo sapiens	98-102
29034069-0	2017	Scaffold hopping via ANCHOR.QUERY: beta-lactams as potent p53-MDM2 antagonists .	beta-Lactams	35-47	MDM2 proto-oncogene	Homo sapiens	62-66
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	MDM2 proto-oncogene	Homo sapiens	169-173
28415963-9	2017	CONCLUSION: Although MDM2-B induced slight changes in the cell cycle profile, overall, we found the impact of the three MDM2 splice variants on potential cellular endpoints upon doxorubicin treatment to be limited.	Doxorubicin	178-189	MDM2 proto-oncogene	Homo sapiens	120-124
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	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	155-159
28351583-10	2017	The presence of G allele of MDM2 or Thr allele of ERCC1 was associated with a significantly higher risk of acute and/or early DMEX toxicity.	dmex	126-130	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	15-19
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	MDM2 proto-oncogene	Homo sapiens	38-42
28274247-0	2017	Gossypol has anti-cancer effects by dual-targeting MDM2 and VEGF in human breast cancer.	Gossypol	0-8	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	149-153
28274247-4	2017	Because MDM2 is an RNA-binding protein and its targets include VEGF mRNA, we investigated whether gossypol has an inhibitory effect on MDM2-VEGF.	Gossypol	98-106	MDM2 proto-oncogene	Homo sapiens	135-144
28274247-5	2017	METHODS: UV cross-linking and RNA binding assay, isothermal titration calorimetry assay, and ubiquitination assay were performed to determine mechanisms by which gossypol functions as a dual inhibitor of MDM2 and VEGF.	Gossypol	162-170	MDM2 proto-oncogene	Homo sapiens	204-208
28274247-6	2017	The effect of gossypol on MDM2 and VEGF expression, cancer cell apoptosis, tumor growth and VEGF-mediated angiogenesis were studied in vitro and in vivo in different human breast cancer models with a different p53 status.	Gossypol	14-22	MDM2 proto-oncogene	Homo sapiens	26-30
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	MDM2 proto-oncogene	Homo sapiens	64-68
28274247-8	2017	A nechanistic study further demonstrated that, through disrupting the interaction between MDM2 protein and VEGF mRNA, gossypol induced MDM2 self-ubiquitination and decreased VEGF translation simultaneously, which resulted in both apoptosis and anti-angiogenesis effects.	Gossypol	118-126	MDM2 proto-oncogene	Homo sapiens	90-94
28274247-11	2017	CONCLUSION: Gossypol has anti-cancer effects by dual-targeting MDM2 and VEGF in human breast cancer.	Gossypol	12-20	MDM2 proto-oncogene	Homo sapiens	63-67
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.	Diterpenes	16-25	MDM2 proto-oncogene	Homo sapiens	149-153
28147328-4	2017	The purpose of this study is to study anti-MDM2 autoantibody in pSS patients.	pss	64-67	MDM2 proto-oncogene	Homo sapiens	43-47
29354330-2	2017	Thus, the objective of this study was to synthesize compounds based computational modeling that indicated the pyrido[3,4-b]indole class bind to MDM2, a new cancer target for which there are still no drug on the market.	pyrido[3,4-b]indole	110-129	MDM2 proto-oncogene	Homo sapiens	144-148
29354330-9	2017	Docking at on MDM2 suggested a hydrogen bond interaction between the 6-methoxy Tyr106, hydrophobic interaction with Val93, pi-pi stacking interactions with Tyr100 and His96 and hydrophobic interactions with Leu54 and Ile99.	Hydrogen	31-39	MDM2 proto-oncogene	Homo sapiens	14-18
29354330-9	2017	Docking at on MDM2 suggested a hydrogen bond interaction between the 6-methoxy Tyr106, hydrophobic interaction with Val93, pi-pi stacking interactions with Tyr100 and His96 and hydrophobic interactions with Leu54 and Ile99.	6-methoxy tyr106	69-85	MDM2 proto-oncogene	Homo sapiens	14-18
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	MDM2 proto-oncogene	Homo sapiens	276-280
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	MDM2 proto-oncogene	Homo sapiens	276-280
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	MDM2 proto-oncogene	Homo sapiens	276-280
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	MDM2 proto-oncogene	Homo sapiens	276-280
28147328-9	2017	RESULTS: The presence of anti-MDM2 autoantibody in pSS patients was 21.0%, significantly higher than normal controls (5.40%).	pss	51-54	MDM2 proto-oncogene	Homo sapiens	30-34
28147328-12	2017	Prevalence of anemia, thrombocytopenia and anti-SSB was significantly higher in pSS patients with anti-MDM2 autoantibody.	pss	80-83	MDM2 proto-oncogene	Homo sapiens	103-107
28147328-15	2017	Study on the role of anti-MDM2 or MDM2 in pSS may help us know the pathogenesis mechanism of pSS better.	pss	42-45	MDM2 proto-oncogene	Homo sapiens	26-30
28147328-15	2017	Study on the role of anti-MDM2 or MDM2 in pSS may help us know the pathogenesis mechanism of pSS better.	pss	42-45	MDM2 proto-oncogene	Homo sapiens	34-38
28147328-15	2017	Study on the role of anti-MDM2 or MDM2 in pSS may help us know the pathogenesis mechanism of pSS better.	pss	93-96	MDM2 proto-oncogene	Homo sapiens	26-30
28147328-15	2017	Study on the role of anti-MDM2 or MDM2 in pSS may help us know the pathogenesis mechanism of pSS better.	pss	93-96	MDM2 proto-oncogene	Homo sapiens	34-38
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	MDM2 proto-oncogene	Homo sapiens	83-87
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	MDM2 proto-oncogene	Homo sapiens	83-87
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	MDM2 proto-oncogene	Homo sapiens	136-140
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	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	109-113
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	MDM2 proto-oncogene	Homo sapiens	73-77
27177180-0	2017	Combination therapy in a xenograft model of glioblastoma: enhancement of the antitumor activity of temozolomide by an MDM2 antagonist.	Temozolomide	99-111	MDM2 proto-oncogene	Homo sapiens	118-122
27177180-11	2017	CONCLUSIONS Modulation of MDM2/p53-associated signaling pathways is a novel approach for decreasing TMZ resistance in GBM.	Temozolomide	100-103	MDM2 proto-oncogene	Homo sapiens	26-30
27177180-12	2017	To the authors" knowledge, this is the first study in a humanized intracranial patient-derived xenograft model to demonstrate the efficacy of combining front-line TMZ therapy and an inhibitor of MDM2 protein-protein interactions.	Temozolomide	163-166	MDM2 proto-oncogene	Homo sapiens	195-199
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	MDM2 proto-oncogene	Homo sapiens	187-191
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	MDM2 proto-oncogene	Homo sapiens	187-191
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	MDM2 proto-oncogene	Homo sapiens	89-93
27888811-11	2017	Several promising MDM2 inhibitors have been described such as nutlins, benzodiazepinediones or spiro-oxindoles as well as novel compound classes such as xanthone derivatives and trisubstituted aminothiophenes.	nutlins	62-69	MDM2 proto-oncogene	Homo sapiens	18-22
27888811-11	2017	Several promising MDM2 inhibitors have been described such as nutlins, benzodiazepinediones or spiro-oxindoles as well as novel compound classes such as xanthone derivatives and trisubstituted aminothiophenes.	benzodiazepinediones	71-91	MDM2 proto-oncogene	Homo sapiens	18-22
27888811-11	2017	Several promising MDM2 inhibitors have been described such as nutlins, benzodiazepinediones or spiro-oxindoles as well as novel compound classes such as xanthone derivatives and trisubstituted aminothiophenes.	spiro-oxindoles	95-110	MDM2 proto-oncogene	Homo sapiens	18-22
27999193-2	2017	MDM2 (human homolog of the murine double minute-2) inhibitors such as Nutlin-3 have been shown to induce apoptosis in a p53-dependent manner in CML cells and sensitize cells to Imatinib.	Imatinib Mesylate	177-185	MDM2 proto-oncogene	Homo sapiens	0-4
27888811-11	2017	Several promising MDM2 inhibitors have been described such as nutlins, benzodiazepinediones or spiro-oxindoles as well as novel compound classes such as xanthone derivatives and trisubstituted aminothiophenes.	xanthone	153-161	MDM2 proto-oncogene	Homo sapiens	18-22
27888811-11	2017	Several promising MDM2 inhibitors have been described such as nutlins, benzodiazepinediones or spiro-oxindoles as well as novel compound classes such as xanthone derivatives and trisubstituted aminothiophenes.	trisubstituted aminothiophenes	178-208	MDM2 proto-oncogene	Homo sapiens	18-22
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	MDM2 proto-oncogene	Homo sapiens	90-94
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	MDM2 proto-oncogene	Homo sapiens	262-266
28035066-5	2017	Results showed that 10x10-13Mestradiol elevated the expression of hnRNPA1 regardless ER expression in cells, and then down-regulated the expression of MDM2.	10x10-13mestradiol	20-38	MDM2 proto-oncogene	Homo sapiens	151-155
28035066-7	2017	While, knocking down hnRNPA1 through the transfection of hnRNPA1 siRNA led to the increase of MDM2 at both protein level and gene level In vivo experiment, subcutaneous injection with estradiol every two days near the tumor at doses of 2.5mg/kg/d suppressed tumor growth and reduced MDM2 expression.	Estradiol	184-193	MDM2 proto-oncogene	Homo sapiens	94-98
28035066-7	2017	While, knocking down hnRNPA1 through the transfection of hnRNPA1 siRNA led to the increase of MDM2 at both protein level and gene level In vivo experiment, subcutaneous injection with estradiol every two days near the tumor at doses of 2.5mg/kg/d suppressed tumor growth and reduced MDM2 expression.	Estradiol	184-193	MDM2 proto-oncogene	Homo sapiens	283-287
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	MDM2 proto-oncogene	Homo sapiens	140-144
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	MDM2 proto-oncogene	Homo sapiens	260-264
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	MDM2 proto-oncogene	Homo sapiens	10-14
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	MDM2 proto-oncogene	Homo sapiens	42-46
28099510-5	2017	Instead of promoting the conjugation of polyubiquitin chains and the subsequent proteasomal degradation of NUB1, Mdm2 rather induces its di-ubiquitination on lysine 159.	Lysine	158-164	MDM2 proto-oncogene	Homo sapiens	113-117
28099510-7	2017	We conclude that Mdm2 acts as a positive regulator of NUB1 function, by modulating NUB1 ubiquitination on lysine 159.	Lysine	106-112	MDM2 proto-oncogene	Homo sapiens	17-21
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	MDM2 proto-oncogene	Homo sapiens	183-187
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	MDM2 proto-oncogene	Homo sapiens	99-103
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	MDM2 proto-oncogene	Homo sapiens	99-103
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	MDM2 proto-oncogene	Homo sapiens	10-14
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	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	187-191
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	MDM2 proto-oncogene	Homo sapiens	95-99
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	MDM2 proto-oncogene	Homo sapiens	191-195
28721806-10	2017	L-THP caused down-regulation of XIAP protein via inhibiting the expression of MDM2 and involving proteasomedependent pathway.	tetrahydropalmatine	0-5	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	138-142
28054709-5	2017	RA binds to the RING-finger region of MDM2 and stabilizes p53.	Radium	0-2	MDM2 proto-oncogene	Homo sapiens	38-42
28054709-6	2017	SARAH binds RA and blocks the interaction between RA and MDM2.	Radium	2-4	MDM2 proto-oncogene	Homo sapiens	57-61
28054709-6	2017	SARAH binds RA and blocks the interaction between RA and MDM2.	Radium	12-14	MDM2 proto-oncogene	Homo sapiens	57-61
28054709-8	2017	In the presence of active KRas, the interaction between RA and MDM2 is recovered.	Radium	56-58	MDM2 proto-oncogene	Homo sapiens	63-67
27372348-5	2017	WA prevents p53 alterations and inactivates overexpressed MDM2 through ARF and ROS production.	ros	79-82	MDM2 proto-oncogene	Homo sapiens	58-62
27959389-7	2017	The matrine-induced downregulation of MDM2 led to an inhibition of inhibitor of apoptosis protein 3, which might serve a critical role in matrine-induced apoptosis in MDM2-overexpressing Hep3B cells.	matrine	4-11	MDM2 proto-oncogene	Homo sapiens	38-42
27959389-7	2017	The matrine-induced downregulation of MDM2 led to an inhibition of inhibitor of apoptosis protein 3, which might serve a critical role in matrine-induced apoptosis in MDM2-overexpressing Hep3B cells.	matrine	4-11	MDM2 proto-oncogene	Homo sapiens	167-171
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	MDM2 proto-oncogene	Homo sapiens	165-169
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	MDM2 proto-oncogene	Homo sapiens	9-13
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	MDM2 proto-oncogene	Homo sapiens	119-123
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	MDM2 proto-oncogene	Homo sapiens	90-94
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	MDM2 proto-oncogene	Homo sapiens	96-100
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	MDM2 proto-oncogene	Homo sapiens	9-13
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	MDM2 proto-oncogene	Homo sapiens	96-100
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	MDM2 proto-oncogene	Homo sapiens	91-95
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	MDM2 proto-oncogene	Homo sapiens	91-95
27709883-5	2016	In particular, the 6-chloroindole group does not occupy the usual Trp-23 pocket of Mdm2 but instead is engaged in dimerization.	6-chloroindole	19-33	MDM2 proto-oncogene	Homo sapiens	83-87
27764791-5	2016	Herein, we show that MDM2 inhibitor SAR405838 is a potent therapeutic drug for NB.	SAR405838	36-45	MDM2 proto-oncogene	Homo sapiens	21-25
27986870-0	2016	MEK-ERK-mediated phosphorylation of Mdm2 at Ser-166 in hepatocytes.	Serine	44-47	MDM2 proto-oncogene	Homo sapiens	36-40
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	MDM2 proto-oncogene	Homo sapiens	43-47
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	MDM2 proto-oncogene	Homo sapiens	229-233
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	MDM2 proto-oncogene	Homo sapiens	94-98
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	MDM2 proto-oncogene	Homo sapiens	94-98
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	MDM2 proto-oncogene	Homo sapiens	175-179
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	MDM2 proto-oncogene	Homo sapiens	111-115
27614128-0	2016	Pioglitazone inhibits EGFR/MDM2 signaling-mediated PPARgamma degradation.	Pioglitazone	0-12	MDM2 proto-oncogene	Homo sapiens	27-31
27764791-0	2016	Novel MDM2 inhibitor SAR405838 (MI-773) induces p53-mediated apoptosis in neuroblastoma.	SAR405838	21-30	MDM2 proto-oncogene	Homo sapiens	6-10
27764791-0	2016	Novel MDM2 inhibitor SAR405838 (MI-773) induces p53-mediated apoptosis in neuroblastoma.	SAR405838	32-38	MDM2 proto-oncogene	Homo sapiens	6-10
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	MDM2 proto-oncogene	Homo sapiens	129-133
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	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	49-53
27780924-9	2016	Using the cellular thermal shift assay and the drug affinity responsive target stability assay, we further demonstrated that CDDO-Me directly binds to USP7 in cells, which leads to the decrease of its substrates such as MDM2, MDMX and UHRF1.	bardoxolone methyl	125-132	MDM2 proto-oncogene	Homo sapiens	220-224
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	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	119-123
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	MDM2 proto-oncogene	Homo sapiens	63-67
27659528-7	2016	Mechanistic analysis revealed that administration of geridonin in combination with paclitaxel up-regulated the tumor suppressor PTEN and inhibited phosphorylation of Akt and MDM2.	geridonin	53-62	MDM2 proto-oncogene	Homo sapiens	174-178
27871033-6	2016	Docking of A1 with human mdm2 indicated the lowest binding energy (-6.111Kcal/mol) thereby showing strong affinity of the ligand molecule with the receptor which has been stabilized by strong hydrogen bond interactions in the binding pocket.	Hydrogen	192-200	MDM2 proto-oncogene	Homo sapiens	25-29
27729622-6	2016	Finally, we demonstrate that the unrelated MDM2 antagonist Mi-63 also impinges upon AR signalling, supporting the concept of future treatment of prostate cancer with MDM2 antagonists.	MI-63	59-64	MDM2 proto-oncogene	Homo sapiens	43-47
27729622-6	2016	Finally, we demonstrate that the unrelated MDM2 antagonist Mi-63 also impinges upon AR signalling, supporting the concept of future treatment of prostate cancer with MDM2 antagonists.	MI-63	59-64	MDM2 proto-oncogene	Homo sapiens	166-170
27659528-7	2016	Mechanistic analysis revealed that administration of geridonin in combination with paclitaxel up-regulated the tumor suppressor PTEN and inhibited phosphorylation of Akt and MDM2.	Paclitaxel	83-93	MDM2 proto-oncogene	Homo sapiens	174-178
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	MDM2 proto-oncogene	Homo sapiens	123-127
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	123-127
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	74-78
26993060-0	2016	Antitumour activity of the glycoengineered type II anti-CD20 antibody obinutuzumab (GA101) in combination with the MDM2-selective antagonist idasanutlin (RG7388).	RG7388	141-152	MDM2 proto-oncogene	Homo sapiens	115-119
26993060-1	2016	OBJECTIVES: To investigate whether the glycoengineered type II anti-CD20 monoclonal antibody obinutuzumab (GA101) combined with the selective MDM2 antagonist idasanutlin (RG7388) offers superior efficacy to monotherapy in treating B-lymphoid malignancies in preclinical models.	RG7388	158-169	MDM2 proto-oncogene	Homo sapiens	142-146
27649550-0	2016	Molecular design and validation of halogen bonding orthogonal to hydrogen bonding in breast cancer MDM2-peptide complex.	Halogens	35-42	MDM2 proto-oncogene	Homo sapiens	99-103
27649550-0	2016	Molecular design and validation of halogen bonding orthogonal to hydrogen bonding in breast cancer MDM2-peptide complex.	Hydrogen	65-73	MDM2 proto-oncogene	Homo sapiens	99-103
27649550-2	2016	Here, we performed molecular design of halogen bonding orthogonal to hydrogen bonding at the complex interface of MDM2 protein with its cognate peptide ligand to improve the peptide binding affinity and specificity.	Halogens	39-46	MDM2 proto-oncogene	Homo sapiens	114-118
27649550-2	2016	Here, we performed molecular design of halogen bonding orthogonal to hydrogen bonding at the complex interface of MDM2 protein with its cognate peptide ligand to improve the peptide binding affinity and specificity.	Hydrogen	69-77	MDM2 proto-oncogene	Homo sapiens	114-118
27792778-3	2016	To this end, we conduct a series of hydrogen bond propensity calculations in different contexts: 1) computational alanine-scanning studies of the MDM2-p53 interface; 2) the formation of the complex of MDM2 with the disruptive small molecule Nutlin-3a (dissecting the contribution of the different molecular fragments) and 3) the binding of a series of small molecules (drugs) with different affinities for MDM2.	Hydrogen	36-44	MDM2 proto-oncogene	Homo sapiens	201-205
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	MDM2 proto-oncogene	Homo sapiens	199-203
27735941-9	2016	MDM2 inhibitor-induced p53 activation further enhanced YM155 activity.	YM 155	55-60	MDM2 proto-oncogene	Homo sapiens	0-4
27626308-10	2016	GSK2830371 and the MDM2 inhibitor Nutlin-3a acted synergistically in p53 wild-type cells.	nutlin 3	34-43	MDM2 proto-oncogene	Homo sapiens	19-23
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	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	78-82
27792778-3	2016	To this end, we conduct a series of hydrogen bond propensity calculations in different contexts: 1) computational alanine-scanning studies of the MDM2-p53 interface; 2) the formation of the complex of MDM2 with the disruptive small molecule Nutlin-3a (dissecting the contribution of the different molecular fragments) and 3) the binding of a series of small molecules (drugs) with different affinities for MDM2.	Hydrogen	36-44	MDM2 proto-oncogene	Homo sapiens	201-205
27666947-6	2016	Importantly, one of the MDM2/XIAP inhibitors, MX69, showed minimal inhibitory effect on normal human hematopoiesis in vitro and was very well tolerated in animal models.	MX69	46-50	MDM2 proto-oncogene	Homo sapiens	24-28
27698494-9	2016	Additionally, we identify lysine residues at positions 152 and 154 in the N-terminal domain of ORF50 critically involved in MDM2-mediated downregulation of ORF50 levels.	Lysine	26-32	MDM2 proto-oncogene	Homo sapiens	124-128
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	MDM2 proto-oncogene	Homo sapiens	53-57
27798881-7	2016	In the multivariate analysis, the combination of low MDM4 and high MDM2 was significant for RFS and CSS (HR=14.9; p=0.001; HR=5.63; p=0.019).	thiocysteine	100-103	MDM2 proto-oncogene	Homo sapiens	67-71
27798881-8	2016	CONCLUSION: The combination of MDM2 and MDM4 expression is an independent predictor in patients undergoing RC for MIBC.	4-METHYL-2-PENTANOL	114-118	MDM2 proto-oncogene	Homo sapiens	31-35
27542305-4	2016	The conception of these new inhibitors originated in a consideration on the MDM2 bound conformation of the dihydroisoquinolinone class of inhibitors to which NVP-CGM097 belongs.	CHEMBL1824269	107-128	MDM2 proto-oncogene	Homo sapiens	76-80
27688096-7	2016	Together, these results suggest that miR-367-3p may function as an AR enhancer to increase Sorafenib chemotherapy efficacy via altering the MDM2/AR/FKBP5/PHLPP/(pAKT and pERK) signals to better suppress HCC metastasis.	Sorafenib	91-100	MDM2 proto-oncogene	Homo sapiens	140-144
27785069-5	2016	Overall, compared with the control group, a significantly increased SCC risk was observed for the MDM2 rs2279744 polymorphism in the Asian population (test of association: odds ratio [OR] 1.12, P=0.027 for G vs T; OR 1.26, P=0.016 for GG vs TT; OR 1.25, P&lt;0.001 for GG vs TT + TG; and OR 1.08, P=0.023 for carrier G vs T).	Thioguanine	280-282	MDM2 proto-oncogene	Homo sapiens	98-102
27238606-0	2016	Initial Testing (Stage 1) of MK-8242-A Novel MDM2 Inhibitor-by the Pediatric Preclinical Testing Program.	mk-8242	29-36	MDM2 proto-oncogene	Homo sapiens	45-49
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	MDM2 proto-oncogene	Homo sapiens	101-105
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	MDM2 proto-oncogene	Homo sapiens	39-43
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	MDM2 proto-oncogene	Homo sapiens	115-119
27591897-0	2016	The Vascular Endothelial Growth Factor-A phosphorylates Murine Double Minute-2 on its Serine 166 via the Extracellular Signal-Regulated Kinase 1/2 and p90 Ribosomal S6 Kinase in primary human endothelial cells.	Serine	86-92	MDM2 proto-oncogene	Homo sapiens	56-78
27591897-2	2016	We have recently demonstrated that the pro-angiogenic Vascular Endothelial Growth Factor-A (VEGF-A) is a potent upstream regulator of Mdm2 phosphorylation on its Serine 166 (p-Ser166-Mdm2), a protein modification leading to an increase in endothelial cell migration.	Serine	162-168	MDM2 proto-oncogene	Homo sapiens	134-138
27591897-2	2016	We have recently demonstrated that the pro-angiogenic Vascular Endothelial Growth Factor-A (VEGF-A) is a potent upstream regulator of Mdm2 phosphorylation on its Serine 166 (p-Ser166-Mdm2), a protein modification leading to an increase in endothelial cell migration.	Serine	162-168	MDM2 proto-oncogene	Homo sapiens	183-187
27591897-6	2016	We therefore next analyzed which of these kinases could be responsible for VEGF-A-dependent Mdm2 phosphorylation on Serine 166 by using kinase-specific pharmacological inhibitors.	Serine	116-122	MDM2 proto-oncogene	Homo sapiens	92-96
27591897-7	2016	Inhibition of ERK1/2 phosphorylation by UO126 entirely abrogated the response of p-Ser166-Mdm2 to VEGF-A treatment, while Akt phosphorylation inhibition by wortmannin led to further elevations in p-Ser166-Mdm2.	U 0126	40-45	MDM2 proto-oncogene	Homo sapiens	90-94
27532490-4	2016	Here, we report the use of benzenes as probe molecules in ligand-mapping MD (LMMD) simulations to predict the existence of two novel binding sites on the surface of the oncoprotein MDM2.	Benzene	27-35	MDM2 proto-oncogene	Homo sapiens	169-185
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	MDM2 proto-oncogene	Homo sapiens	189-193
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	246-255	MDM2 proto-oncogene	Homo sapiens	27-31
26776160-0	2016	The E3 ubiquitin protein ligase MDM2 dictates all-trans retinoic acid-induced osteoblastic differentiation of osteosarcoma cells by modulating the degradation of RARalpha.	Tretinoin	56-69	MDM2 proto-oncogene	Homo sapiens	32-36
27432230-0	2016	Platycodin D, a metabolite of Platycodin grandiflorum, inhibits highly metastatic MDA-MB-231 breast cancer growth in vitro and in vivo by targeting the MDM2 oncogene.	platycodin D	0-12	MDM2 proto-oncogene	Homo sapiens	152-156
27273042-11	2016	This coincides with an increase in MDM2/dihydrolipoamide dehydrogenase complexes in the nucleus that was further enhanced by the nuclear export inhibitor Leptomycin B.	leptomycin B	154-166	MDM2 proto-oncogene	Homo sapiens	35-39
26776160-7	2016	Moreover, MDM2 impairs the ATRA-induced osteoblastic differentiation of osteosarcoma cells, whereas an inhibitor of the MDM2 ubiquitin ligase synergizes with ATRA to enhance the differentiation of osteosarcoma cells and primary osteosarcoma blasts.	Tretinoin	27-31	MDM2 proto-oncogene	Homo sapiens	10-14
26776160-7	2016	Moreover, MDM2 impairs the ATRA-induced osteoblastic differentiation of osteosarcoma cells, whereas an inhibitor of the MDM2 ubiquitin ligase synergizes with ATRA to enhance the differentiation of osteosarcoma cells and primary osteosarcoma blasts.	Tretinoin	158-162	MDM2 proto-oncogene	Homo sapiens	120-124
26776160-8	2016	Therefore, our study indicates that MDM2 serves as an E3 ubiquitin ligase to regulate the degradation of RARalpha and suggests that MDM2 is a novel therapeutic target for ATRA-based differentiation therapeutic approaches in osteosarcoma.	Tretinoin	171-175	MDM2 proto-oncogene	Homo sapiens	36-40
26776160-8	2016	Therefore, our study indicates that MDM2 serves as an E3 ubiquitin ligase to regulate the degradation of RARalpha and suggests that MDM2 is a novel therapeutic target for ATRA-based differentiation therapeutic approaches in osteosarcoma.	Tretinoin	171-175	MDM2 proto-oncogene	Homo sapiens	132-136
26586447-2	2016	Idasanutlin (RG7388) is a potent p53-MDM2 antagonist currently in clinical development for treatment of cancer.	RG7388	0-11	MDM2 proto-oncogene	Homo sapiens	37-41
27576846-0	2016	TP53 mutations emerge with HDM2 inhibitor SAR405838 treatment in de-differentiated liposarcoma.	SAR405838	42-51	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	71-75
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	MDM2 proto-oncogene	Homo sapiens	195-199
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	MDM2 proto-oncogene	Homo sapiens	195-199
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	MDM2 proto-oncogene	Homo sapiens	195-199
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	MDM2 proto-oncogene	Homo sapiens	195-199
27259273-0	2016	MDM2 knockdown mediated by a triazine-modified dendrimer in the treatment of non-small cell lung cancer.	Triazines	29-37	MDM2 proto-oncogene	Homo sapiens	0-4
27259273-7	2016	The triazine-modified dendrimer efficiently stimulates the down-regulation of MDM2 gene in NSCLC PC9 cells, which induces significant cell apoptosis through the activation of apoptosis markers such as caspase-8 and poly(ADP-ribose) polymerase (PARP) cleavage.	Triazines	4-12	MDM2 proto-oncogene	Homo sapiens	78-82
27533941-0	2016	Identification of lineariifolianoid A as a novel dual NFAT1 and MDM2 inhibitor for human cancer therapy.	Lineariifolianoid A	18-37	MDM2 proto-oncogene	Homo sapiens	64-68
27533941-3	2016	The present study was designed to examine the anticancer activity and underlying mechanisms of action of lineariifolianoid A (LinA), a novel natural product inhibitor of the NFAT1-MDM2 pathway.	lineariifolianoid	105-122	MDM2 proto-oncogene	Homo sapiens	180-184
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	MDM2 proto-oncogene	Homo sapiens	87-91
26392091-4	2016	The analysis of the changes in the expression of genes involved in the response to DNA damage (CDKN1A, GADD45A, MDM2), apoptosis (BAX, BCL2) and oncogenesis (MYC, JUN) showed that 5-FU, CDDP and ET upregulated the genes involved in DNA damage response, while the anti-apoptotic gene BCL2 and oncogene MYC were downregulated.	Fluorouracil	180-184	MDM2 proto-oncogene	Homo sapiens	112-116
26392091-4	2016	The analysis of the changes in the expression of genes involved in the response to DNA damage (CDKN1A, GADD45A, MDM2), apoptosis (BAX, BCL2) and oncogenesis (MYC, JUN) showed that 5-FU, CDDP and ET upregulated the genes involved in DNA damage response, while the anti-apoptotic gene BCL2 and oncogene MYC were downregulated.	Cisplatin	186-190	MDM2 proto-oncogene	Homo sapiens	112-116
27283770-7	2016	Consistently, MGCD in combination with Nutlin-3, a MDM2 inhibitor showed synergistic effect on inducing apoptosis in 2D and 3D cultured CNE2 cells.	mocetinostat	14-18	MDM2 proto-oncogene	Homo sapiens	51-55
27283770-7	2016	Consistently, MGCD in combination with Nutlin-3, a MDM2 inhibitor showed synergistic effect on inducing apoptosis in 2D and 3D cultured CNE2 cells.	nutlin 3	39-47	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	202-206
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	MDM2 proto-oncogene	Homo sapiens	137-141
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	MDM2 proto-oncogene	Homo sapiens	54-58
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	MDM2 proto-oncogene	Homo sapiens	103-107
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	MDM2 proto-oncogene	Homo sapiens	60-64
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	MDM2 proto-oncogene	Homo sapiens	209-213
26586447-2	2016	Idasanutlin (RG7388) is a potent p53-MDM2 antagonist currently in clinical development for treatment of cancer.	RG7388	13-19	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	19-23
27362806-5	2016	Interestingly, rather than influencing all cAMP-stimulated genes, inhibition of the kinases directly responsible for STAT activation, namely JAKs, or ablation of MDM2, each resulted in abolished induction of a subset of cAMP-stimulated genes, with Cebpd being among the most affected.	Cyclic AMP	220-224	MDM2 proto-oncogene	Homo sapiens	162-166
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	MDM2 proto-oncogene	Homo sapiens	83-87
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	MDM2 proto-oncogene	Homo sapiens	19-23
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	MDM2 proto-oncogene	Homo sapiens	127-131
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	MDM2 proto-oncogene	Homo sapiens	127-131
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	MDM2 proto-oncogene	Homo sapiens	177-181
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	MDM2 proto-oncogene	Homo sapiens	153-157
27147566-7	2016	Moreover, JNK2 phosphorylated p53 at Thr-81, thus protecting p53 from MDM2-induced proteasome degradation.	Threonine	37-40	MDM2 proto-oncogene	Homo sapiens	70-74
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	MDM2 proto-oncogene	Homo sapiens	54-58
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	MDM2 proto-oncogene	Homo sapiens	185-189
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	MDM2 proto-oncogene	Homo sapiens	157-161
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	MDM2 proto-oncogene	Homo sapiens	215-219
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	MDM2 proto-oncogene	Homo sapiens	122-126
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	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	87-91
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	MDM2 proto-oncogene	Homo sapiens	86-90
27129163-0	2016	Downregulation of cyclin D1 sensitizes cancer cells to MDM2 antagonist Nutlin-3.	nutlin 3	71-79	MDM2 proto-oncogene	Homo sapiens	55-59
26959882-6	2016	We compared its effect to MI-219 and Nutlin, which are less potent MDM2 antagonists than SAR405838.	nutlin	37-43	MDM2 proto-oncogene	Homo sapiens	67-71
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	MDM2 proto-oncogene	Homo sapiens	171-175
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	MDM2 proto-oncogene	Homo sapiens	171-175
27050388-4	2016	Phosphorylation of serine 17 in the MDM2 lid region is thought to modulate the equilibrium between "open" and "closed" lid states, but contradictory findings on the favored lid conformational state upon phosphorylation have been reported.	Serine	19-25	MDM2 proto-oncogene	Homo sapiens	36-40
27038437-4	2016	In combination with NMR data, the nanopore measurements showed that the addition of Nutlin-3 rescued MDM2 translocation, indicating that Nutlin-3 disrupted the MDM2/GST-p53TAD complex, thereby releasing MDM2.	nutlin 3	84-92	MDM2 proto-oncogene	Homo sapiens	101-105
27038437-4	2016	In combination with NMR data, the nanopore measurements showed that the addition of Nutlin-3 rescued MDM2 translocation, indicating that Nutlin-3 disrupted the MDM2/GST-p53TAD complex, thereby releasing MDM2.	nutlin 3	137-145	MDM2 proto-oncogene	Homo sapiens	101-105
27038437-4	2016	In combination with NMR data, the nanopore measurements showed that the addition of Nutlin-3 rescued MDM2 translocation, indicating that Nutlin-3 disrupted the MDM2/GST-p53TAD complex, thereby releasing MDM2.	nutlin 3	137-145	MDM2 proto-oncogene	Homo sapiens	160-164
27038437-4	2016	In combination with NMR data, the nanopore measurements showed that the addition of Nutlin-3 rescued MDM2 translocation, indicating that Nutlin-3 disrupted the MDM2/GST-p53TAD complex, thereby releasing MDM2.	nutlin 3	137-145	MDM2 proto-oncogene	Homo sapiens	160-164
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	MDM2 proto-oncogene	Homo sapiens	215-219
26869629-0	2016	Acute myeloid leukemia patients" clinical response to idasanutlin (RG7388) is associated with pre-treatment MDM2 protein expression in leukemic blasts.	RG7388	54-65	MDM2 proto-oncogene	Homo sapiens	108-112
27569097-0	2016	MDM2 344T&gt;A polymorphism; could it be a predictive marker of anthracycline resistance?	Anthracyclines	64-77	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	104-108
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	MDM2 proto-oncogene	Homo sapiens	27-31
27004407-10	2016	The inhibitory effect of triptolide on MDM2-mediated Akt activation was eliminated with MDM2 overexpression.	triptolide	25-35	MDM2 proto-oncogene	Homo sapiens	39-43
27004407-0	2016	Triptolide has anticancer and chemosensitization effects by down-regulating Akt activation through the MDM2/REST pathway in human breast cancer.	triptolide	0-10	MDM2 proto-oncogene	Homo sapiens	103-107
27004407-3	2016	Herein we report a novel signaling pathway, MDM2/Akt, is involved in the anticancer mechanism of triptolide.	triptolide	97-107	MDM2 proto-oncogene	Homo sapiens	44-48
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	MDM2 proto-oncogene	Homo sapiens	37-41
27004407-6	2016	More specifically, triptolide interfered with the interaction between MDM2 and the transcription factor REST to increase expression of the regulatory subunit of PI3-kinase p85 and consequently inhibit Akt activation.	triptolide	19-29	MDM2 proto-oncogene	Homo sapiens	70-74
27044814-0	2016	Tryptanthrin reduces mast cell proliferation promoted by TSLP through modulation of MDM2 and p53.	tryptanthrine	0-12	MDM2 proto-oncogene	Homo sapiens	84-88
27642319-0	2016	Celecoxib Treatment Alters p53 and MDM2 Expression via COX-2 Crosstalk in A549 Cells.	Celecoxib	0-9	MDM2 proto-oncogene	Homo sapiens	35-39
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	MDM2 proto-oncogene	Homo sapiens	206-210
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	MDM2 proto-oncogene	Homo sapiens	206-210
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	MDM2 proto-oncogene	Homo sapiens	206-210
27642319-9	2016	Moreover, our data point toward the possibility that Celecoxib treatment may not be a proper therapeutic strategy in lung cancer cells owing to its potential role in the activation of oncogenes, including COX-2 and MDM2 which seemingly confers a chemoresistance circumstance to the cell.	Celecoxib	53-62	MDM2 proto-oncogene	Homo sapiens	215-219
27108384-2	2016	We assessed MI-219, a small molecule inhibitor of MDM2 with improved pharmacokinetics over nutlin-3, for sensitization of prostate cancer cells to radiotherapy and androgen deprivation therapy, a standard treatment option for men with high-risk prostate cancer.	MI-219	12-18	MDM2 proto-oncogene	Homo sapiens	50-54
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	MDM2 proto-oncogene	Homo sapiens	9-13
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	MDM2 proto-oncogene	Homo sapiens	12-16
27108384-12	2016	We demonstrate that treatment with MI-219 (an inhibitor of MDM2) results in prostate cancer cell sensitization to radiation and androgen deprivation therapy in vitro and in vivo.	MI-219	35-41	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	75-79
26883108-0	2016	Inhibition of WIP1 phosphatase sensitizes breast cancer cells to genotoxic stress and to MDM2 antagonist nutlin-3.	nutlin 3	105-113	MDM2 proto-oncogene	Homo sapiens	89-93
26883108-6	2016	Over time cells treated with GSK2830371 accumulated in G1 and G2 phases of the cell cycle in a p21-dependent manner and were prone to induction of senescence by a low dose of MDM2 antagonist nutlin-3.	GSK2830371	29-39	MDM2 proto-oncogene	Homo sapiens	175-179
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	MDM2 proto-oncogene	Homo sapiens	134-138
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	MDM2 proto-oncogene	Homo sapiens	134-138
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	MDM2 proto-oncogene	Homo sapiens	69-73
27004407-10	2016	The inhibitory effect of triptolide on MDM2-mediated Akt activation was eliminated with MDM2 overexpression.	triptolide	25-35	MDM2 proto-oncogene	Homo sapiens	88-92
27004407-11	2016	MDM2-overexpressing tumor cells, in turn, were less susceptible to the anticancer and chemosensitization effects of triptolide than control cells.	triptolide	116-126	MDM2 proto-oncogene	Homo sapiens	0-4
27004407-14	2016	In summary, triptolide has anticancer and chemosensitization effects by down-regulating Akt activation through the MDM2/REST pathway in human breast cancer.	triptolide	12-22	MDM2 proto-oncogene	Homo sapiens	115-119
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	117-121
26475335-0	2016	SAR405838: A Novel and Potent Inhibitor of the MDM2:p53 Axis for the Treatment of Dedifferentiated Liposarcoma.	SAR405838	0-9	MDM2 proto-oncogene	Homo sapiens	47-51
26475335-3	2016	Here, we report on the preclinical effects of SAR405838, a novel and highly selective MDM2 small-molecule inhibitor, in both in vitro and in vivo DDLPS models.	SAR405838	46-55	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	123-127
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	MDM2 proto-oncogene	Homo sapiens	89-93
26937175-3	2016	MATERIALS AND METHODS: A498 cells treated with MDM2 antagonist MI-319 and/or mTOR inhibitor rapamycin were employed in the present study.	MI 319	63-69	MDM2 proto-oncogene	Homo sapiens	47-51
26926790-0	2016	Homozygous G/G variant of SNP309 in the human MDM2 gene is associated with earlier tumor onset in Caucasian female renal cell carcinoma patients.	snp309	26-32	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	42-46
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	MDM2 proto-oncogene	Homo sapiens	333-337
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	MDM2 proto-oncogene	Homo sapiens	262-266
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	MDM2 proto-oncogene	Homo sapiens	17-21
26863418-0	2016	Hydrophobic Interactions Are a Key to MDM2 Inhibition by Polyphenols as Revealed by Molecular Dynamics Simulations and MM/PBSA Free Energy Calculations.	Polyphenols	57-68	MDM2 proto-oncogene	Homo sapiens	38-42
26863418-0	2016	Hydrophobic Interactions Are a Key to MDM2 Inhibition by Polyphenols as Revealed by Molecular Dynamics Simulations and MM/PBSA Free Energy Calculations.	poly(tetramethylene succinate-co-tetramethylene adipate)	122-126	MDM2 proto-oncogene	Homo sapiens	38-42
26863418-3	2016	In the present study, we elucidated the MDM2 inhibition potential of polyphenols (Apigenin, Fisetin, Galangin and Luteolin) by MD simulation and MM/PBSA free energy calculations.	Polyphenols	69-80	MDM2 proto-oncogene	Homo sapiens	40-44
26863418-4	2016	All polyphenols bind to hydrophobic groove of MDM2 and the binding was found to be stable throughout MD simulation.	Polyphenols	4-15	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	83-87
26549658-5	2016	Functional validation demonstrated that TBMS1-induced NCI-H460 cell cytotoxicity involved nucleolar stress-induced p53/murine double minute clone 2 (MDM2), mTOR, and NF-kappaB signaling pathways.	tubeimoside I	40-45	MDM2 proto-oncogene	Homo sapiens	115-147
25867069-0	2016	The NEDD8 inhibitor MLN4924 increases the size of the nucleolus and activates p53 through the ribosomal-Mdm2 pathway.	pevonedistat	20-27	MDM2 proto-oncogene	Homo sapiens	104-108
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	MDM2 proto-oncogene	Homo sapiens	50-54
26985323-2	2016	Research focused on optimization of a crucial HDM2 Trp23-ligand interaction led to the identification of 2-(trifluoromethyl)thiophene as the preferred moiety.	2-(Trifluoromethyl)thiophene	105-133	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	109-113
26636645-5	2016	Moreover, we find that the PP1alpha inhibitor tautomycin increases phosphorylation of AR ubiquitin ligases including SKP2 and MDM2 at sites that enhance their activity, providing a mechanism by which PP1alpha may suppress AR degradation.	tautomycin	46-56	MDM2 proto-oncogene	Homo sapiens	126-130
26694802-0	2016	Inhibition of MDM2 expression by rosmarinic acid in TSLP-stimulated mast cell.	rosmarinic acid	33-48	MDM2 proto-oncogene	Homo sapiens	14-18
26694802-9	2016	These effects of RA are likely to be mediated through inhibiting the MDM2 increased by TSLP.	rosmarinic acid	17-19	MDM2 proto-oncogene	Homo sapiens	69-73
26748827-5	2016	MDM2 physically associated with EZH2 on chromatin, enhancing the trimethylation of histone 3 at lysine 27 and the ubiquitination of histone 2A at lysine 119 (H2AK119) at its target genes.	Lysine	96-102	MDM2 proto-oncogene	Homo sapiens	0-4
26748827-5	2016	MDM2 physically associated with EZH2 on chromatin, enhancing the trimethylation of histone 3 at lysine 27 and the ubiquitination of histone 2A at lysine 119 (H2AK119) at its target genes.	Lysine	146-152	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	225-229
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	MDM2 proto-oncogene	Homo sapiens	225-229
27825169-7	2016	RESULTS: Rapamycin treatment suppresses the expression of MDM2 and exogenous overexpression of MDM2 in A498 cells contributes to rapamycin resistance.	Sirolimus	9-18	MDM2 proto-oncogene	Homo sapiens	58-62
27825169-7	2016	RESULTS: Rapamycin treatment suppresses the expression of MDM2 and exogenous overexpression of MDM2 in A498 cells contributes to rapamycin resistance.	Sirolimus	9-18	MDM2 proto-oncogene	Homo sapiens	95-99
27825169-11	2016	In both in vitro and in vivo models, the combination of rapamycin with the MDM2 inhibitor, MI-319, demonstrated a synergistic inhibitory effect on rapamycin resistant cells.	Sirolimus	147-156	MDM2 proto-oncogene	Homo sapiens	75-79
27825169-7	2016	RESULTS: Rapamycin treatment suppresses the expression of MDM2 and exogenous overexpression of MDM2 in A498 cells contributes to rapamycin resistance.	Sirolimus	129-138	MDM2 proto-oncogene	Homo sapiens	95-99
27825169-8	2016	By establishing a rapamycin resistant cell line, we observed that MDM2 was significantly upregulated in rapamycin resistant cells than that in rapamycin sensitive cells.	Sirolimus	18-27	MDM2 proto-oncogene	Homo sapiens	66-70
27825169-8	2016	By establishing a rapamycin resistant cell line, we observed that MDM2 was significantly upregulated in rapamycin resistant cells than that in rapamycin sensitive cells.	Sirolimus	104-113	MDM2 proto-oncogene	Homo sapiens	66-70
27825169-10	2016	Moreover, the inhibition of MDM2 by siMDM2 sensitizes A498 cells to rapamycin through the activation of p53.	Sirolimus	68-77	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	136-140
25808617-0	2016	Computational analysis of spiro-oxindole inhibitors of the MDM2-p53 interaction: insights and selection of novel inhibitors.	spiro-oxindole	26-40	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	114-118
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	MDM2 proto-oncogene	Homo sapiens	113-117
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	MDM2 proto-oncogene	Homo sapiens	163-167
29375730-3	2016	We previously reported that MDM2 promotes degradation of another ubiquitin E3 ligase HUWE1 by ubiquitination, particularly, which confers HER2+ breast cancer cells resistance to the HER2 inhibitor lapatinib.	Lapatinib	197-206	MDM2 proto-oncogene	Homo sapiens	28-32
25808617-2	2016	Here, we used molecular dynamics simulations followed by free energy decomposition analysis to study conformational changes in MDM2 induced by three known spiro-oxindole inhibitors.	2-oxindole	161-169	MDM2 proto-oncogene	Homo sapiens	127-131
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	MDM2 proto-oncogene	Homo sapiens	143-147
26585176-4	2016	In silico studies also performed to predict the binding mechanism of DHMA with MDM2-p53 protein.	dhma	69-73	MDM2 proto-oncogene	Homo sapiens	79-83
27213086-1	2016	Structural basis for exploration into MDM2 and MDM2-DHFR interaction plays a vital role in analyzing the obstruction in folate metabolism, nonsynthesis of purines, and further epigenetic regulation in Homo sapiens.	Folic Acid	120-126	MDM2 proto-oncogene	Homo sapiens	38-42
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	MDM2 proto-oncogene	Homo sapiens	158-162
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	MDM2 proto-oncogene	Homo sapiens	158-162
27213086-1	2016	Structural basis for exploration into MDM2 and MDM2-DHFR interaction plays a vital role in analyzing the obstruction in folate metabolism, nonsynthesis of purines, and further epigenetic regulation in Homo sapiens.	Folic Acid	120-126	MDM2 proto-oncogene	Homo sapiens	47-51
27213086-1	2016	Structural basis for exploration into MDM2 and MDM2-DHFR interaction plays a vital role in analyzing the obstruction in folate metabolism, nonsynthesis of purines, and further epigenetic regulation in Homo sapiens.	Purines	155-162	MDM2 proto-oncogene	Homo sapiens	38-42
27213086-1	2016	Structural basis for exploration into MDM2 and MDM2-DHFR interaction plays a vital role in analyzing the obstruction in folate metabolism, nonsynthesis of purines, and further epigenetic regulation in Homo sapiens.	Purines	155-162	MDM2 proto-oncogene	Homo sapiens	47-51
27213086-8	2016	Lysine residues from MDM2 played a predominant role.	Lysine	0-6	MDM2 proto-oncogene	Homo sapiens	21-25
26584879-0	2015	2,30-Bis(10H-indole) heterocycles: New p53/MDM2/MDMX antagonists.	2,30-bis(10h-indole)	0-20	MDM2 proto-oncogene	Homo sapiens	43-47
26228206-10	2015	Immunoprecipitation indicated enhanced MDM2-mediated polyubiquitination of RRM1 through Lys-48-mediated linkage following pimasertib treatment, an effect mediated, in part, by AKT.	lys-48	88-94	MDM2 proto-oncogene	Homo sapiens	39-43
26228206-10	2015	Immunoprecipitation indicated enhanced MDM2-mediated polyubiquitination of RRM1 through Lys-48-mediated linkage following pimasertib treatment, an effect mediated, in part, by AKT.	N-(2,3-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamide	122-132	MDM2 proto-oncogene	Homo sapiens	39-43
26475964-0	2015	Enhanced cytotoxicity of prenylated chalcone against tumour cells via disruption of the p53-MDM2 interaction.	Chalcone	36-44	MDM2 proto-oncogene	Homo sapiens	92-96
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	MDM2 proto-oncogene	Homo sapiens	58-62
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	MDM2 proto-oncogene	Homo sapiens	79-83
26350565-0	2015	The cholesterol metabolite 27-hydroxycholesterol regulates p53 activity and increases cell proliferation via MDM2 in breast cancer cells.	Cholesterol	4-15	MDM2 proto-oncogene	Homo sapiens	109-113
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	MDM2 proto-oncogene	Homo sapiens	109-113
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	MDM2 proto-oncogene	Homo sapiens	105-109
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	MDM2 proto-oncogene	Homo sapiens	133-137
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.	nutlin 3	120-128	MDM2 proto-oncogene	Homo sapiens	105-109
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	MDM2 proto-oncogene	Homo sapiens	119-123
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	MDM2 proto-oncogene	Homo sapiens	170-174
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	MDM2 proto-oncogene	Homo sapiens	71-75
26428461-0	2015	A stapled peptide antagonist of MDM2 carried by polymeric micelles sensitizes glioblastoma to temozolomide treatment through p53 activation.	Temozolomide	94-106	MDM2 proto-oncogene	Homo sapiens	32-36
26428461-3	2015	To circumvent these problems, we developed a cyclic RGD peptide-conjugated poly(ethylene glycol)-co-poly(lactic acid) polymeric micelle (RGD-M) that carried a stapled peptide antagonist of both MDM2 and MDMX (sPMI).	poly(ethylene glycol)-co-poly(lactic acid)	75-117	MDM2 proto-oncogene	Homo sapiens	194-198
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	MDM2 proto-oncogene	Homo sapiens	102-106
26206331-0	2015	Inhibition of Wild-Type p53-Expressing AML by the Novel Small Molecule HDM2 Inhibitor CGM097.	NVP-CGM097	86-92	MDM2 proto-oncogene	Homo sapiens	71-75
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	MDM2 proto-oncogene	Homo sapiens	47-51
26427060-0	2015	Design, Synthesis and Evaluation of 2,5-Diketopiperazines as Inhibitors of the MDM2-p53 Interaction.	2,5-dioxopiperazine	36-57	MDM2 proto-oncogene	Homo sapiens	79-83
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	MDM2 proto-oncogene	Homo sapiens	90-94
26256638-6	2015	Docking results indicated that compound 3d fitted well into the MDM2 active site 1RV1 by interacting with Lys94 and Thr101 residues.	Thr101	116-122	MDM2 proto-oncogene	Homo sapiens	64-68
26115576-0	2015	Identification of a new p53/MDM2 inhibitor motif inspired by studies of chlorofusin.	chlorofusin	72-83	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	165-169
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	MDM2 proto-oncogene	Homo sapiens	165-169
26115576-3	2015	From this small library the first ever non-azaphilone containing chlorofusin analog with MDM2/p53 activity was identified.	azaphilone	43-53	MDM2 proto-oncogene	Homo sapiens	89-93
26115576-3	2015	From this small library the first ever non-azaphilone containing chlorofusin analog with MDM2/p53 activity was identified.	chlorofusin	65-76	MDM2 proto-oncogene	Homo sapiens	89-93
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	MDM2 proto-oncogene	Homo sapiens	151-155
26416444-9	2015	We demonstrated that T/T and G/G mdm2 SNP309 cells were equally sensitive to 8-amino-adenosine induced cell death.	8-aminoadenosine	77-94	MDM2 proto-oncogene	Homo sapiens	33-37
26378044-6	2015	Mdm2 recognizes phosphorylated serine 213 of AR-v7, and induces AR-v7 ubiquitination and protein degradation.	Serine	31-37	MDM2 proto-oncogene	Homo sapiens	0-4
26431163-6	2015	We pretreated such cells with Nutlin-3a, a prototype inhibitor of the p53-antagonist Mdm2.	nutlin 3	30-39	MDM2 proto-oncogene	Homo sapiens	85-89
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	MDM2 proto-oncogene	Homo sapiens	51-55
25605253-3	2015	SAHA and/or HDAC2 siRNA increased Mdm2 ubiquitination, and MG132, an inhibitor of proteosome function, prevented HDAC2 inhibition-induced degradation of Mdm2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	MDM2 proto-oncogene	Homo sapiens	153-157
26141769-0	2015	Discovery of dihydroisoquinolinone derivatives as novel inhibitors of the p53-MDM2 interaction with a distinct binding mode.	CHEMBL1824269	13-34	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	131-135
25818095-10	2015	CONCLUSION: The results of our study suggest that SNPs in MDM2 might be used to predict the toxicities of platinum-based chemotherapy and overall survival in patients with advanced NSCLC.	Platinum	106-114	MDM2 proto-oncogene	Homo sapiens	58-62
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	MDM2 proto-oncogene	Homo sapiens	89-93
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	MDM2 proto-oncogene	Homo sapiens	92-96
26041888-0	2015	Oral nano-delivery of anticancer ginsenoside 25-OCH3-PPD, a natural inhibitor of the MDM2 oncogene: Nanoparticle preparation, characterization, in vitro and in vivo anti-prostate cancer activity, and mechanisms of action.	25-methoxylprotopanaxadiol	33-56	MDM2 proto-oncogene	Homo sapiens	85-89
26041888-3	2015	We have recently identified a novel ginsenoside, 25-OCH3-PPD (GS25), one of the most active anticancer ginsenosides discovered thus far, and have demonstrated its MDM2 inhibition and anticancer activity in various human cancer models, including prostate cancer.	Ginsenosides	36-47	MDM2 proto-oncogene	Homo sapiens	163-167
26041888-3	2015	We have recently identified a novel ginsenoside, 25-OCH3-PPD (GS25), one of the most active anticancer ginsenosides discovered thus far, and have demonstrated its MDM2 inhibition and anticancer activity in various human cancer models, including prostate cancer.	25-methoxylprotopanaxadiol	62-66	MDM2 proto-oncogene	Homo sapiens	163-167
26041888-6	2015	After GS25 was successfully encapsulated into PEG-PLGA nanoparticles (GS25NP) and its physicochemical properties were characterized, the efficiency of MDM2 targeting, anticancer efficacy, pharmacokinetics, and safety were evaluated in in vitro and in vivo models of human prostate cancer.	25-methoxylprotopanaxadiol	6-10	MDM2 proto-oncogene	Homo sapiens	151-155
26041888-7	2015	Our results indicated that, compared with the unencapsulated GS25, GS25NP demonstrated better MDM2 inhibition, improved oral bioavailability and enhanced in vitro and in vivo activities.	gs25np	67-73	MDM2 proto-oncogene	Homo sapiens	94-98
25388787-1	2015	Two libraries of substituted benzimidazoles were designed using a "scaffold-hopping" approach based on reported MDM2-p53 inhibitors.	Benzimidazoles	29-43	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	116-120
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	MDM2 proto-oncogene	Homo sapiens	150-154
26070072-0	2015	Significant Differences in the Development of Acquired Resistance to the MDM2 Inhibitor SAR405838 between In Vitro and In Vivo Drug Treatment.	SAR405838	88-97	MDM2 proto-oncogene	Homo sapiens	73-77
25989210-5	2015	Actinomycin D promotes phosphorylation and accumulation of p53 via a mechanism that involves high expression of MDM2.	Dactinomycin	0-13	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	170-174
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	MDM2 proto-oncogene	Homo sapiens	116-120
26070072-1	2015	SAR405838 is a potent and specific MDM2 inhibitor currently being evaluated in Phase I clinical trials for the treatment of human cancer.	SAR405838	0-9	MDM2 proto-oncogene	Homo sapiens	35-39
26070072-14	2015	Our data thus show that SJSA-1 tumor cells acquire very different levels of resistance in vitro and in vivo to the MDM2 inhibitor SAR405838.	SAR405838	130-139	MDM2 proto-oncogene	Homo sapiens	115-119
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	MDM2 proto-oncogene	Homo sapiens	99-103
25754349-1	2015	PURPOSE: Two clinical-stage anticancer drugs, the Bcl-2 inhibitor ABT-263, and the MDM2 inhibitor SAR405838 achieve complete tumor regression in animal models of leukemia but also induce acquired resistance.	SAR405838	98-107	MDM2 proto-oncogene	Homo sapiens	83-87
26046940-7	2015	25-fold affinity improvement of the piperidinone family of inhibitors for MDM2 constructs that include the full lid correlates with interactions between ligand hydrophobic groups and the C-terminal lid region that is already partially ordered in apo MDM2.	2-piperidone	36-48	MDM2 proto-oncogene	Homo sapiens	74-78
26046940-7	2015	25-fold affinity improvement of the piperidinone family of inhibitors for MDM2 constructs that include the full lid correlates with interactions between ligand hydrophobic groups and the C-terminal lid region that is already partially ordered in apo MDM2.	2-piperidone	36-48	MDM2 proto-oncogene	Homo sapiens	250-254
26046940-8	2015	By contrast, Nutlin or benzodiazepinedione inhibitors, that bind with similar affinity to full lid and lid-truncated MDM2 constructs, interact additionally through their solubilizing groups with N-terminal lid residues that are more disordered in apo MDM2.	nutlin	13-19	MDM2 proto-oncogene	Homo sapiens	117-121
26046940-8	2015	By contrast, Nutlin or benzodiazepinedione inhibitors, that bind with similar affinity to full lid and lid-truncated MDM2 constructs, interact additionally through their solubilizing groups with N-terminal lid residues that are more disordered in apo MDM2.	nutlin	13-19	MDM2 proto-oncogene	Homo sapiens	251-255
26046940-8	2015	By contrast, Nutlin or benzodiazepinedione inhibitors, that bind with similar affinity to full lid and lid-truncated MDM2 constructs, interact additionally through their solubilizing groups with N-terminal lid residues that are more disordered in apo MDM2.	benzodiazepinedione	23-42	MDM2 proto-oncogene	Homo sapiens	117-121
26046940-8	2015	By contrast, Nutlin or benzodiazepinedione inhibitors, that bind with similar affinity to full lid and lid-truncated MDM2 constructs, interact additionally through their solubilizing groups with N-terminal lid residues that are more disordered in apo MDM2.	benzodiazepinedione	23-42	MDM2 proto-oncogene	Homo sapiens	251-255
25840370-0	2015	The cis conformation of proline leads to weaker binding of a p53 peptide to MDM2 compared to trans.	Proline	24-31	MDM2 proto-oncogene	Homo sapiens	76-80
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	MDM2 proto-oncogene	Homo sapiens	127-131
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	MDM2 proto-oncogene	Homo sapiens	134-138
25882531-0	2015	Discovery of DS-5272 as a promising candidate: A potent and orally active p53-MDM2 interaction inhibitor.	DS-5272	13-20	MDM2 proto-oncogene	Homo sapiens	78-82
25882531-1	2015	We have published p53-MDM2 interaction inhibitors possessing a novel dihydroimidazothiazole scaffold.	dihydroimidazothiazole	69-91	MDM2 proto-oncogene	Homo sapiens	22-26
25965177-0	2015	A distinct p53 target gene set predicts for response to the selective p53-HDM2 inhibitor NVP-CGM097.	NVP-CGM097	93-99	MDM2 proto-oncogene	Homo sapiens	74-78
25942498-0	2015	8-Triazolylpurines: Towards Fluorescent Inhibitors of the MDM2/p53 Interaction.	8-triazolylpurines	0-18	MDM2 proto-oncogene	Homo sapiens	58-62
25773666-0	2015	Acteoside attenuates TSLP-induced mast cell proliferation via down-regulating MDM2.	acteoside	0-9	MDM2 proto-oncogene	Homo sapiens	78-82
25773666-3	2015	Here, we investigate whether acteoside attenuates the MDM2 expression in a TSLP-stimulated human mast cell line (HMC-1 cells).	acteoside	29-38	MDM2 proto-oncogene	Homo sapiens	54-58
25773666-8	2015	In conclusion, these results indicate that acteoside is a specific regulator of MDM2 activation in TSLP-stimulated mast cells, which indicates its potential use for the treatment of mast cell-mediated inflammatory diseases.	acteoside	43-52	MDM2 proto-oncogene	Homo sapiens	80-84
25668009-0	2015	MDM2 is an important prognostic and predictive factor for platin-pemetrexed therapy in malignant pleural mesotheliomas and deregulation of P14/ARF (encoded by CDKN2A) seems to contribute to an MDM2-driven inactivation of P53.	Pemetrexed	65-75	MDM2 proto-oncogene	Homo sapiens	0-4
25668009-12	2015	CONCLUSIONS: MDM2 is a prognostic and predictive marker for a platin-pemetrexed therapy of patients with MPMs.	Pemetrexed	69-79	MDM2 proto-oncogene	Homo sapiens	13-17
25482373-7	2015	Because hMED17 associates with p53 upon UV-C irradiation, we treated human MCF-7 cells with either UV-C or the MDM2 inhibitor Nutlin-3.	nutlin 3	126-134	MDM2 proto-oncogene	Homo sapiens	111-115
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	MDM2 proto-oncogene	Homo sapiens	140-144
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	MDM2 proto-oncogene	Homo sapiens	91-95
25814188-6	2015	In addition, similar tumor cytotoxic effects were observed for OXAZ-1 against MDMX-overexpressing breast adenocarcinoma MCF-7 tumor cells, commonly described as highly resistant to MDM2-only inhibitors.	oxaz-1	63-69	MDM2 proto-oncogene	Homo sapiens	181-185
25845590-3	2015	Here we explore MDM2 splicing regulation by utilizing a novel minigene that mimics endogenous MDM2 splicing in response to UV and cisplatinum-induced DNA damage.	Cisplatin	130-141	MDM2 proto-oncogene	Homo sapiens	16-20
25845590-3	2015	Here we explore MDM2 splicing regulation by utilizing a novel minigene that mimics endogenous MDM2 splicing in response to UV and cisplatinum-induced DNA damage.	Cisplatin	130-141	MDM2 proto-oncogene	Homo sapiens	94-98
25845590-8	2015	Notably, we demonstrate that MDM2-ALT1 splicing can be blocked by targeting SRSF1 sites on exon 11 using antisense oligonucleotides.	Oligonucleotides	115-131	MDM2 proto-oncogene	Homo sapiens	29-33
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	MDM2 proto-oncogene	Homo sapiens	101-105
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	MDM2 proto-oncogene	Homo sapiens	101-105
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	MDM2 proto-oncogene	Homo sapiens	81-85
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	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	83-87
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	MDM2 proto-oncogene	Homo sapiens	135-139
25902914-11	2015	In further studies, we found that oroxylin A induced a reduction in MDM2 transcription by promoting the lipid phosphatase activity of phosphatase and tensin homolog, which was upregulated via sirtuin3-mediated deacetylation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	34-44	MDM2 proto-oncogene	Homo sapiens	68-72
25902914-13	2015	The expression of MDM2 protein in tumor tissue was downregulated by oroxylin A as well.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	68-78	MDM2 proto-oncogene	Homo sapiens	18-22
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	MDM2 proto-oncogene	Homo sapiens	80-84
25706509-6	2015	Additionally, the hydrophobic staple shields a network of water molecules, kinetically stabilizing a water chain hydrogen-bonded between the peptide and MDM2.	Water	58-63	MDM2 proto-oncogene	Homo sapiens	153-157
25706509-6	2015	Additionally, the hydrophobic staple shields a network of water molecules, kinetically stabilizing a water chain hydrogen-bonded between the peptide and MDM2.	Water	101-106	MDM2 proto-oncogene	Homo sapiens	153-157
25706509-6	2015	Additionally, the hydrophobic staple shields a network of water molecules, kinetically stabilizing a water chain hydrogen-bonded between the peptide and MDM2.	Hydrogen	113-121	MDM2 proto-oncogene	Homo sapiens	153-157
24882579-0	2015	miR-339-5p regulates the p53 tumor-suppressor pathway by targeting MDM2.	mir-339-5p	0-10	MDM2 proto-oncogene	Homo sapiens	67-71
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	MDM2 proto-oncogene	Homo sapiens	122-126
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	MDM2 proto-oncogene	Homo sapiens	142-146
25880782-13	2015	MDM2 positivity was significantly higher in the Failure group than in the CR group in cStageIII (P = 0.014).	Chromium	74-76	MDM2 proto-oncogene	Homo sapiens	0-4
25639470-0	2015	An mTORC1-Mdm2-Drosha axis for miRNA biogenesis in response to glucose- and amino acid-deprivation.	Glucose	63-70	MDM2 proto-oncogene	Homo sapiens	10-14
25639470-7	2015	These miRNA was regulated by glucose through the mTORC1-MDM2-DROSHA axis.	Glucose	29-36	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	134-138
25415135-5	2015	There was, however, a statistically significant association of T309G MDM2 with CSS (p=0.022): patients with TT had significantly worse survival than GG/GT (p=0.009), while those with GT and GG had similar outcomes (p=0.92).	thiocysteine	79-82	MDM2 proto-oncogene	Homo sapiens	69-73
25444910-5	2015	When HK-2 cells were treated with the MDM2 antagonist inducing p53, nutlin-3, or p53 transcriptional activator, tenovin-1, cell growth decreased but cisplatin toxicity was unaffected.	Cisplatin	149-158	MDM2 proto-oncogene	Homo sapiens	38-42
25663456-8	2015	In xenograft tumors, CP-31398 modulated the expression of Bax, Bcl-2, caspase 3, cyclin D, and Mdm2 and then blocked the growth of xenograft tumors.	CP 31398	21-29	MDM2 proto-oncogene	Homo sapiens	95-99
25461314-5	2015	Additionally, N9 also potentiates the production of the pro-apoptotic markers Bax and p53 via inhibition of MDM2.	Nonoxynol	14-16	MDM2 proto-oncogene	Homo sapiens	108-112
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	MDM2 proto-oncogene	Homo sapiens	130-134
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	MDM2 proto-oncogene	Homo sapiens	162-166
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	MDM2 proto-oncogene	Homo sapiens	205-209
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	MDM2 proto-oncogene	Homo sapiens	70-74
25312347-11	2015	Finally, the molecular docking analysis of the interactions between the synthesized compounds and MDM2 revealed that oxazoloisoindolinone 3a binds to MDM2.	oxazoloisoindolinone	117-137	MDM2 proto-oncogene	Homo sapiens	98-102
25312347-11	2015	Finally, the molecular docking analysis of the interactions between the synthesized compounds and MDM2 revealed that oxazoloisoindolinone 3a binds to MDM2.	oxazoloisoindolinone	117-137	MDM2 proto-oncogene	Homo sapiens	150-154
25524737-0	2015	PI3K/AKT and Mdm2 activation are associated with inhibitory effect of cAMP increasing agents on DNA damage-induced cell death in human pre-B NALM-6 cells.	Cyclic AMP	70-74	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	111-115
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	MDM2 proto-oncogene	Homo sapiens	266-270
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	MDM2 proto-oncogene	Homo sapiens	127-131
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	MDM2 proto-oncogene	Homo sapiens	127-131
25377899-0	2015	Identification of antipsychotic drug fluspirilene as a potential p53-MDM2 inhibitor: a combined computational and experimental study.	Fluspirilene	37-49	MDM2 proto-oncogene	Homo sapiens	69-73
25377899-6	2015	These studies identified fluspirilene, an approved antipsychotic drug, as a top hit with MDM2 binding mode and energy similar to that of a native MDM2 crystal ligand.	Fluspirilene	25-37	MDM2 proto-oncogene	Homo sapiens	89-93
25377899-6	2015	These studies identified fluspirilene, an approved antipsychotic drug, as a top hit with MDM2 binding mode and energy similar to that of a native MDM2 crystal ligand.	Fluspirilene	25-37	MDM2 proto-oncogene	Homo sapiens	146-150
25377899-7	2015	The molecular dynamics simulations suggested stable binding of fluspirilene to the p53-binding pocket on MDM2 protein.	Fluspirilene	63-75	MDM2 proto-oncogene	Homo sapiens	105-109
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	MDM2 proto-oncogene	Homo sapiens	129-133
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	MDM2 proto-oncogene	Homo sapiens	136-140
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	MDM2 proto-oncogene	Homo sapiens	148-152
25431082-5	2015	MDM2 silencing (transiently by siRNA-MDM2) increased the PD-induced FOXO3a protein expression, while MDM2 overexpression (in cells transiently transfected with a pcDNA3-MDM2 plasmid) decreased the PD-induced expression of the FOXO3a protein.	platycodin D	57-59	MDM2 proto-oncogene	Homo sapiens	0-4
25431082-5	2015	MDM2 silencing (transiently by siRNA-MDM2) increased the PD-induced FOXO3a protein expression, while MDM2 overexpression (in cells transiently transfected with a pcDNA3-MDM2 plasmid) decreased the PD-induced expression of the FOXO3a protein.	platycodin D	57-59	MDM2 proto-oncogene	Homo sapiens	37-41
25431082-5	2015	MDM2 silencing (transiently by siRNA-MDM2) increased the PD-induced FOXO3a protein expression, while MDM2 overexpression (in cells transiently transfected with a pcDNA3-MDM2 plasmid) decreased the PD-induced expression of the FOXO3a protein.	platycodin D	57-59	MDM2 proto-oncogene	Homo sapiens	37-41
25431082-5	2015	MDM2 silencing (transiently by siRNA-MDM2) increased the PD-induced FOXO3a protein expression, while MDM2 overexpression (in cells transiently transfected with a pcDNA3-MDM2 plasmid) decreased the PD-induced expression of the FOXO3a protein.	platycodin D	57-59	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	125-129
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	MDM2 proto-oncogene	Homo sapiens	125-129
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	MDM2 proto-oncogene	Homo sapiens	125-129
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	MDM2 proto-oncogene	Homo sapiens	92-96
24986024-0	2015	ROS and p53 in regulation of UVB-induced HDM2 alternative splicing.	ros	0-3	MDM2 proto-oncogene	Homo sapiens	41-45
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	MDM2 proto-oncogene	Homo sapiens	169-173
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	MDM2 proto-oncogene	Homo sapiens	169-173
25384157-0	2014	Discovery of AM-7209, a potent and selective 4-amidobenzoic acid inhibitor of the MDM2-p53 interaction.	am-7209	13-20	MDM2 proto-oncogene	Homo sapiens	82-86
25584963-3	2015	To study the spatiotemporal characteristics of this molecular process we carried out Brownian dynamics simulations of the interactions of the MDM2 protein with a p53 peptide in its wild type state and when phosphorylated at Thr18 (pThr18) and Ser20 (pSer20).	UNII-PYZ33YLR8A	224-229	MDM2 proto-oncogene	Homo sapiens	142-146
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	MDM2 proto-oncogene	Homo sapiens	82-86
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	MDM2 proto-oncogene	Homo sapiens	162-166
25354189-2	2014	The optimal combination of azido amino acids and dialkynyl linker length for MDM2 binding was determined.	azido amino acids	27-44	MDM2 proto-oncogene	Homo sapiens	77-81
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	MDM2 proto-oncogene	Homo sapiens	64-68
25512388-7	2014	In contrast, FL118 stimulates Mdm2-mediated MdmX ubiquitination.	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	13-18	MDM2 proto-oncogene	Homo sapiens	30-34
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	MDM2 proto-oncogene	Homo sapiens	61-65
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	MDM2 proto-oncogene	Homo sapiens	108-112
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	MDM2 proto-oncogene	Homo sapiens	108-112
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	MDM2 proto-oncogene	Homo sapiens	68-72
25214240-6	2014	In addition, inhibition of p53 by pifithrin-alpha orthe activation of Mdm2 by Nutlin-3 co-treatment did not alter EBR induced PARP cleavage.	nutlin 3	78-86	MDM2 proto-oncogene	Homo sapiens	70-74
24292333-6	2014	RESULTS: Negative, cytoplasm-positive, nucleus-positive, and N+&amp;C+ expressions of Mdm2 were observed in 59.2, 10.9, 27.8, and 2.1 % of patients, respectively.	n+&amp	61-67	MDM2 proto-oncogene	Homo sapiens	86-90
25622680-12	2014	Cisplatin up-regulated p53, Mdm2 and p21 in both cell lines.	Cisplatin	0-9	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	156-160
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	MDM2 proto-oncogene	Homo sapiens	64-68
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	MDM2 proto-oncogene	Homo sapiens	64-68
26281353-8	2015	In cancer cells MDM2 stimulates cytostatic-induced DSBs repair, thus leading to chemoresistance.	dsbs	51-55	MDM2 proto-oncogene	Homo sapiens	16-20
25218545-10	2014	RESULTS: The allelic and genotypic frequencies did not differ between the groups when analyzed separately, however, the interaction between the TP63 TT and MDM2 TT genotypes was shown to increase the risk of RPL (OR=2.19, CI 95%: 1.28-3.75, p=0.004), even when adjusted for alcohol consumption, smoking, number of pregnancies and ethnicity (OR=1.97, CI 95%: 1.27-3.58, p=0.025).	Alcohols	274-281	MDM2 proto-oncogene	Homo sapiens	156-160
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	MDM2 proto-oncogene	Homo sapiens	221-225
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	MDM2 proto-oncogene	Homo sapiens	221-225
25341038-12	2014	Concurrently, stress-activated JNK phosphorylates TAp73 at multiple serine and threonine residues, which is crucial to ablate TAp73/MDM2 complex and to promote TAp73 transcriptional function and induction of robust apoptosis.	Serine	68-74	MDM2 proto-oncogene	Homo sapiens	132-136
25341038-12	2014	Concurrently, stress-activated JNK phosphorylates TAp73 at multiple serine and threonine residues, which is crucial to ablate TAp73/MDM2 complex and to promote TAp73 transcriptional function and induction of robust apoptosis.	Threonine	79-88	MDM2 proto-oncogene	Homo sapiens	132-136
24292333-10	2014	In multivariate analysis, nuclear Mdm2 expression including the N+&amp;C+ group was significantly related to poor prognosis.	n+&amp	64-70	MDM2 proto-oncogene	Homo sapiens	34-38
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	MDM2 proto-oncogene	Homo sapiens	114-118
25271708-0	2014	The pyrido[b]indole MDM2 inhibitor SP-141 exerts potent therapeutic effects in breast cancer models.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	35-41	MDM2 proto-oncogene	Homo sapiens	20-24
25271708-3	2014	Here we use a high-throughput screening and computer-aided, structure-based rational drug design, and identify a lead compound, SP-141, which can directly bind to MDM2, inhibit MDM2 expression and induce its autoubiquitination and proteasomal degradation.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	128-134	MDM2 proto-oncogene	Homo sapiens	163-167
25271708-3	2014	Here we use a high-throughput screening and computer-aided, structure-based rational drug design, and identify a lead compound, SP-141, which can directly bind to MDM2, inhibit MDM2 expression and induce its autoubiquitination and proteasomal degradation.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	128-134	MDM2 proto-oncogene	Homo sapiens	177-181
25181509-0	2014	Inhibition of the MDM2 E3 Ligase induces apoptosis and autophagy in wild-type and mutant p53 models of multiple myeloma, and acts synergistically with ABT-737.	ABT-737	151-158	MDM2 proto-oncogene	Homo sapiens	18-22
25382556-10	2014	To investigate hMED15 localization, we treated human MCF-7 cells with the MDM2 inhibitor Nutlin-3, thus inducing p21 transcription.	nutlin 3	89-97	MDM2 proto-oncogene	Homo sapiens	74-78
25198897-0	2014	Design, synthesis and biological evaluation of sulfamide and triazole benzodiazepines as novel p53-MDM2 inhibitors.	fusarubin	47-56	MDM2 proto-oncogene	Homo sapiens	99-103
25198897-0	2014	Design, synthesis and biological evaluation of sulfamide and triazole benzodiazepines as novel p53-MDM2 inhibitors.	triazole benzodiazepines	61-85	MDM2 proto-oncogene	Homo sapiens	99-103
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	MDM2 proto-oncogene	Homo sapiens	166-170
24994714-8	2014	OSU-53 activated Foxo3a through two Akt-dependent pathways, one at the level of nuclear localization by blocking Akt- and IKKbeta-mediated phosphorylation, and a second at the level of protein stabilization via cytoplasmic sequestration of MDM2, an E3 ligase responsible for Foxo3a degradation.	osu	0-3	MDM2 proto-oncogene	Homo sapiens	240-244
25151861-0	2014	MiR-181b sensitizes glioma cells to teniposide by targeting MDM2.	mir-181b	0-8	MDM2 proto-oncogene	Homo sapiens	60-64
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	MDM2 proto-oncogene	Homo sapiens	63-67
25410780-9	2014	Western blot showed that Numb expression was much higher in well differentiated PDAC than that in paired normal pancreas (t = 1.092, P = 0.020) , while the expression of MDM2 and p53 was significantly increased in 16 cases of PDAC (t = 3.263, P = 0.005; t = 3.607, P = 0.003, respectively).	pdac	226-230	MDM2 proto-oncogene	Homo sapiens	170-174
25151861-0	2014	MiR-181b sensitizes glioma cells to teniposide by targeting MDM2.	Teniposide	36-46	MDM2 proto-oncogene	Homo sapiens	60-64
25151861-11	2014	Cell sensitivity to teniposide was detected on miR-181b over expressed and MDM2 down regulated cells.	Teniposide	20-30	MDM2 proto-oncogene	Homo sapiens	75-79
25151861-16	2014	Further study revealed that miR-181b binds to the 3"-UTR region of MDM2 leading to the decrease in MDM2 levels and subsequent increase in teniposide sensitivity.	mir-181b	28-36	MDM2 proto-oncogene	Homo sapiens	67-71
25151861-16	2014	Further study revealed that miR-181b binds to the 3"-UTR region of MDM2 leading to the decrease in MDM2 levels and subsequent increase in teniposide sensitivity.	mir-181b	28-36	MDM2 proto-oncogene	Homo sapiens	99-103
25151861-16	2014	Further study revealed that miR-181b binds to the 3"-UTR region of MDM2 leading to the decrease in MDM2 levels and subsequent increase in teniposide sensitivity.	Teniposide	138-148	MDM2 proto-oncogene	Homo sapiens	67-71
25221773-0	2014	In silico study of fragile histidine triad interaction domains with MDM2 and p53.	Histidine	27-36	MDM2 proto-oncogene	Homo sapiens	68-72
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	MDM2 proto-oncogene	Homo sapiens	118-122
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	MDM2 proto-oncogene	Homo sapiens	118-122
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	MDM2 proto-oncogene	Homo sapiens	103-107
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	MDM2 proto-oncogene	Homo sapiens	233-237
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	MDM2 proto-oncogene	Homo sapiens	233-237
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	MDM2 proto-oncogene	Homo sapiens	104-108
25115702-8	2014	Additionally, as seen in other stapled peptide structures, the hydrocarbon staple itself contributes to binding through favourable interactions with Mdm2.	Hydrocarbons	63-74	MDM2 proto-oncogene	Homo sapiens	149-153
24921920-2	2014	Nutlin-3, an MDM2-p53 antagonist, has previously been reported to be a competitive MDR-1 inhibitor.	nutlin 3	0-8	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	27-31
25088421-7	2014	Together, these findings suggest that Npas4 regulates Mdm2 expression to ubiquitinate and degrade Dcx during dendritic spine development in newborn OB GCs after sensory experience.	dcx	98-101	MDM2 proto-oncogene	Homo sapiens	54-58
25074979-3	2014	In various breast cancer cell lines, we found that SIRT6 was phosphorylated at Ser(338) by the kinase AKT1, which induced the interaction and ubiquitination of SIRT6 by MDM2, targeting SIRT6 for protease-dependent degradation.	Serine	79-82	MDM2 proto-oncogene	Homo sapiens	169-173
24997575-0	2014	Discovery of potent and selective spiroindolinone MDM2 inhibitor, RO8994, for cancer therapy.	spiroindolinone	34-49	MDM2 proto-oncogene	Homo sapiens	50-54
24997575-0	2014	Discovery of potent and selective spiroindolinone MDM2 inhibitor, RO8994, for cancer therapy.	RO8994	66-72	MDM2 proto-oncogene	Homo sapiens	50-54
24997575-4	2014	Here, we report the discovery and optimization of a highly potent and selective series of spiroindolinone small-molecule MDM2 inhibitors, culminating in RO8994.	spiroindolinone	90-105	MDM2 proto-oncogene	Homo sapiens	121-125
24997575-4	2014	Here, we report the discovery and optimization of a highly potent and selective series of spiroindolinone small-molecule MDM2 inhibitors, culminating in RO8994.	RO8994	153-159	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	131-135
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	MDM2 proto-oncogene	Homo sapiens	224-228
24920214-0	2014	Melatonin down-regulates MDM2 gene expression and enhances p53 acetylation in MCF-7 cells.	Melatonin	0-9	MDM2 proto-oncogene	Homo sapiens	25-29
25075210-9	2014	Furthermore, in the analysis of contraceptives, a significant association was found between the use of contraceptives and the MDM2 variant in the development of high-grade cervical lesions for the TG genotype (p = 0.019; OR = 2.21) when HSIL was compared with control.	Thioguanine	197-199	MDM2 proto-oncogene	Homo sapiens	126-130
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	MDM2 proto-oncogene	Homo sapiens	46-50
24968304-0	2014	Inhibition of MDM2 by nilotinib contributes to cytotoxicity in both Philadelphia-positive and negative acute lymphoblastic leukemia.	nilotinib	22-31	MDM2 proto-oncogene	Homo sapiens	14-18
24968304-4	2014	In studying ALL cell lines, we found that the expression of MDM2 in both Philadelphia positive (Ph+) and Philadelphia negative (Ph-) ALL cells was remarkably inhibited by nilotinib, in a dose- and time-dependent manner.	nilotinib	171-180	MDM2 proto-oncogene	Homo sapiens	60-64
24968304-5	2014	Further studies demonstrated that nilotinib inhibited MDM2 at the post-translational level by inducing MDM2 self-ubiquitination and degradation.	nilotinib	34-43	MDM2 proto-oncogene	Homo sapiens	54-58
24968304-5	2014	Further studies demonstrated that nilotinib inhibited MDM2 at the post-translational level by inducing MDM2 self-ubiquitination and degradation.	nilotinib	34-43	MDM2 proto-oncogene	Homo sapiens	103-107
24968304-6	2014	Nilotinib-mediated MDM2 downregulation did not result in accumulation and activation of p53.	nilotinib	0-9	MDM2 proto-oncogene	Homo sapiens	19-23
24968304-7	2014	Inhibition of MDM2 in nilotinib-treated ALL cells led to downregulation of the anti-apoptotic protein X-linked inhibitor of apoptosis protein (XIAP), a translational target of MDM2, resulting in activation of caspases.	nilotinib	22-31	MDM2 proto-oncogene	Homo sapiens	14-18
24920214-10	2014	Herein, we demonstrated that melatonin drastically down-regulates MDM2 gene expression and inhibits MDM2 shuttling into the nucleus, given that melatonin increases L11 and inhibits Akt-PI3K-dependent MDM2 phosphorylation.	Melatonin	29-38	MDM2 proto-oncogene	Homo sapiens	66-70
24920214-10	2014	Herein, we demonstrated that melatonin drastically down-regulates MDM2 gene expression and inhibits MDM2 shuttling into the nucleus, given that melatonin increases L11 and inhibits Akt-PI3K-dependent MDM2 phosphorylation.	Melatonin	29-38	MDM2 proto-oncogene	Homo sapiens	100-104
24920214-10	2014	Herein, we demonstrated that melatonin drastically down-regulates MDM2 gene expression and inhibits MDM2 shuttling into the nucleus, given that melatonin increases L11 and inhibits Akt-PI3K-dependent MDM2 phosphorylation.	Melatonin	29-38	MDM2 proto-oncogene	Homo sapiens	100-104
24920214-10	2014	Herein, we demonstrated that melatonin drastically down-regulates MDM2 gene expression and inhibits MDM2 shuttling into the nucleus, given that melatonin increases L11 and inhibits Akt-PI3K-dependent MDM2 phosphorylation.	Melatonin	144-153	MDM2 proto-oncogene	Homo sapiens	66-70
24920214-10	2014	Herein, we demonstrated that melatonin drastically down-regulates MDM2 gene expression and inhibits MDM2 shuttling into the nucleus, given that melatonin increases L11 and inhibits Akt-PI3K-dependent MDM2 phosphorylation.	Melatonin	144-153	MDM2 proto-oncogene	Homo sapiens	100-104
24920214-10	2014	Herein, we demonstrated that melatonin drastically down-regulates MDM2 gene expression and inhibits MDM2 shuttling into the nucleus, given that melatonin increases L11 and inhibits Akt-PI3K-dependent MDM2 phosphorylation.	Melatonin	144-153	MDM2 proto-oncogene	Homo sapiens	100-104
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	MDM2 proto-oncogene	Homo sapiens	87-91
24968304-7	2014	Inhibition of MDM2 in nilotinib-treated ALL cells led to downregulation of the anti-apoptotic protein X-linked inhibitor of apoptosis protein (XIAP), a translational target of MDM2, resulting in activation of caspases.	nilotinib	22-31	MDM2 proto-oncogene	Homo sapiens	176-180
24968304-8	2014	Inhibition of XIAP following nilotinib-mediated downregulation of MDM2 resulted in apoptosis of MDM2-expressing ALL; however, similar nilotinib treatment induced stronger apoptosis in Ph+/MDM2+ ALL than in Ph-/MDM2+ or Ph+/MDM2- ALL.	nilotinib	29-38	MDM2 proto-oncogene	Homo sapiens	66-70
24968304-9	2014	The ALL cells that were Ph-/MDM2- were totally resistant to nilotinib.	nilotinib	60-69	MDM2 proto-oncogene	Homo sapiens	28-32
24849437-0	2014	[Effect of quercetin on glioma cell U87 apoptosis and feedback regulation of MDM2-p53].	Quercetin	11-20	MDM2 proto-oncogene	Homo sapiens	77-81
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	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	224-228
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	MDM2 proto-oncogene	Homo sapiens	51-55
24813735-0	2014	Discovery of 1-arylpyrrolidone derivatives as potent p53-MDM2 inhibitors based on molecule fusing strategy.	1-arylpyrrolidone	13-30	MDM2 proto-oncogene	Homo sapiens	57-61
24418072-4	2014	The binding affinity calculations by WaterMap provided over one hundred hydration sites in the MDM2 binding pocket where water density is greater than twice that of the bulk, and the relative value of free energy released by displacing these hydration sites.	Water	121-126	MDM2 proto-oncogene	Homo sapiens	95-99
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	MDM2 proto-oncogene	Homo sapiens	156-160
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	MDM2 proto-oncogene	Homo sapiens	109-113
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	MDM2 proto-oncogene	Homo sapiens	140-144
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	MDM2 proto-oncogene	Homo sapiens	225-229
24579771-3	2014	AREAS COVERED: In this review, the authors discuss the challenges and prospective remedies for minimizing the significant haematological toxicities of the cis-imidazole Nutlin HDM2-binding antagonists.	cis-imidazole	155-168	MDM2 proto-oncogene	Homo sapiens	176-180
24579771-6	2014	EXPERT OPINION: Medicinal chemistry strategies, based on structure-based drug design, are required to re-engineer cis-imidazoline Nutlin HDM2-binding antagonists into less haematologically toxic drugs.	cis-imidazoline	114-129	MDM2 proto-oncogene	Homo sapiens	137-141
24673452-6	2014	RESULTS: The results of our meta-analysis suggested that MDM2 T309G polymorphism might be strongly correlated with an increased risk of NSCLC (G allele vs. T allele: OR=1.63, 95% CI: 1.42-1.89, p&lt;0.001; TG+GG vs. TT: OR=1.54, 95% CI: 1.31-1.80, p&lt;0.001; respectively).	Thioguanine	206-208	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	90-94
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	MDM2 proto-oncogene	Homo sapiens	195-199
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	MDM2 proto-oncogene	Homo sapiens	53-57
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	MDM2 proto-oncogene	Homo sapiens	142-146
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	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	58-62
24810962-5	2014	MDM2 inhibitors also synergized strongly with BH3 mimetics, BCR-ABL antagonists, and HDAC inhibitors.	BH 3	46-49	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	197-201
24601644-0	2014	Novel inhibitors of the MDM2-p53 interaction featuring hydrogen bond acceptors as carboxylic acid isosteres.	Hydrogen	55-63	MDM2 proto-oncogene	Homo sapiens	24-28
24601644-0	2014	Novel inhibitors of the MDM2-p53 interaction featuring hydrogen bond acceptors as carboxylic acid isosteres.	carboxylic acid isosteres	82-107	MDM2 proto-oncogene	Homo sapiens	24-28
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	MDM2 proto-oncogene	Homo sapiens	109-113
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	MDM2 proto-oncogene	Homo sapiens	109-113
24601644-2	2014	These inhibitors have in common a carboxylic acid moiety that engages in an electrostatic interaction with MDM2-His96.	Carboxylic Acids	34-49	MDM2 proto-oncogene	Homo sapiens	107-111
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	MDM2 proto-oncogene	Homo sapiens	139-143
24656661-0	2014	Core modification of substituted piperidines as novel inhibitors of HDM2-p53 protein-protein interaction.	Piperidines	33-44	MDM2 proto-oncogene	Homo sapiens	68-72
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	MDM2 proto-oncogene	Homo sapiens	61-65
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	MDM2 proto-oncogene	Homo sapiens	61-65
24656661-2	2014	Conformational restrictions and further functionalization of the piperidine core were investigated as a strategy to gain additional interactions with HDM2.	piperidine	65-75	MDM2 proto-oncogene	Homo sapiens	150-154
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	MDM2 proto-oncogene	Homo sapiens	96-100
26580383-7	2014	We further found that the presence of a hydrophobic staple in the peptide-MDM2 interface tends to trap a network of water molecules prior to binding.	Water	116-121	MDM2 proto-oncogene	Homo sapiens	74-78
24286312-3	2014	Nutlin-3, a MDM2 antagonist, has antitumor activity in various cancers.	nutlin 3	0-8	MDM2 proto-oncogene	Homo sapiens	12-16
24377313-6	2014	We have also demonstrated that synthetic herboxidiene and its analogs can potently modulate the alternate splicing of MDM-2 pre-mRNA.	herboxidiene	41-53	MDM2 proto-oncogene	Homo sapiens	118-123
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	MDM2 proto-oncogene	Homo sapiens	48-52
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	MDM2 proto-oncogene	Homo sapiens	48-52
24548297-0	2014	Selective and potent morpholinone inhibitors of the MDM2-p53 protein-protein interaction.	Morpholin-3-one	21-33	MDM2 proto-oncogene	Homo sapiens	52-56
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	MDM2 proto-oncogene	Homo sapiens	109-113
24548297-2	2014	Our continued search for potent and diverse analogues led to the discovery of novel morpholinone MDM2 inhibitors.	Morpholin-3-one	84-96	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	78-82
23884452-3	2014	In this study, we investigated the interaction of the MDM2 SNP285 and 309 in a large series of 195 LFS patients.	snp285	59-65	MDM2 proto-oncogene	Homo sapiens	54-58
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	MDM2 proto-oncogene	Homo sapiens	184-188
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	MDM2 proto-oncogene	Homo sapiens	184-188
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	MDM2 proto-oncogene	Homo sapiens	104-108
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	MDM2 proto-oncogene	Homo sapiens	104-108
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	MDM2 proto-oncogene	Homo sapiens	79-83
24659749-3	2014	As such, AMLs are excellent candidates for therapeutics involving the reactivation of their WTp53 to restrict and destroy cancer cells, and the Mdm2 antagonist nutlin-3 is one such promising agent.	nutlin 3	160-168	MDM2 proto-oncogene	Homo sapiens	144-148
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	MDM2 proto-oncogene	Homo sapiens	104-108
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	MDM2 proto-oncogene	Homo sapiens	104-108
24456472-2	2014	Continued research investigation of the N-alkyl substituent of this series, focused in particular on a previously underutilized interaction in a shallow cleft on the MDM2 surface, led to the discovery of a one-carbon tethered sulfone which gave rise to substantial improvements in biochemical and cellular potency.	Nitrogen	40-41	MDM2 proto-oncogene	Homo sapiens	166-170
24456472-2	2014	Continued research investigation of the N-alkyl substituent of this series, focused in particular on a previously underutilized interaction in a shallow cleft on the MDM2 surface, led to the discovery of a one-carbon tethered sulfone which gave rise to substantial improvements in biochemical and cellular potency.	Carbon	210-216	MDM2 proto-oncogene	Homo sapiens	166-170
24456472-2	2014	Continued research investigation of the N-alkyl substituent of this series, focused in particular on a previously underutilized interaction in a shallow cleft on the MDM2 surface, led to the discovery of a one-carbon tethered sulfone which gave rise to substantial improvements in biochemical and cellular potency.	Sulfones	226-233	MDM2 proto-oncogene	Homo sapiens	166-170
24900882-1	2014	Introduction of an aliphatic side chain to a key position of a novel piperidine-based HDM2 inhibitor scaffold resulted in significant potency gains, enabling further series progression.	piperidine	69-79	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	52-56
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	MDM2 proto-oncogene	Homo sapiens	58-62
24525337-1	2014	At high cytotoxic concentrations, actinomycin D (ActD) blocks transcription, decreasing levels of MDM2 and thus causing p53 stabilization.	Dactinomycin	34-47	MDM2 proto-oncogene	Homo sapiens	98-102
24486134-0	2014	Substituted piperidines as HDM2 inhibitors.	Piperidines	12-23	MDM2 proto-oncogene	Homo sapiens	27-31
24486134-1	2014	Novel small molecule HDM2 inhibitor, substituted piperidine, was identified.	piperidine	49-59	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	139-143
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	MDM2 proto-oncogene	Homo sapiens	139-143
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	MDM2 proto-oncogene	Homo sapiens	48-52
24356969-4	2014	Specifically, we showed that Rbm24 is induced by DNA damage and Mdm2 inhibitor Nutlin-3.	nutlin 3	79-87	MDM2 proto-oncogene	Homo sapiens	64-68
24268795-2	2014	We herein report the synthesis and evaluation of eighteen spiroisoxazoline oxindoles derivatives as p53-MDM2 interaction inhibitors.	spiroisoxazoline oxindoles	58-84	MDM2 proto-oncogene	Homo sapiens	104-108
24189165-8	2014	Moreover, the levels of Mdm2 and caspase-3 expression were reduced in the cells exposed to spermine compared to blank group.	Spermine	91-99	MDM2 proto-oncogene	Homo sapiens	24-28
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	MDM2 proto-oncogene	Homo sapiens	26-30
23907365-11	2014	RESULTS: In both MCF-7 and MDA-MB-468 cells, VEGF expression and secretion were reduced, resulting from specific inhibition of MDM2 expression by ASO.	Oligonucleotides, Antisense	146-149	MDM2 proto-oncogene	Homo sapiens	127-131
23907365-14	2014	CONCLUSION: In summary, the ASO construct targeting MDM2 specifically suppresses VEGF expression in vitro and VEGF-mediated tumor angiogenesis in vivo in breast cancer.	Oligonucleotides, Antisense	28-31	MDM2 proto-oncogene	Homo sapiens	52-56
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	18-22
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	MDM2 proto-oncogene	Homo sapiens	55-59
25482940-4	2014	We determine that MDM2 c.14 + 309T &gt; G was significantly associated with severe hematologic and overall toxicities for advanced NSCLC patients treated with platinum-based chemotherapy, especially for patients aged 57 and younger.	Platinum	159-167	MDM2 proto-oncogene	Homo sapiens	18-22
25482940-8	2014	Moreover, patients carrying the MDM2 c.-461 &gt; G -c.14 + 309T &gt; G CG/CT diplotype exhibited higher toxicities than those carrying CG/CG.	cysteinylglycine	71-73	MDM2 proto-oncogene	Homo sapiens	32-36
25482940-11	2014	In summary, we found that the p53 p. Pro72Arg, MDM2 c.14 + 309T &gt; G and MDM2 c.-461C &gt; G polymorphisms are associated with toxicity risks following platinum-based chemotherapy treatment in advanced NSCLC patients.	Platinum	154-162	MDM2 proto-oncogene	Homo sapiens	47-51
25482940-11	2014	In summary, we found that the p53 p. Pro72Arg, MDM2 c.14 + 309T &gt; G and MDM2 c.-461C &gt; G polymorphisms are associated with toxicity risks following platinum-based chemotherapy treatment in advanced NSCLC patients.	Platinum	154-162	MDM2 proto-oncogene	Homo sapiens	75-79
25482940-12	2014	We suggest that MDM2 c.14 + 309T &gt; G may be used as a candidate biomarker to predict adverse events in advanced NSCLC patients who had platinum-based chemotherapy treatment.	Platinum	138-146	MDM2 proto-oncogene	Homo sapiens	16-20
25482947-13	2014	Indeed, rapamycin increased the levels of endogenous MDM2 despite inhibition of its phosphorylation at Ser-166.	Serine	103-106	MDM2 proto-oncogene	Homo sapiens	53-57
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	MDM2 proto-oncogene	Homo sapiens	105-109
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	MDM2 proto-oncogene	Homo sapiens	144-148
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	MDM2 proto-oncogene	Homo sapiens	66-70
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	MDM2 proto-oncogene	Homo sapiens	12-16
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	MDM2 proto-oncogene	Homo sapiens	159-163
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	MDM2 proto-oncogene	Homo sapiens	159-163
25022573-6	2014	MDM2 ASONs downregulated MDM2 expression in a dose-dependent manner and increased the rate of paclitaxel-induced cell growth inhibition.	Paclitaxel	94-104	MDM2 proto-oncogene	Homo sapiens	0-4
24390485-3	2014	Sequential posttranslational modifications of the C134W mutant occur where hyperphosphorylation at serine 33 (S33) by GSK3beta induces MDM2-mediated ubiquitination and proteasomal degradation.	Serine	99-105	MDM2 proto-oncogene	Homo sapiens	135-139
25201196-0	2014	Crosstalk between Mdm2, p53 and HIF1-alpha: distinct responses to oxygen stress and implications for tumour hypoxia.	Oxygen	66-72	MDM2 proto-oncogene	Homo sapiens	18-22
24132698-7	2014	Concomitantly, DEX induced a time-dependent increase in cytosolic alpha(2) AR-beta-arrestin interaction and a decrease in beta-arrestin interaction with Mdm2 E3 ubiquitin ligase.	Dexamethasone	15-18	MDM2 proto-oncogene	Homo sapiens	153-157
24163099-4	2014	MDM2 activates chk1 phosphorylation, elevates mixed lineage lymphoma histone methyl transferase levels and promotes checkpoint-dependent tri-methylation of histone H3 at lysine 4, known to prevent firing of late replication origins at the early S phase.	Lysine	170-176	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	0-4
24391839-9	2013	The elevated resistance of U87-MCSF cells towards 5-FU was due to the increase in the expressions (10.2 and 6 fold) of ABCB1 and mdm2, respectively.	Fluorouracil	50-54	MDM2 proto-oncogene	Homo sapiens	129-133
24391839-10	2013	Furthermore, increase in expressions of ABCG1, mdm2 and CD24 was also observed in U87MG cells after prolonged incubation with 5-FU.	Fluorouracil	126-130	MDM2 proto-oncogene	Homo sapiens	47-51
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	MDM2 proto-oncogene	Homo sapiens	7-11
24900784-0	2014	Discovery of Potent and Orally Active p53-MDM2 Inhibitors RO5353 and RO2468 for Potential Clinical Development.	ro5353	58-64	MDM2 proto-oncogene	Homo sapiens	42-46
24900784-0	2014	Discovery of Potent and Orally Active p53-MDM2 Inhibitors RO5353 and RO2468 for Potential Clinical Development.	ro2468	69-75	MDM2 proto-oncogene	Homo sapiens	42-46
24900784-2	2014	In a previous communication, the efforts leading to the identification of a non-imidazoline MDM2 inhibitor, RG7388, was disclosed and revealed the desirable in vitro and in vivo pharmacological properties that this class of pyrrolidine-based inhibitors possesses.	Imidazolines	80-91	MDM2 proto-oncogene	Homo sapiens	92-96
24900784-2	2014	In a previous communication, the efforts leading to the identification of a non-imidazoline MDM2 inhibitor, RG7388, was disclosed and revealed the desirable in vitro and in vivo pharmacological properties that this class of pyrrolidine-based inhibitors possesses.	pyrrolidine	224-235	MDM2 proto-oncogene	Homo sapiens	92-96
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	MDM2 proto-oncogene	Homo sapiens	64-68
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	MDM2 proto-oncogene	Homo sapiens	64-68
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	MDM2 proto-oncogene	Homo sapiens	82-86
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	MDM2 proto-oncogene	Homo sapiens	234-238
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	MDM2 proto-oncogene	Homo sapiens	234-238
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	MDM2 proto-oncogene	Homo sapiens	82-86
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	MDM2 proto-oncogene	Homo sapiens	234-238
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	MDM2 proto-oncogene	Homo sapiens	234-238
24207125-2	2013	We present the cocrystal structures of two complexes of MDM2 with inhibitors based on 6-chloroindole scaffolds.	6-chloroindole	86-100	MDM2 proto-oncogene	Homo sapiens	56-60
24349524-0	2013	Inhibition of PI3K/mTOR overcomes nilotinib resistance in BCR-ABL1 positive leukemia cells through translational down-regulation of MDM2.	nilotinib	34-43	MDM2 proto-oncogene	Homo sapiens	132-136
24349524-10	2013	The main role of PI3K/mTOR inhibitor BEZ235 and the reason for apoptosis in the nilotinib-resistant cells was the block of the translational machinery, leading to the rapid downregulation of the anti-apoptotic protein MDM2 (human homolog of the murine double minute-2).	nilotinib	80-89	MDM2 proto-oncogene	Homo sapiens	218-222
24349246-7	2013	Significant differences were observed comparing MDM2 genotype frequencies at position 309 of intron 1 between cases (GG: 21.6%, TG: 54.5%, TT: 23.8%) and controls (GG: 7.3%, TG: 43.9%, TT: 48.7%).	Thioguanine	174-176	MDM2 proto-oncogene	Homo sapiens	48-52
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	MDM2 proto-oncogene	Homo sapiens	147-151
24403256-4	2013	In combination studies, we show that histone deacetylase (HDAC) inhibitors, the HDM2 inhibitor Nutlin-3, and the anthracycline daunorubicin all enhance the apoptotic response of JQ1.	nutlin 3	95-103	MDM2 proto-oncogene	Homo sapiens	80-84
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	MDM2 proto-oncogene	Homo sapiens	92-96
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	MDM2 proto-oncogene	Homo sapiens	151-156
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	MDM2 proto-oncogene	Homo sapiens	251-255
23912932-0	2013	Current evidence on the relationship between SNP309 polymorphism in the MDM2 gene and colorectal cancer risk.	snp309	45-51	MDM2 proto-oncogene	Homo sapiens	72-76
24113239-0	2013	5-Deazaflavin derivatives as inhibitors of p53 ubiquitination by HDM2.	5-deazaflavin	0-13	MDM2 proto-oncogene	Homo sapiens	65-69
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	MDM2 proto-oncogene	Homo sapiens	192-196
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	MDM2 proto-oncogene	Homo sapiens	192-196
24177565-0	2013	Protective roles of Gadd45 and MDM2 in blueberry anthocyanins mediated DNA repair of fragmented and non-fragmented DNA damage in UV-irradiated HepG2 cells.	Anthocyanins	49-61	MDM2 proto-oncogene	Homo sapiens	31-35
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	MDM2 proto-oncogene	Homo sapiens	228-232
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	MDM2 proto-oncogene	Homo sapiens	128-132
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	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	93-97
24040331-1	2013	Serdemetan (JNJ-26854165), an antagonist to Mdm2, was anticipated to promote the activation of p53.	JNJ 26854165	0-10	MDM2 proto-oncogene	Homo sapiens	44-48
24040331-1	2013	Serdemetan (JNJ-26854165), an antagonist to Mdm2, was anticipated to promote the activation of p53.	JNJ 26854165	12-24	MDM2 proto-oncogene	Homo sapiens	44-48
24040331-3	2013	We investigated if Serdemetan would alter the Mdm2-HIF1alpha axis and affect cell survival in human glioblastoma cells independently of p53.	JNJ 26854165	19-29	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	134-138
23812671-7	2013	RESULTS: Dual targeting of BRAF(V600E) and Hdm2 with vemurafenib and Nt-3, respectively, synergistically induced apoptosis and suppressed melanoma viability in vitro and tumor growth in vivo.	Vemurafenib	53-64	MDM2 proto-oncogene	Homo sapiens	43-47
23812671-7	2013	RESULTS: Dual targeting of BRAF(V600E) and Hdm2 with vemurafenib and Nt-3, respectively, synergistically induced apoptosis and suppressed melanoma viability in vitro and tumor growth in vivo.	nutlin 3	69-73	MDM2 proto-oncogene	Homo sapiens	43-47
23934659-0	2013	Cisplatin causes cell death via TAB1 regulation of p53/MDM2/MDMX circuitry.	Cisplatin	0-9	MDM2 proto-oncogene	Homo sapiens	55-59
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	MDM2 proto-oncogene	Homo sapiens	85-89
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	MDM2 proto-oncogene	Homo sapiens	94-98
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	MDM2 proto-oncogene	Homo sapiens	85-89
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	MDM2 proto-oncogene	Homo sapiens	94-98
23776060-0	2013	Identification of a second Nutlin-3 responsive interaction site in the N-terminal domain of MDM2 using hydrogen/deuterium exchange mass spectrometry.	Hydrogen	103-111	MDM2 proto-oncogene	Homo sapiens	92-96
23776060-0	2013	Identification of a second Nutlin-3 responsive interaction site in the N-terminal domain of MDM2 using hydrogen/deuterium exchange mass spectrometry.	Deuterium	112-121	MDM2 proto-oncogene	Homo sapiens	92-96
23776060-4	2013	We present a methodology using a hydrogen/deuterium (H/D) exchange platform that measures Nutlin-3 binding to the N-terminal domain of MDM2 (MDM2(1-126)) in order to begin to develop dynamic assays that evaluate MDM2 allostery.	Hydrogen	33-41	MDM2 proto-oncogene	Homo sapiens	135-139
23776060-4	2013	We present a methodology using a hydrogen/deuterium (H/D) exchange platform that measures Nutlin-3 binding to the N-terminal domain of MDM2 (MDM2(1-126)) in order to begin to develop dynamic assays that evaluate MDM2 allostery.	Deuterium	42-51	MDM2 proto-oncogene	Homo sapiens	135-139
23720736-7	2013	RUNX2 protein levels decrease upon stabilization of p53 with the MDM2 inhibitor Nutlin-3.	nutlin 3	80-88	MDM2 proto-oncogene	Homo sapiens	65-69
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	MDM2 proto-oncogene	Homo sapiens	119-123
23843462-7	2013	The activated AKT phosphorylated MDM2 at Ser(166) and promoted degradation of the tumor suppressor p53.	Serine	41-44	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	14-18
23808545-4	2013	Here, we report the discovery and characterization of a second generation clinical MDM2 inhibitor, RG7388, with superior potency and selectivity.	RG7388	99-105	MDM2 proto-oncogene	Homo sapiens	83-87
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	MDM2 proto-oncogene	Homo sapiens	181-185
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	MDM2 proto-oncogene	Homo sapiens	158-162
23685175-1	2013	We have discovered and reported potent p53-MDM2 interaction inhibitors possessing dihydroimidazothiazole scaffold.	dihydroimidazothiazole	82-104	MDM2 proto-oncogene	Homo sapiens	43-47
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	MDM2 proto-oncogene	Homo sapiens	158-162
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	MDM2 proto-oncogene	Homo sapiens	186-190
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	MDM2 proto-oncogene	Homo sapiens	18-22
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	MDM2 proto-oncogene	Homo sapiens	129-133
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	MDM2 proto-oncogene	Homo sapiens	87-91
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	MDM2 proto-oncogene	Homo sapiens	111-115
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	MDM2 proto-oncogene	Homo sapiens	105-109
22789708-0	2013	Benzimidazole-2-one: a novel anchoring principle for antagonizing p53-Mdm2.	benzimidazole-2-one	0-19	MDM2 proto-oncogene	Homo sapiens	70-74
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	MDM2 proto-oncogene	Homo sapiens	145-149
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	MDM2 proto-oncogene	Homo sapiens	145-149
22789708-4	2013	The finding of the benzimidazolone moiety as a tryptophan replacement in mdm2 is significant as it offers access to novel scaffolds with potentially higher selectivity and potency and improved biological activities.	benzimidazolone	19-34	MDM2 proto-oncogene	Homo sapiens	73-77
22789708-4	2013	The finding of the benzimidazolone moiety as a tryptophan replacement in mdm2 is significant as it offers access to novel scaffolds with potentially higher selectivity and potency and improved biological activities.	Tryptophan	47-57	MDM2 proto-oncogene	Homo sapiens	73-77
22789708-5	2013	Observing low muM affinities to mdm2 by NMR and fluorescence polarization we conclude that the 2-(2-oxo-2,3-dihydro-1H-benzo[d]imidazol-1-yl)acetamide scaffold might be a good starting point to further optimize the affinities to Mdm2.	2-(2-oxo-2,3-dihydro-1h-benzo[d]imidazol-1-yl)acetamide	95-150	MDM2 proto-oncogene	Homo sapiens	32-36
22789708-5	2013	Observing low muM affinities to mdm2 by NMR and fluorescence polarization we conclude that the 2-(2-oxo-2,3-dihydro-1H-benzo[d]imidazol-1-yl)acetamide scaffold might be a good starting point to further optimize the affinities to Mdm2.	2-(2-oxo-2,3-dihydro-1h-benzo[d]imidazol-1-yl)acetamide	95-150	MDM2 proto-oncogene	Homo sapiens	229-233
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	MDM2 proto-oncogene	Homo sapiens	95-99
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	MDM2 proto-oncogene	Homo sapiens	111-115
22292771-0	2013	A small-molecule inhibitor, 5"-O-tritylthymidine, targets FAK and Mdm-2 interaction, and blocks breast and colon tumorigenesis in vivo.	5'-O-Tritylthymidine	28-48	MDM2 proto-oncogene	Homo sapiens	66-71
23682023-0	2013	3T3-L1 adipocytes possess anandamide- and epinephrine-responsive machinery for MDM2 distribution to the plasma membrane.	anandamide	26-36	MDM2 proto-oncogene	Homo sapiens	79-83
23682023-0	2013	3T3-L1 adipocytes possess anandamide- and epinephrine-responsive machinery for MDM2 distribution to the plasma membrane.	Epinephrine	42-53	MDM2 proto-oncogene	Homo sapiens	79-83
23682023-2	2013	We examined MDM2 level in the plasma membrane (PM) and total MDM2 level of 3T3-L1 adipocytes treated with biomolecular anandamide, epinephrine, and other agents for 15 min.	anandamide	119-129	MDM2 proto-oncogene	Homo sapiens	12-16
23682023-2	2013	We examined MDM2 level in the plasma membrane (PM) and total MDM2 level of 3T3-L1 adipocytes treated with biomolecular anandamide, epinephrine, and other agents for 15 min.	Epinephrine	131-142	MDM2 proto-oncogene	Homo sapiens	12-16
23682023-5	2013	PM MDM2 distribution caused by a biomolecular concentration was maintained by treatment with mithramycin A and exposure of cells to 28 C or 32 C but not to 18 C, and PM MDM2 levels after treatment with high concentrations of biomolecules were altered upon exposure to the inhibitor and mild hypothermia.	mithramycin A	93-106	MDM2 proto-oncogene	Homo sapiens	3-7
22920093-0	2013	Synthesis and biological evaluation of novel pyrimido[4,5-b]quinoline-2,4- dione derivatives as MDM2 ubiquitin ligase inhibitors.	pyrimido[4,5-b]quinoline-2,4- dione	45-80	MDM2 proto-oncogene	Homo sapiens	96-100
22920093-3	2013	Among tested compounds, four sulfur-containing compounds (4-7) displayed enhanced cytotoxic activities and better MDM2 E3 ligase inhibitoty activities in comparison with that of HLI98c.	Sulfur	29-35	MDM2 proto-oncogene	Homo sapiens	114-118
23862226-7	2013	RT-PCR and Western blot showed markedly up-regulated expressions of GSK3 P3 a3beta down-regulated expressions of MDM2 mRNA and proteins in the PC-3 cells treated with deguelin.	deguelin	167-175	MDM2 proto-oncogene	Homo sapiens	113-117
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	MDM2 proto-oncogene	Homo sapiens	91-95
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	16-20	MDM2 proto-oncogene	Homo sapiens	148-152
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	MDM2 proto-oncogene	Homo sapiens	148-152
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	MDM2 proto-oncogene	Homo sapiens	148-152
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	MDM2 proto-oncogene	Homo sapiens	32-36
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	MDM2 proto-oncogene	Homo sapiens	106-110
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	MDM2 proto-oncogene	Homo sapiens	106-110
23597064-2	2013	The cocrystal structure of 10 with MDM2 inspired two independent optimization strategies and resulted in the discovery of morpholinones 16 and 27 possessing distinct binding modes.	morpholinones	122-135	MDM2 proto-oncogene	Homo sapiens	35-39
23597064-3	2013	Both analogues were potent MDM2 inhibitors in biochemical and cellular assays, and morpholinone 27 (IC50 = 0.10 muM) also displayed suitable PK profile for in vivo animal experiments.	Morpholin-3-one	83-95	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	157-161
23347235-6	2013	The effect of adjuvant fluorouracil-leucovorin-oxaliplatin (FLO) in improving OS compared with surgery alone was evident only in the high MDM2 group (hazard ratio = 0.57; 95% confidence interval, 0.37-0.89; P = 0.013).	fluorouracil-leucovorin-oxaliplatin	23-58	MDM2 proto-oncogene	Homo sapiens	138-142
23641733-0	2013	Diastereomeric spirooxindoles as highly potent and efficacious MDM2 inhibitors.	spirooxindoles	15-29	MDM2 proto-oncogene	Homo sapiens	63-67
23641733-2	2013	We previously published a series of spirooxindole-containing compounds as a new class of MDM2 small-molecule inhibitors.	Spirooxindole	36-49	MDM2 proto-oncogene	Homo sapiens	89-93
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	MDM2 proto-oncogene	Homo sapiens	312-316
23652204-6	2013	In HER2-positive breast cancer cells treated with the HER2 tyrosine kinase inhibitor lapatinib, MDM2 was degraded and HUWE1 was stabilized.	Lapatinib	85-94	MDM2 proto-oncogene	Homo sapiens	96-100
23652204-7	2013	In contrast, in breast cancer cells that acquired resistance to lapatinib, the abundance of MDM2 was not decreased and HUWE1 was degraded, which inhibited apoptosis, regardless of p53 status.	Lapatinib	64-73	MDM2 proto-oncogene	Homo sapiens	92-96
23652204-8	2013	MDM2 inhibition overcame lapatinib resistance in cells with either wild-type or mutant p53 and in xenograft models.	Lapatinib	25-34	MDM2 proto-oncogene	Homo sapiens	0-4
23652204-9	2013	These findings demonstrate broader, p53-independent roles for MDM2 and HUWE1 in apoptosis and specifically suggest the potential for therapy directed against MDM2 to overcome lapatinib resistance.	Lapatinib	175-184	MDM2 proto-oncogene	Homo sapiens	158-162
23347235-6	2013	The effect of adjuvant fluorouracil-leucovorin-oxaliplatin (FLO) in improving OS compared with surgery alone was evident only in the high MDM2 group (hazard ratio = 0.57; 95% confidence interval, 0.37-0.89; P = 0.013).	flo	60-63	MDM2 proto-oncogene	Homo sapiens	138-142
23347235-9	2013	For the first time, our data suggest that MDM2 is a potent prognostic and predictive factor for benefit from adjuvant fluorouracil-leucovorin-oxaliplatin chemotherapy in resectable gastric cancer.	fluorouracil-leucovorin	118-141	MDM2 proto-oncogene	Homo sapiens	42-46
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	MDM2 proto-oncogene	Homo sapiens	90-94
23347235-9	2013	For the first time, our data suggest that MDM2 is a potent prognostic and predictive factor for benefit from adjuvant fluorouracil-leucovorin-oxaliplatin chemotherapy in resectable gastric cancer.	Oxaliplatin	142-153	MDM2 proto-oncogene	Homo sapiens	42-46
23563151-0	2013	Ribosomal protein S7 regulates arsenite-induced GADD45alpha expression by attenuating MDM2-mediated GADD45alpha ubiquitination and degradation.	arsenite	31-39	MDM2 proto-oncogene	Homo sapiens	86-90
23563151-7	2013	Further investigations indicated that arsenite treatment enhanced S7-MDM2 interaction, resulting in attenuation of MDM2-dependent GADD45alpha ubiquitination and degradation, thereby leading to GADD45alpha-dependent cell death pathway activation.	arsenite	38-46	MDM2 proto-oncogene	Homo sapiens	69-73
23563151-7	2013	Further investigations indicated that arsenite treatment enhanced S7-MDM2 interaction, resulting in attenuation of MDM2-dependent GADD45alpha ubiquitination and degradation, thereby leading to GADD45alpha-dependent cell death pathway activation.	arsenite	38-46	MDM2 proto-oncogene	Homo sapiens	115-119
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	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	130-134
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	MDM2 proto-oncogene	Homo sapiens	23-27
23218882-2	2013	We hypothesized that functional polymorphisms in the promoters of MDM2 and p14(ARF) contribute to the interindividual difference in predisposition to DTC.	dtc	150-153	MDM2 proto-oncogene	Homo sapiens	66-70
23218882-5	2013	RESULTS: MDM2-rs2279744 and p14(ARF)-rs3731217 were associated with a significantly increased risk of DTC (MDM2-rs2279744: TT versus TG/GG; OR, 1.5; 95% CI, 1.1-2.0; p14(ARF)-rs3731217: TG/GG versus TT; OR, 1.7; 95% CI, 1.2-2.3).	Thioguanine	133-135	MDM2 proto-oncogene	Homo sapiens	9-13
23218882-5	2013	RESULTS: MDM2-rs2279744 and p14(ARF)-rs3731217 were associated with a significantly increased risk of DTC (MDM2-rs2279744: TT versus TG/GG; OR, 1.5; 95% CI, 1.1-2.0; p14(ARF)-rs3731217: TG/GG versus TT; OR, 1.7; 95% CI, 1.2-2.3).	Thioguanine	133-135	MDM2 proto-oncogene	Homo sapiens	107-111
23218882-5	2013	RESULTS: MDM2-rs2279744 and p14(ARF)-rs3731217 were associated with a significantly increased risk of DTC (MDM2-rs2279744: TT versus TG/GG; OR, 1.5; 95% CI, 1.1-2.0; p14(ARF)-rs3731217: TG/GG versus TT; OR, 1.7; 95% CI, 1.2-2.3).	Thioguanine	186-188	MDM2 proto-oncogene	Homo sapiens	9-13
23218882-5	2013	RESULTS: MDM2-rs2279744 and p14(ARF)-rs3731217 were associated with a significantly increased risk of DTC (MDM2-rs2279744: TT versus TG/GG; OR, 1.5; 95% CI, 1.1-2.0; p14(ARF)-rs3731217: TG/GG versus TT; OR, 1.7; 95% CI, 1.2-2.3).	Thioguanine	186-188	MDM2 proto-oncogene	Homo sapiens	107-111
23218882-10	2013	CONCLUSION: Our results suggest that polymorphisms of MDM2 and p14(ARF) contribute to the interindividual difference in susceptibility to DTC, either alone or more likely jointly.	dtc	138-141	MDM2 proto-oncogene	Homo sapiens	54-58
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	MDM2 proto-oncogene	Homo sapiens	145-149
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	MDM2 proto-oncogene	Homo sapiens	187-191
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	MDM2 proto-oncogene	Homo sapiens	90-94
22961628-0	2013	Mdm2 antagonists induce apoptosis and synergize with cisplatin overcoming chemoresistance in TP53 wild-type ovarian cancer cells.	Cisplatin	53-62	MDM2 proto-oncogene	Homo sapiens	0-4
23352573-3	2013	On this regard, a new pH-responsive diblock copolymer of poly(methacryloyloxy ethyl phosphorylcholine)-block-poly(diisopropanolamine ethyl methacrylate) (PMPC-b-PDPA)/siRNA-MDM2 complex nanoparticle with minimized surface charge and suitable particle size was designed and developed for siRNA-MDM2 delivery in vitro and in vivo.	diblock copolymer	36-53	MDM2 proto-oncogene	Homo sapiens	173-177
23352573-3	2013	On this regard, a new pH-responsive diblock copolymer of poly(methacryloyloxy ethyl phosphorylcholine)-block-poly(diisopropanolamine ethyl methacrylate) (PMPC-b-PDPA)/siRNA-MDM2 complex nanoparticle with minimized surface charge and suitable particle size was designed and developed for siRNA-MDM2 delivery in vitro and in vivo.	poly(methacryloyloxy ethyl phosphorylcholine)-block	57-108	MDM2 proto-oncogene	Homo sapiens	173-177
23352573-3	2013	On this regard, a new pH-responsive diblock copolymer of poly(methacryloyloxy ethyl phosphorylcholine)-block-poly(diisopropanolamine ethyl methacrylate) (PMPC-b-PDPA)/siRNA-MDM2 complex nanoparticle with minimized surface charge and suitable particle size was designed and developed for siRNA-MDM2 delivery in vitro and in vivo.	pmpc-b-pdpa	154-165	MDM2 proto-oncogene	Homo sapiens	173-177
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	MDM2 proto-oncogene	Homo sapiens	58-62
23398638-7	2013	The role of MDM2 binding was explored by inhibiting MDM2/p53 binding with nutlin-3.	nutlin 3	74-82	MDM2 proto-oncogene	Homo sapiens	12-16
23238568-4	2013	MDM2 requires phosphatidylinositol (PI)3-kinase activity for enhancing Akt phosphorylation and upregulates this activity by repressing transcription of the regulatory subunit p85 of PI3-kinase.	Phosphatidylinositols	14-34	MDM2 proto-oncogene	Homo sapiens	0-4
23506213-5	2013	The functionality of MDM2 SNP309, with or without H. pylori lipopolysaccharide (LPS), was examined by dual-luciferase assay.	snp309	26-32	MDM2 proto-oncogene	Homo sapiens	21-25
23497256-2	2013	METHODS: Nude/beige mice bearing human RCC xenografts were treated with various combinations of sunitinib and the HDM2 antagonist MI-319.	MI 319	130-136	MDM2 proto-oncogene	Homo sapiens	114-118
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	MDM2 proto-oncogene	Homo sapiens	131-135
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	MDM2 proto-oncogene	Homo sapiens	127-131
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	MDM2 proto-oncogene	Homo sapiens	167-171
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	MDM2 proto-oncogene	Homo sapiens	127-131
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	MDM2 proto-oncogene	Homo sapiens	167-171
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	MDM2 proto-oncogene	Homo sapiens	98-102
23585871-5	2013	Conversely, treatment of prostate cancer cells with an inhibitor of miR-125b (anti-miR-125b) resulted in increased expression of p14(ARF), decreased level of Mdm2, and induction of apoptosis.	mir-125b	68-76	MDM2 proto-oncogene	Homo sapiens	158-162
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	MDM2 proto-oncogene	Homo sapiens	77-81
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	MDM2 proto-oncogene	Homo sapiens	66-70
22525275-0	2013	Lenalidomide promotes p53 degradation by inhibiting MDM2 auto-ubiquitination in myelodysplastic syndrome with chromosome 5q deletion.	Lenalidomide	0-12	MDM2 proto-oncogene	Homo sapiens	52-56
22525275-4	2013	More importantly, we show that lenalidomide (Len) acts to stabilize MDM2, thereby accelerating p53 degradation.	Lenalidomide	31-43	MDM2 proto-oncogene	Homo sapiens	68-72
22525275-4	2013	More importantly, we show that lenalidomide (Len) acts to stabilize MDM2, thereby accelerating p53 degradation.	Lenalidomide	45-48	MDM2 proto-oncogene	Homo sapiens	68-72
22525275-5	2013	Biochemical and molecular analyses showed that Len inhibits the haplodeficient protein phosphatase 2A catalytic domain alpha (PP2Acalpha) phosphatase resulting in hyperphosphorylation of inhibitory serine-166 and serine-186 residues on MDM2, and displaces binding of RPS14 to suppress MDM2 autoubiquitination whereas PP2Acalpha overexpression promotes drug resistance.	Serine	198-204	MDM2 proto-oncogene	Homo sapiens	236-240
22525275-5	2013	Biochemical and molecular analyses showed that Len inhibits the haplodeficient protein phosphatase 2A catalytic domain alpha (PP2Acalpha) phosphatase resulting in hyperphosphorylation of inhibitory serine-166 and serine-186 residues on MDM2, and displaces binding of RPS14 to suppress MDM2 autoubiquitination whereas PP2Acalpha overexpression promotes drug resistance.	Serine	198-204	MDM2 proto-oncogene	Homo sapiens	285-289
22525275-5	2013	Biochemical and molecular analyses showed that Len inhibits the haplodeficient protein phosphatase 2A catalytic domain alpha (PP2Acalpha) phosphatase resulting in hyperphosphorylation of inhibitory serine-166 and serine-186 residues on MDM2, and displaces binding of RPS14 to suppress MDM2 autoubiquitination whereas PP2Acalpha overexpression promotes drug resistance.	Serine	213-219	MDM2 proto-oncogene	Homo sapiens	236-240
22525275-5	2013	Biochemical and molecular analyses showed that Len inhibits the haplodeficient protein phosphatase 2A catalytic domain alpha (PP2Acalpha) phosphatase resulting in hyperphosphorylation of inhibitory serine-166 and serine-186 residues on MDM2, and displaces binding of RPS14 to suppress MDM2 autoubiquitination whereas PP2Acalpha overexpression promotes drug resistance.	Serine	213-219	MDM2 proto-oncogene	Homo sapiens	285-289
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	MDM2 proto-oncogene	Homo sapiens	117-121
23398638-7	2013	The role of MDM2 binding was explored by inhibiting MDM2/p53 binding with nutlin-3.	nutlin 3	74-82	MDM2 proto-oncogene	Homo sapiens	52-56
23356442-10	2013	We also detected an obvious decrease in the level of HDM2 gene expression after both individual and combination treatments with resveratrol and genistein.	Resveratrol	128-139	MDM2 proto-oncogene	Homo sapiens	53-57
23356442-10	2013	We also detected an obvious decrease in the level of HDM2 gene expression after both individual and combination treatments with resveratrol and genistein.	Genistein	144-153	MDM2 proto-oncogene	Homo sapiens	53-57
23356442-11	2013	Our findings suggest that resveratrol and genistein when combined can induce apoptosis at doses lower than usual doses, through the activation of caspases cascade, and by decreasing the expression of HDM2.	Resveratrol	26-37	MDM2 proto-oncogene	Homo sapiens	200-204
23356442-11	2013	Our findings suggest that resveratrol and genistein when combined can induce apoptosis at doses lower than usual doses, through the activation of caspases cascade, and by decreasing the expression of HDM2.	Genistein	42-51	MDM2 proto-oncogene	Homo sapiens	200-204
27481281-0	2013	Molecular Dynamics Investigation on the Inhibition of MDM2-p53 Interaction by Polyphenols.	Polyphenols	78-89	MDM2 proto-oncogene	Homo sapiens	54-58
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	MDM2 proto-oncogene	Homo sapiens	66-70
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	MDM2 proto-oncogene	Homo sapiens	66-70
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	MDM2 proto-oncogene	Homo sapiens	55-59
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	MDM2 proto-oncogene	Homo sapiens	97-101
22391559-5	2013	This RPS14-MDM2 binding was induced upon ribosomal stress caused by actinomycin D or mycophenolic acid.	Dactinomycin	68-81	MDM2 proto-oncogene	Homo sapiens	11-15
22391559-5	2013	This RPS14-MDM2 binding was induced upon ribosomal stress caused by actinomycin D or mycophenolic acid.	Mycophenolic Acid	85-102	MDM2 proto-oncogene	Homo sapiens	11-15
23268733-0	2013	Siladenoserinols A-L: new sulfonated serinol derivatives from a tunicate as inhibitors of p53-Hdm2 interaction.	siladenoserinols a-l	0-20	MDM2 proto-oncogene	Homo sapiens	94-98
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	16-20
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	MDM2 proto-oncogene	Homo sapiens	73-77
22955948-8	2013	Thus, these findings established a novel oxidative stress-responsive pathway that involves IKK-beta, p85 S6K1 and Mdm2, which is response for H(2)O(2)-induced cell death.	Hydrogen Peroxide	142-150	MDM2 proto-oncogene	Homo sapiens	114-118
22349818-6	2013	Mutation of CBP Thr-1872 or Mdm2 Ser-186/188 Akt sites resulted in a dissociation of the ERbeta-CBP-Mdm2 complex and reduced ERbeta turnover.	Threonine	16-19	MDM2 proto-oncogene	Homo sapiens	100-104
22349818-6	2013	Mutation of CBP Thr-1872 or Mdm2 Ser-186/188 Akt sites resulted in a dissociation of the ERbeta-CBP-Mdm2 complex and reduced ERbeta turnover.	Serine	33-36	MDM2 proto-oncogene	Homo sapiens	28-32
22349818-6	2013	Mutation of CBP Thr-1872 or Mdm2 Ser-186/188 Akt sites resulted in a dissociation of the ERbeta-CBP-Mdm2 complex and reduced ERbeta turnover.	Serine	33-36	MDM2 proto-oncogene	Homo sapiens	100-104
24335171-9	2013	Berberine induced down-regulation of XIAP protein involving inhibition of MDM2 expression and a proteasome-dependent pathway.	Berberine	0-9	MDM2 proto-oncogene	Homo sapiens	74-78
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	MDM2 proto-oncogene	Homo sapiens	307-311
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	MDM2 proto-oncogene	Homo sapiens	210-214
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	MDM2 proto-oncogene	Homo sapiens	210-214
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.	nac	46-49	MDM2 proto-oncogene	Homo sapiens	192-196
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	MDM2 proto-oncogene	Homo sapiens	192-196
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	MDM2 proto-oncogene	Homo sapiens	266-270
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	MDM2 proto-oncogene	Homo sapiens	266-270
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	MDM2 proto-oncogene	Homo sapiens	130-134
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	MDM2 proto-oncogene	Homo sapiens	130-134
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	MDM2 proto-oncogene	Homo sapiens	34-38
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	MDM2 proto-oncogene	Homo sapiens	34-38
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	MDM2 proto-oncogene	Homo sapiens	74-78
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	MDM2 proto-oncogene	Homo sapiens	137-141
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	MDM2 proto-oncogene	Homo sapiens	137-141
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	MDM2 proto-oncogene	Homo sapiens	91-95
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	MDM2 proto-oncogene	Homo sapiens	41-45
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	MDM2 proto-oncogene	Homo sapiens	96-100
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	MDM2 proto-oncogene	Homo sapiens	124-128
23187804-0	2012	p53 expression controls prostate cancer sensitivity to chemotherapy and the MDM2 inhibitor Nutlin-3.	nutlin 3	91-99	MDM2 proto-oncogene	Homo sapiens	76-80
22487911-1	2012	Conflicting reports exist regarding the contribution of SNP309 in MDM2 to cancer risk.	snp309	56-62	MDM2 proto-oncogene	Homo sapiens	66-70
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	MDM2 proto-oncogene	Homo sapiens	116-120
23046248-2	2012	Novel p53-MDM2 inhibitors bearing pyrrolidone scaffolds were successfully identified by structure-based design.	Pyrrolidinones	34-45	MDM2 proto-oncogene	Homo sapiens	10-14
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	MDM2 proto-oncogene	Homo sapiens	45-49
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	MDM2 proto-oncogene	Homo sapiens	148-152
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	MDM2 proto-oncogene	Homo sapiens	117-121
23046248-8	2012	The novel pyrrolidone p53-MDM2 inhibitors represent promising lead structures for the development of novel antitumor agents.	Pyrrolidinones	10-21	MDM2 proto-oncogene	Homo sapiens	26-30
23039052-4	2012	Six of these proteins were previously identified MDM2 interactors, and the effects of Nutlin-3 on the MDM2-nucleophosmin interaction (NPM) was further validated.	nutlin 3	86-94	MDM2 proto-oncogene	Homo sapiens	102-106
23125243-0	2012	A novel combination therapy approach for the treatment of acute myeloid leukemia: the multi-kinase inhibitor sorafenib and the HDM2 inhibitor nutlin-3.	nutlin 3	142-150	MDM2 proto-oncogene	Homo sapiens	127-131
22872685-0	2012	Combination treatment in vitro with Nutlin, a small-molecule antagonist of MDM2, and pegylated interferon-alpha 2a specifically targets JAK2V617F-positive polycythemia vera cells.	nutlin	36-42	MDM2 proto-oncogene	Homo sapiens	75-79
23035244-0	2012	Lithocholic acid is an endogenous inhibitor of MDM4 and MDM2.	Lithocholic Acid	0-16	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	129-133
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	MDM2 proto-oncogene	Homo sapiens	68-72
22991965-2	2012	Here, we present kinetic, thermodynamic, and structural rationale for the remarkable potency of a new class of MDM2 inhibitors, the piperidinones.	2-piperidone	132-145	MDM2 proto-oncogene	Homo sapiens	111-115
22991965-3	2012	While these compounds bind to the same site as previously reported for small molecule inhibitors, such as the Nutlins, data presented here demonstrate that the piperidinones also engage the N-terminal region (residues 10-16) of human MDM2, in particular, Val14 and Thr16.	2-piperidone	160-173	MDM2 proto-oncogene	Homo sapiens	234-238
22991965-4	2012	This portion of MDM2 is unstructured in both the apo form of the protein and in MDM2 complexes with p53 or Nutlin, but adopts a novel beta-strand structure when complexed with the piperidinones.	2-piperidone	180-193	MDM2 proto-oncogene	Homo sapiens	16-20
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	MDM2 proto-oncogene	Homo sapiens	94-98
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	MDM2 proto-oncogene	Homo sapiens	129-133
23035244-9	2012	Binding was weakened by structural changes in LCA, and so it may be a natural ligand of MDM2 and MDM4, raising the possibility that MDM proteins may be sensors for specific steroids.	Lithocholic Acid	46-49	MDM2 proto-oncogene	Homo sapiens	88-92
23035244-9	2012	Binding was weakened by structural changes in LCA, and so it may be a natural ligand of MDM2 and MDM4, raising the possibility that MDM proteins may be sensors for specific steroids.	Steroids	173-181	MDM2 proto-oncogene	Homo sapiens	88-92
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	MDM2 proto-oncogene	Homo sapiens	61-65
22995624-2	2012	As a result, we discovered novel MDM2 inhibitors possessing a dihydroimidazothiazole scaffold.	dihydroimidazothiazole	62-84	MDM2 proto-oncogene	Homo sapiens	33-37
22990650-7	2012	MDM2 (P=0.032) and ERBB2 (P=0.064) expression was increased in platinum-sensitive patients, and FGF1 (adjusted log-rank test P=0.006), FGFR2 (P=0.04) and PDRFRB expression (P=0.037) significantly inversely influenced progression-free survival.	Platinum	63-71	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	136-140
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	MDM2 proto-oncogene	Homo sapiens	0-4
22989009-4	2012	Previously, we examined the anti-lymphoma activity of MI-319, the laboratory grade of a new class of HDM2 SMI, the spiro-oxindole, in follicular lymphoma.	spiro-oxindole	115-129	MDM2 proto-oncogene	Homo sapiens	101-105
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	MDM2 proto-oncogene	Homo sapiens	134-138
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	MDM2 proto-oncogene	Homo sapiens	50-54
22976441-8	2012	We further demonstrated that DNA damage-induced activation of ATM directly phosphorylated CKIdelta at two well-conserved S/TQ sites, which promotes CKIdelta nuclear localization to increase CKIdelta-mediated phosphorylation of Mdm2, thereby facilitating subsequent Mdm2 ubiquitination by SCFbeta-TRCP.	N-(6-methoxy-8-quinolyl)-4-toluenesulfonamide	123-125	MDM2 proto-oncogene	Homo sapiens	227-231
22119201-0	2012	SNP285C modulates oestrogen receptor/Sp1 binding to the MDM2 promoter and reduces the risk of endometrial but not prostatic cancer.	snp285c	0-7	MDM2 proto-oncogene	Homo sapiens	56-60
22707197-4	2012	Triptolide treatment can suppress Akt/Hdm2 signaling pathway, and lead to p53 accumulation, thereby up-regulating DR5 expression.	triptolide	0-10	MDM2 proto-oncogene	Homo sapiens	38-42
22976441-8	2012	We further demonstrated that DNA damage-induced activation of ATM directly phosphorylated CKIdelta at two well-conserved S/TQ sites, which promotes CKIdelta nuclear localization to increase CKIdelta-mediated phosphorylation of Mdm2, thereby facilitating subsequent Mdm2 ubiquitination by SCFbeta-TRCP.	N-(6-methoxy-8-quinolyl)-4-toluenesulfonamide	123-125	MDM2 proto-oncogene	Homo sapiens	265-269
22733537-4	2012	The effects of Nutlin-3, an MDM2 antagonist, on tumor growth in relation to DNMT3A expression and TSG methylation status were examined by xenograft model.	nutlin 3	15-23	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	141-145
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	MDM2 proto-oncogene	Homo sapiens	141-145
22733537-9	2012	Treatment with Nutlin-3, an MDM2 antagonist, significantly suppressed tumor growth and reduced DNA methylation level of TSGs through downregulation of DNMT3A expression in xenograft studies.	nutlin 3	15-23	MDM2 proto-oncogene	Homo sapiens	28-32
22624960-0	2012	AM-8553: a novel MDM2 inhibitor with a promising outlook for potential clinical development.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(2-hydroxypentan-3-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	0-7	MDM2 proto-oncogene	Homo sapiens	17-21
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	MDM2 proto-oncogene	Homo sapiens	155-159
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	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	66-70
22472959-6	2012	MDM2 amplification was analyzed using FISH on formalin-fixed, paraffin-embedded material in 26 cases.	Formaldehyde	46-54	MDM2 proto-oncogene	Homo sapiens	0-4
22472959-6	2012	MDM2 amplification was analyzed using FISH on formalin-fixed, paraffin-embedded material in 26 cases.	Paraffin	62-70	MDM2 proto-oncogene	Homo sapiens	0-4
22397761-0	2012	Functionalization of single-walled carbon nanotubes enables efficient intracellular delivery of siRNA targeting MDM2 to inhibit breast cancer cells growth.	Carbon	35-41	MDM2 proto-oncogene	Homo sapiens	112-116
22397761-6	2012	It was obvious that MDM2 can serve as a novel therapeutic target by an effective carrier system of DSPE-PEG-Amine-functionalized SWNTs, which would be very advanced and significant to therapy of breast cancer further.	pegamine	104-113	MDM2 proto-oncogene	Homo sapiens	20-24
24250508-0	2012	Docking Analysis and Multidimensional Hybrid QSAR Model of 1,4-Benzodiazepine-2,5-Diones as HDM2 Antagonists.	Bz-423	59-88	MDM2 proto-oncogene	Homo sapiens	92-96
24250508-3	2012	The docking results indicate that pi-pi interaction between the imidazole group in HIS96 and the aryl ring at 4-N of 1,4-benzodiazepine-2,5-dione may be one of the key factors for the combination of ligands with HDM2.	imidazole	64-73	MDM2 proto-oncogene	Homo sapiens	212-216
24250508-3	2012	The docking results indicate that pi-pi interaction between the imidazole group in HIS96 and the aryl ring at 4-N of 1,4-benzodiazepine-2,5-dione may be one of the key factors for the combination of ligands with HDM2.	Bz-423	117-145	MDM2 proto-oncogene	Homo sapiens	212-216
22356895-0	2012	MDM2 309 polymorphism predicts outcome in platinum-treated locally advanced head and neck cancer.	Platinum	42-50	MDM2 proto-oncogene	Homo sapiens	0-4
22578852-0	2012	Comparison of the antitumor effects of an MDM2 inhibitor, nutlin-3, in feline lymphoma cell lines with or without p53 mutation.	nutlin 3	58-66	MDM2 proto-oncogene	Homo sapiens	42-46
22584579-5	2012	We also showed that PIM-1S induced Ser-213 phosphorylation destabilizes AR by recruiting the ubiquitin E3 ligase Mdm2 and promotes AR degradation in a cell cycle-dependent manner, while PIM-1L-induced Thr-850 phosphorylation stabilizes AR by recruiting the ubiquitin E3 ligase RNF6 and promotes AR-mediated transcription under low-androgen conditions.	Serine	35-38	MDM2 proto-oncogene	Homo sapiens	113-117
22524527-2	2012	The affinity of these compounds for MDM2 was improved through conformational control of both the piperidinone ring and the appended N-alkyl substituent.	2-piperidone	97-109	MDM2 proto-oncogene	Homo sapiens	36-40
22524527-2	2012	The affinity of these compounds for MDM2 was improved through conformational control of both the piperidinone ring and the appended N-alkyl substituent.	n-alkyl	132-139	MDM2 proto-oncogene	Homo sapiens	36-40
22524527-3	2012	Optimization afforded 29 (AM-8553), a potent and selective MDM2 inhibitor with excellent pharmacokinetic properties and in vivo efficacy.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(2-hydroxypentan-3-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	26-33	MDM2 proto-oncogene	Homo sapiens	59-63
22940704-0	2012	Structure-activity relationship and antitumor activity of thio-benzodiazepines as p53-MDM2 protein-protein interaction inhibitors.	thio-benzodiazepines	58-78	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	143-147
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	MDM2 proto-oncogene	Homo sapiens	32-36
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	MDM2 proto-oncogene	Homo sapiens	44-48
22622028-9	2012	Nutlin-3, an HDM2 inhibitor, mimicked the effects of alpha-MSH resulting in reduced phosphorylation of H2AX (gamma-H2AX), a marker of DNA damage.	nutlin 3	0-8	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	231-235
22499437-6	2012	Perifosine treatment suppressed the phosphorylation of Akt downstream targets such as GSK3alpha/beta, MDM2, and p70S6K and induced apoptosis.	perifosine	0-10	MDM2 proto-oncogene	Homo sapiens	102-106
22233482-0	2012	QSAR models for isoindolinone-based p53-MDM2 interaction inhibitors using linear and non-linear statistical methods.	phthalimidine	16-29	MDM2 proto-oncogene	Homo sapiens	40-44
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	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	38-42
22337874-4	2012	Contrary to p53, where two separate domains form the interface with MDM2, only one region within the phosphotyrosine binding domain of NUMB (amino acids 113-148) mediates binding to both these regions of MDM2.	Phosphotyrosine	101-116	MDM2 proto-oncogene	Homo sapiens	204-208
21706156-0	2012	MDM2 SNP309 and TP53 R72P associated with severe and febrile neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide.	snp309	5-11	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	0-4
21706156-0	2012	MDM2 SNP309 and TP53 R72P associated with severe and febrile neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide.	Epirubicin	117-127	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	87-91
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).	Epirubicin	188-198	MDM2 proto-oncogene	Homo sapiens	87-91
22095636-7	2012	HuR is stabilized by Mdm2-mediated NEDDylation in at least three lysine residues, ensuring its nuclear localization and protection from degradation.	Lysine	65-71	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	220-224
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	MDM2 proto-oncogene	Homo sapiens	30-34
22343310-0	2012	MDM2 antagonism by nutlin-3 induces death in human medulloblastoma cells.	nutlin 3	19-27	MDM2 proto-oncogene	Homo sapiens	0-4
22318725-0	2012	Ubiquitin- and MDM2 E3 ligase-independent proteasomal turnover of nucleostemin in response to GTP depletion.	Guanosine Triphosphate	94-97	MDM2 proto-oncogene	Homo sapiens	15-19
22318725-12	2012	Hence, these results indicate that NS undergoes a ubiquitin- and MDM2-independent proteasomal degradation when intracellular GTP levels are markedly reduced and also suggest that ubiquitination of NS may be involved in regulation of its function rather than stability.	Guanosine Triphosphate	125-128	MDM2 proto-oncogene	Homo sapiens	65-69
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	MDM2 proto-oncogene	Homo sapiens	42-46
22694121-4	2012	Herein, we report the design of a superactive d-peptide antagonist of MDM2, termed (D)PMI-delta, of which the binding affinity for ((25-109))MDM2 has been improved over (D)PMI-alpha by 3 orders of magnitude (K(d) = 220 pM).	pmi-delta	86-95	MDM2 proto-oncogene	Homo sapiens	70-74
22694121-4	2012	Herein, we report the design of a superactive d-peptide antagonist of MDM2, termed (D)PMI-delta, of which the binding affinity for ((25-109))MDM2 has been improved over (D)PMI-alpha by 3 orders of magnitude (K(d) = 220 pM).	pmi-delta	86-95	MDM2 proto-oncogene	Homo sapiens	141-145
22694121-4	2012	Herein, we report the design of a superactive d-peptide antagonist of MDM2, termed (D)PMI-delta, of which the binding affinity for ((25-109))MDM2 has been improved over (D)PMI-alpha by 3 orders of magnitude (K(d) = 220 pM).	pmi	86-89	MDM2 proto-oncogene	Homo sapiens	70-74
22694121-4	2012	Herein, we report the design of a superactive d-peptide antagonist of MDM2, termed (D)PMI-delta, of which the binding affinity for ((25-109))MDM2 has been improved over (D)PMI-alpha by 3 orders of magnitude (K(d) = 220 pM).	pmi	86-89	MDM2 proto-oncogene	Homo sapiens	141-145
22694121-4	2012	Herein, we report the design of a superactive d-peptide antagonist of MDM2, termed (D)PMI-delta, of which the binding affinity for ((25-109))MDM2 has been improved over (D)PMI-alpha by 3 orders of magnitude (K(d) = 220 pM).	methylphenyl carbinol	176-181	MDM2 proto-oncogene	Homo sapiens	70-74
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	MDM2 proto-oncogene	Homo sapiens	99-103
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	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	189-193
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	MDM2 proto-oncogene	Homo sapiens	211-215
22301280-5	2012	Using measurement of surface plasmon resonance, we demonstrated that active 5-deazaflavin analogs bind to the MDM2 RING, whereas inactive compounds show no binding.	5-deazaflavin	76-89	MDM2 proto-oncogene	Homo sapiens	110-114
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	MDM2 proto-oncogene	Homo sapiens	122-126
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	MDM2 proto-oncogene	Homo sapiens	168-172
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	MDM2 proto-oncogene	Homo sapiens	133-137
22579006-0	2012	Preclinical pharmacokinetics of MI-219, a novel human double minute 2 (HDM2) inhibitor and prediction of human pharmacokinetics.	MI-219	32-38	MDM2 proto-oncogene	Homo sapiens	71-75
22108807-7	2012	Selection cloning and sequence analysis of MDM2 DNA binding sequences, unlike             RNA binding sequences, revealed no obvious DNA binding consensus sequence, but             preferential binding to oligopurine:pyrimidine-rich stretches.	oligopurine	205-216	MDM2 proto-oncogene	Homo sapiens	43-47
22108807-7	2012	Selection cloning and sequence analysis of MDM2 DNA binding sequences, unlike             RNA binding sequences, revealed no obvious DNA binding consensus sequence, but             preferential binding to oligopurine:pyrimidine-rich stretches.	pyrimidine	217-227	MDM2 proto-oncogene	Homo sapiens	43-47
21725357-0	2012	MYCN sensitizes neuroblastoma to the MDM2-p53 antagonists Nutlin-3 and MI-63.	nutlin 3	58-66	MDM2 proto-oncogene	Homo sapiens	37-41
21725357-0	2012	MYCN sensitizes neuroblastoma to the MDM2-p53 antagonists Nutlin-3 and MI-63.	MI-63	71-76	MDM2 proto-oncogene	Homo sapiens	37-41
22056306-7	2012	In contrast, ectopically expression of Mdm2 decreases PolH expression, which can be abrogated by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	MDM2 proto-oncogene	Homo sapiens	39-43
22233735-0	2012	Fibroid explants reveal a higher sensitivity against MDM2-inhibitor nutlin-3 than matching myometrium.	nutlin 3	68-76	MDM2 proto-oncogene	Homo sapiens	53-57
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	MDM2 proto-oncogene	Homo sapiens	142-146
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	MDM2 proto-oncogene	Homo sapiens	38-42
23167335-0	2012	MDM2 T309G has a synergistic effect with P21 ser31arg single nucleotide polymorphisms on the risk of acute myeloid leukemia.	ser31arg	45-53	MDM2 proto-oncogene	Homo sapiens	0-4
23167335-6	2012	In contrast, a SNP in position 309 of MDM2 results in increased expression due to substitution of thymine by guanine.	Thymine	98-105	MDM2 proto-oncogene	Homo sapiens	38-42
23167335-6	2012	In contrast, a SNP in position 309 of MDM2 results in increased expression due to substitution of thymine by guanine.	Guanine	109-116	MDM2 proto-oncogene	Homo sapiens	38-42
23167335-10	2012	Although the MDM2 309G allele was itself without affect, it showed a synergistic effect with P21 ser/arg polymorphism (P value=0.003, OR= 6.807, 95% CI= 1.909-24.629).	Serine	97-100	MDM2 proto-oncogene	Homo sapiens	13-17
23167335-10	2012	Although the MDM2 309G allele was itself without affect, it showed a synergistic effect with P21 ser/arg polymorphism (P value=0.003, OR= 6.807, 95% CI= 1.909-24.629).	Arginine	101-104	MDM2 proto-oncogene	Homo sapiens	13-17
22134502-0	2012	MDM2 SNP309 modifies the prognostic significance of the p53 mutational             status in patients with ovarian cancer.	snp309	5-11	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	112-116
22051195-0	2012	Regulation of Actinomycin D induced upregulation of Mdm2 in H1299 cells.	Dactinomycin	14-27	MDM2 proto-oncogene	Homo sapiens	52-56
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	MDM2 proto-oncogene	Homo sapiens	29-33
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	MDM2 proto-oncogene	Homo sapiens	29-33
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	MDM2 proto-oncogene	Homo sapiens	101-105
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	MDM2 proto-oncogene	Homo sapiens	171-175
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	MDM2 proto-oncogene	Homo sapiens	34-38
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	MDM2 proto-oncogene	Homo sapiens	34-38
21954050-0	2012	Exhaustive fluorine scanning toward potent p53-Mdm2 antagonists.	Fluorine	11-19	MDM2 proto-oncogene	Homo sapiens	47-51
22104152-0	2012	Hoiamide D, a marine cyanobacteria-derived inhibitor of p53/MDM2 interaction.	hoiamide D	0-10	MDM2 proto-oncogene	Homo sapiens	60-64
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	MDM2 proto-oncogene	Homo sapiens	53-57
22830335-7	2012	These identified natural MDM2 inhibitors include a plethora of diverse chemical frameworks, ranging from flavonoids, steroids, and sesquiterpenes to alkaloids.	Flavonoids	105-115	MDM2 proto-oncogene	Homo sapiens	25-29
22830335-7	2012	These identified natural MDM2 inhibitors include a plethora of diverse chemical frameworks, ranging from flavonoids, steroids, and sesquiterpenes to alkaloids.	Steroids	117-125	MDM2 proto-oncogene	Homo sapiens	25-29
22830335-7	2012	These identified natural MDM2 inhibitors include a plethora of diverse chemical frameworks, ranging from flavonoids, steroids, and sesquiterpenes to alkaloids.	Sesquiterpenes	131-145	MDM2 proto-oncogene	Homo sapiens	25-29
22830335-7	2012	These identified natural MDM2 inhibitors include a plethora of diverse chemical frameworks, ranging from flavonoids, steroids, and sesquiterpenes to alkaloids.	Alkaloids	149-158	MDM2 proto-oncogene	Homo sapiens	25-29
21523548-0	2012	Structural determinants of benzodiazepinedione/peptide-based p53-HDM2 inhibitors using 3D-QSAR, docking and molecular dynamics.	benzodiazepinedione	27-46	MDM2 proto-oncogene	Homo sapiens	65-69
21833626-2	2011	We have earlier reported that the increased intake of soy isoflavones reduces risk of postmenopausal breast cancer, and experimental studies suggest that dietary isoflavones can down-regulate the expression of the MDM2 oncoprotein.	Isoflavones	162-173	MDM2 proto-oncogene	Homo sapiens	214-218
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	MDM2 proto-oncogene	Homo sapiens	123-127
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	MDM2 proto-oncogene	Homo sapiens	123-127
22911819-0	2012	Natural product ginsenoside 25-OCH3-PPD inhibits breast cancer growth and metastasis through down-regulating MDM2.	25-methoxylprotopanaxadiol	16-39	MDM2 proto-oncogene	Homo sapiens	109-113
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	MDM2 proto-oncogene	Homo sapiens	92-96
22912688-0	2012	Aciculatin induces p53-dependent apoptosis via MDM2 depletion in human cancer cells in vitro and in vivo.	aciculatin	0-10	MDM2 proto-oncogene	Homo sapiens	47-51
22912688-7	2012	Interestingly, the aciculatin-induced downregulation of MDM2, an important negative regulator of p53, contributed to p53 accumulation.	aciculatin	19-29	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	182-186
23650573-7	2012	We also found that MDM2 combined to IGF-1R in response to sunitinib stimulation.	Sunitinib	58-67	MDM2 proto-oncogene	Homo sapiens	19-23
23650573-11	2012	These results mean that sunitinib mediates ubiquitination of IGF-1R dependent on MDM2.	Sunitinib	24-33	MDM2 proto-oncogene	Homo sapiens	81-85
22044530-4	2011	Our data showed that pretreatment with TCDD abolished 1-NP- but not BaP-induced p53 and mouse double minute 2 (MDM2; HDM2 in humans) expressions.	Polychlorinated Dibenzodioxins	39-43	MDM2 proto-oncogene	Homo sapiens	117-121
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	MDM2 proto-oncogene	Homo sapiens	32-36
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	MDM2 proto-oncogene	Homo sapiens	32-36
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	MDM2 proto-oncogene	Homo sapiens	32-36
22044530-7	2011	However, TCDD-activated HDM2 did not distinctly cause the degradation of BaP- or nutlin-3-induced p53 expression.	Polychlorinated Dibenzodioxins	9-13	MDM2 proto-oncogene	Homo sapiens	24-28
22047690-0	2011	Conjugation of spermine enhances cellular uptake of the stapled peptide-based inhibitors of p53-Mdm2 interaction.	Spermine	15-23	MDM2 proto-oncogene	Homo sapiens	96-100
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	MDM2 proto-oncogene	Homo sapiens	114-118
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.	Arsenic	119-126	MDM2 proto-oncogene	Homo sapiens	52-56
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	MDM2 proto-oncogene	Homo sapiens	93-97
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	MDM2 proto-oncogene	Homo sapiens	178-182
21833626-6	2011	Furthermore, the protective effect of dietary soy isoflavones on postmenopausal breast cancer was mainly confined to women homozygous for the high activity MDM2 allele (GG genotype).	Isoflavones	50-61	MDM2 proto-oncogene	Homo sapiens	156-160
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	MDM2 proto-oncogene	Homo sapiens	227-231
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	MDM2 proto-oncogene	Homo sapiens	55-59
21953469-4	2011	We found that K351N substitution abrogates the monoubiquitination of p53 induced by both Mdm2 and MSL2 E3-ligases.	k351n	14-19	MDM2 proto-oncogene	Homo sapiens	89-93
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	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	55-59
21844567-0	2011	HDM-2 inhibition suppresses expression of ribonucleotide reductase subunit M2, and synergistically enhances gemcitabine-induced cytotoxicity in mantle cell lymphoma.	gemcitabine	108-119	MDM2 proto-oncogene	Homo sapiens	0-5
21903592-2	2011	Although a mutation at Cys-305 within the zinc finger domain of MDM2 has been shown to drastically impair MDM2 interaction with RPL11 and thus escapes the inhibition by this ribosomal protein, it still remains elusive whether RPL11 inactivates MDM2 via direct action on this zinc finger domain and what is the chemical nature of this specific interaction.	Cysteine	23-26	MDM2 proto-oncogene	Homo sapiens	64-68
21903592-2	2011	Although a mutation at Cys-305 within the zinc finger domain of MDM2 has been shown to drastically impair MDM2 interaction with RPL11 and thus escapes the inhibition by this ribosomal protein, it still remains elusive whether RPL11 inactivates MDM2 via direct action on this zinc finger domain and what is the chemical nature of this specific interaction.	Cysteine	23-26	MDM2 proto-oncogene	Homo sapiens	106-110
21903592-2	2011	Although a mutation at Cys-305 within the zinc finger domain of MDM2 has been shown to drastically impair MDM2 interaction with RPL11 and thus escapes the inhibition by this ribosomal protein, it still remains elusive whether RPL11 inactivates MDM2 via direct action on this zinc finger domain and what is the chemical nature of this specific interaction.	Cysteine	23-26	MDM2 proto-oncogene	Homo sapiens	106-110
21903592-5	2011	This binding is disrupted by single mutations of non-cysteine amino acids within the zinc finger domain of MDM2.	cysteine amino acids	53-73	MDM2 proto-oncogene	Homo sapiens	107-111
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	MDM2 proto-oncogene	Homo sapiens	106-110
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	MDM2 proto-oncogene	Homo sapiens	36-40
21996465-2	2011	Most of the thio-benzodiazepines had nanomolar to micromolar affinity toward MDM2.	thio-benzodiazepines	12-32	MDM2 proto-oncogene	Homo sapiens	77-81
21996465-6	2011	The thio-benzodiazepines represent a promising class of non-peptide inhibitors of the p53-MDM2 interaction.	thio-benzodiazepines	4-24	MDM2 proto-oncogene	Homo sapiens	90-94
21868571-6	2011	The protective effect of stromal cells was significantly reduced by pre-exposure to the HDM2 inhibitor Nutlin-3a.	nutlin 3	103-112	MDM2 proto-oncogene	Homo sapiens	88-92
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	MDM2 proto-oncogene	Homo sapiens	107-111
21875801-0	2011	MDM2-p53 protein-protein interaction inhibitors: a-ring substituted isoindolinones.	phthalimidine	68-82	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	41-45
21929745-0	2011	Differential modulatory effects of GSK-3beta and HDM2 on sorafenib-induced AIF nuclear translocation (programmed necrosis) in melanoma.	Sorafenib	57-66	MDM2 proto-oncogene	Homo sapiens	49-53
22701761-10	2011	MDM2-mediated increase in p100/NF-kappaB2 expression reduced cell death mediated by paclitaxel.	Paclitaxel	84-94	MDM2 proto-oncogene	Homo sapiens	0-4
21855354-0	2011	Design, synthesis, and biological evaluation of imidazoline derivatives as p53-MDM2 binding inhibitors.	Imidazolines	48-59	MDM2 proto-oncogene	Homo sapiens	79-83
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	MDM2 proto-oncogene	Homo sapiens	102-106
21773579-0	2011	Achieving cell penetration with distance-matching cysteine cross-linkers: a facile route to cell-permeable peptide dual inhibitors of Mdm2/Mdmx.	Cysteine	50-58	MDM2 proto-oncogene	Homo sapiens	134-138
21773579-2	2011	By cross-linking a peptide dual inhibitor of Mdm2/Mdmx containing cysteines at i,i+7 positions, dramatic enhancement in cell permeability was achieved, along with increased helicity and biological activity.	Cysteine	66-75	MDM2 proto-oncogene	Homo sapiens	45-49
21820342-0	2011	Molecular modeling and molecular dynamics simulation studies on pyrrolopyrimidine-based alpha-helix mimetic as dual inhibitors of MDM2 and MDMX.	pyrrolopyrimidine	64-81	MDM2 proto-oncogene	Homo sapiens	130-134
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	MDM2 proto-oncogene	Homo sapiens	138-142
21628454-3	2011	Specifically, the serine/threonine kinase GSK-3beta stabilizes nuclear NFATc2 through phosphorylation of the serine-rich SP2 domain, thus protecting the transcription factor from E3-ubiquitin ligase HDM2-mediated proteolysis.	Serine	18-24	MDM2 proto-oncogene	Homo sapiens	199-203
21628454-4	2011	Zoledronic acid disrupts this NFATc2 stabilization pathway through two mechanisms, namely GSK-3beta inhibition and induction of HDM2 activity.	Zoledronic Acid	0-15	MDM2 proto-oncogene	Homo sapiens	128-132
21628454-5	2011	Upon nuclear accumulation, HDM2 targets unphosphorylated NFATc2 for ubiquitination at acceptor lysine residues Lys-684/Lys-897 and hence labels the factor for subsequent proteasomal degradation.	Lysine	95-101	MDM2 proto-oncogene	Homo sapiens	27-31
21628454-5	2011	Upon nuclear accumulation, HDM2 targets unphosphorylated NFATc2 for ubiquitination at acceptor lysine residues Lys-684/Lys-897 and hence labels the factor for subsequent proteasomal degradation.	Lysine	111-114	MDM2 proto-oncogene	Homo sapiens	27-31
21628454-5	2011	Upon nuclear accumulation, HDM2 targets unphosphorylated NFATc2 for ubiquitination at acceptor lysine residues Lys-684/Lys-897 and hence labels the factor for subsequent proteasomal degradation.	Lysine	119-122	MDM2 proto-oncogene	Homo sapiens	27-31
21628454-6	2011	Conversely, mutagenesis-induced constitutive serine phosphorylation (Ser-215, Ser-219, and Ser-223) of the SP2 domain prevents NFATc2 from HDM2-mediated ubiquitination and degradation and consequently rescues cancer cells from growth suppression by zoledronic acid.	Serine	45-51	MDM2 proto-oncogene	Homo sapiens	139-143
21628454-6	2011	Conversely, mutagenesis-induced constitutive serine phosphorylation (Ser-215, Ser-219, and Ser-223) of the SP2 domain prevents NFATc2 from HDM2-mediated ubiquitination and degradation and consequently rescues cancer cells from growth suppression by zoledronic acid.	Serine	69-72	MDM2 proto-oncogene	Homo sapiens	139-143
21628454-6	2011	Conversely, mutagenesis-induced constitutive serine phosphorylation (Ser-215, Ser-219, and Ser-223) of the SP2 domain prevents NFATc2 from HDM2-mediated ubiquitination and degradation and consequently rescues cancer cells from growth suppression by zoledronic acid.	Serine	78-81	MDM2 proto-oncogene	Homo sapiens	139-143
21628454-6	2011	Conversely, mutagenesis-induced constitutive serine phosphorylation (Ser-215, Ser-219, and Ser-223) of the SP2 domain prevents NFATc2 from HDM2-mediated ubiquitination and degradation and consequently rescues cancer cells from growth suppression by zoledronic acid.	Serine	78-81	MDM2 proto-oncogene	Homo sapiens	139-143
21628454-6	2011	Conversely, mutagenesis-induced constitutive serine phosphorylation (Ser-215, Ser-219, and Ser-223) of the SP2 domain prevents NFATc2 from HDM2-mediated ubiquitination and degradation and consequently rescues cancer cells from growth suppression by zoledronic acid.	Zoledronic Acid	249-264	MDM2 proto-oncogene	Homo sapiens	139-143
21628454-7	2011	In conclusion, this study demonstrates a critical role of the GSK-3beta-HDM2 signaling loop in the regulation of NFATc2 protein stability and growth promotion and suggests that double targeting of this pathway is responsible, at least to a significant part, for the potent and reliable anti-tumoral effects of zoledronic acid.	Zoledronic Acid	310-325	MDM2 proto-oncogene	Homo sapiens	72-76
21791053-3	2011	The recently discovered small-molecule MDM2 inhibitor MI-219 and its analogues are in advanced preclinical development as cancer therapeutics.	MI-219	54-60	MDM2 proto-oncogene	Homo sapiens	39-43
21640377-0	2011	The suppression of prostate LNCaP cancer cells growth by Selenium nanoparticles through Akt/Mdm2/AR controlled apoptosis.	Selenium	57-65	MDM2 proto-oncogene	Homo sapiens	92-96
21640377-6	2011	Moreover, Selenium nanoparticles activate Akt kinase by increasing its phosphorylation, promote Akt-dependent androgen receptor phosphorylation and Mdm2 regulated degradation through proteasome pathway.	Selenium	10-18	MDM2 proto-oncogene	Homo sapiens	148-152
21374733-8	2011	Interestingly, treatment of MG132 restored Mdm2 expression to the steady-state level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	MDM2 proto-oncogene	Homo sapiens	43-47
20972874-9	2011	The observed effects of SF1126 on the p-Akt-MDM2-survivin axis suggest a patient selection paradigm in which NB tumors with increased pAkt-MDM2-survivin signaling may predict response to SF1126 alone or in combination with standard chemotherapy regimens that contain anthracyclines.	SF 1126	24-30	MDM2 proto-oncogene	Homo sapiens	44-48
21929745-5	2011	In this report, we describe the results of studies exploring the effects of GSK-3beta on the cytotoxicity and antitumor activity of sorafenib combined with the HDM2 antagonist MI-319.	MI 319	176-182	MDM2 proto-oncogene	Homo sapiens	160-164
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	MDM2 proto-oncogene	Homo sapiens	177-181
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.	Methotrexate	145-157	MDM2 proto-oncogene	Homo sapiens	166-170
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	MDM2 proto-oncogene	Homo sapiens	53-57
21350558-2	2011	In this study, we show that human homolog double minute 2 (HDM2) inhibition, with MI-219-a novel compound, and consequently p53 stabilization induce chronic myeloid leukemia (CML) blast crisis cells to undergo apoptosis regardless of the presence of the T315I mutation in the BCR-ABL kinase domain.	mi-219-a	82-90	MDM2 proto-oncogene	Homo sapiens	34-57
21350558-2	2011	In this study, we show that human homolog double minute 2 (HDM2) inhibition, with MI-219-a novel compound, and consequently p53 stabilization induce chronic myeloid leukemia (CML) blast crisis cells to undergo apoptosis regardless of the presence of the T315I mutation in the BCR-ABL kinase domain.	mi-219-a	82-90	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	17-22
21623005-0	2011	Network modeling of MDM2 inhibitor-oxaliplatin combination reveals biological synergy in wt-p53 solid tumors.	Oxaliplatin	35-46	MDM2 proto-oncogene	Homo sapiens	20-24
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	MDM2 proto-oncogene	Homo sapiens	162-166
21726810-4	2011	PIDD-induced Caspase-2 directly cleaves the E3 ubiquitin ligase Mdm2 at Asp 367, leading to loss of the C-terminal RING domain responsible for p53 ubiquitination.	Aspartic Acid	72-75	MDM2 proto-oncogene	Homo sapiens	64-68
21561866-6	2011	Interestingly, MDM2 in turn ubiquitinates S27a and promotes proteasomal degradation of S27a in response to actinomycin D treatment, thus forming a mutual-regulatory loop.	Dactinomycin	107-120	MDM2 proto-oncogene	Homo sapiens	15-19
21750655-10	2011	Interestingly, XI-011 acted additively with the MDM2 antagonist Nutlin-3a to inhibit growth of breast cancer cells.	(10-methyl-9-anthryl)methyl imidothiocarbamate	15-21	MDM2 proto-oncogene	Homo sapiens	48-52
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	MDM2 proto-oncogene	Homo sapiens	143-147
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	MDM2 proto-oncogene	Homo sapiens	91-95
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	MDM2 proto-oncogene	Homo sapiens	156-160
21268124-9	2011	MDM2 SNP309 may be used as one of the candidate biomarkers to predict NSCLC survival.	snp309	5-11	MDM2 proto-oncogene	Homo sapiens	0-4
21460101-0	2011	Functional analysis of the p53 pathway in neuroblastoma cells using the small-molecule MDM2 antagonist nutlin-3.	nutlin 3	103-111	MDM2 proto-oncogene	Homo sapiens	87-91
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	MDM2 proto-oncogene	Homo sapiens	131-135
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	MDM2 proto-oncogene	Homo sapiens	166-170
21504235-0	2011	Diosgenin suppresses hepatocyte growth factor (HGF)-induced epithelial-mesenchymal transition by down-regulation of Mdm2 and vimentin.	Diosgenin	0-9	MDM2 proto-oncogene	Homo sapiens	116-120
21504235-6	2011	Moreover, diosgenin effectively inhibited the HGF-induced increases in Mdm2 and vimentin by down-regulating phosphorylated Akt and mTOR.	Diosgenin	10-19	MDM2 proto-oncogene	Homo sapiens	71-75
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	MDM2 proto-oncogene	Homo sapiens	24-28
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	MDM2 proto-oncogene	Homo sapiens	134-138
21466165-7	2011	All parkin mutants tested effectively suppress arrestin ubiquitination, suggesting that bound parkin shields arrestin lysines targeted by Mdm2.	Lysine	118-125	MDM2 proto-oncogene	Homo sapiens	138-142
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	MDM2 proto-oncogene	Homo sapiens	30-34
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	MDM2 proto-oncogene	Homo sapiens	232-236
21123063-0	2011	Improvement of the synthesis and pharmacokinetic properties of chromenotriazolopyrimidine MDM2-p53 protein-protein inhibitors.	chromenotriazolopyrimidine	63-89	MDM2 proto-oncogene	Homo sapiens	90-94
21123063-2	2011	We report several optimizations to the synthesis of the chromenotriazolopyrimidine series of MDM2-p53 protein-protein interaction inhibitors.	chromenotriazolopyrimidine	56-82	MDM2 proto-oncogene	Homo sapiens	93-97
21389118-6	2011	Next we demonstrate that lysine residues at position 11 and 12 of beta-arrestin2 are required for the interaction between Mdm2 RING finger mutant H457S (Mdm2(H457S)) and beta-arrestin2, mutation of which prevents Mdm2(H457S)/beta-arrestin2 interaction and subsequent nuclear localization of beta-arrestin2.	Lysine	25-31	MDM2 proto-oncogene	Homo sapiens	122-126
21389118-6	2011	Next we demonstrate that lysine residues at position 11 and 12 of beta-arrestin2 are required for the interaction between Mdm2 RING finger mutant H457S (Mdm2(H457S)) and beta-arrestin2, mutation of which prevents Mdm2(H457S)/beta-arrestin2 interaction and subsequent nuclear localization of beta-arrestin2.	Lysine	25-31	MDM2 proto-oncogene	Homo sapiens	153-158
21389118-6	2011	Next we demonstrate that lysine residues at position 11 and 12 of beta-arrestin2 are required for the interaction between Mdm2 RING finger mutant H457S (Mdm2(H457S)) and beta-arrestin2, mutation of which prevents Mdm2(H457S)/beta-arrestin2 interaction and subsequent nuclear localization of beta-arrestin2.	Lysine	25-31	MDM2 proto-oncogene	Homo sapiens	213-218
21623005-1	2011	Earlier we had shown that the MDM2 inhibitor (MI-219) belonging to the spiro-oxindole family can synergistically enhance the efficacy of platinum chemotherapeutics leading to 50% tumor free survival in a genetically complex pancreatic ductaladenocarcinoma (PDAC) xenograft model.	MI-219	46-52	MDM2 proto-oncogene	Homo sapiens	30-34
21623005-1	2011	Earlier we had shown that the MDM2 inhibitor (MI-219) belonging to the spiro-oxindole family can synergistically enhance the efficacy of platinum chemotherapeutics leading to 50% tumor free survival in a genetically complex pancreatic ductaladenocarcinoma (PDAC) xenograft model.	spiro-oxindole	71-85	MDM2 proto-oncogene	Homo sapiens	30-34
21623005-1	2011	Earlier we had shown that the MDM2 inhibitor (MI-219) belonging to the spiro-oxindole family can synergistically enhance the efficacy of platinum chemotherapeutics leading to 50% tumor free survival in a genetically complex pancreatic ductaladenocarcinoma (PDAC) xenograft model.	Platinum	137-145	MDM2 proto-oncogene	Homo sapiens	30-34
19523862-2	2011	MDM2 overexpression has shown to be weakly associated with distant tumor metastases, and down-regulation of MDM2 via antisense oligonucleotides in vitro has resulted in the radiosensitization of prostate cancer cell lines.	Oligonucleotides	127-143	MDM2 proto-oncogene	Homo sapiens	108-112
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	MDM2 proto-oncogene	Homo sapiens	55-59
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	MDM2 proto-oncogene	Homo sapiens	55-59
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	MDM2 proto-oncogene	Homo sapiens	48-52
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	MDM2 proto-oncogene	Homo sapiens	32-36
21504832-4	2011	Herein, we report that SirT1 controls global levels of Suv39h1 by increasing its half-life through inhibition of Suv39h1 lysine 87 polyubiquitination by the E3-ubiquitin ligase MDM2.	Lysine	121-127	MDM2 proto-oncogene	Homo sapiens	177-181
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	MDM2 proto-oncogene	Homo sapiens	180-184
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	MDM2 proto-oncogene	Homo sapiens	18-22
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	18-22
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	MDM2 proto-oncogene	Homo sapiens	64-68
21504625-3	2011	JNJ-26854165 and RO5045337 are 2 small-molecule inhibitors of MDM2 in clinical development.	RG7112	17-26	MDM2 proto-oncogene	Homo sapiens	62-66
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	MDM2 proto-oncogene	Homo sapiens	180-184
21132010-4	2011	We found that GNL3L binds MDM2 in vivo and displays the same function as NS in stabilizing MDM2 protein and preventing its ubiquitylation.	ns	73-75	MDM2 proto-oncogene	Homo sapiens	91-95
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	MDM2 proto-oncogene	Homo sapiens	132-136
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	MDM2 proto-oncogene	Homo sapiens	114-118
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	MDM2 proto-oncogene	Homo sapiens	113-117
21091766-0	2011	Melatonin and vitamin D3 synergistically down-regulate Akt and MDM2 leading to TGFbeta-1-dependent growth inhibition of breast cancer cells.	Melatonin	0-9	MDM2 proto-oncogene	Homo sapiens	63-67
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	MDM2 proto-oncogene	Homo sapiens	156-160
20473904-3	2011	The EBNA-5 binding to MDM2 counteracted destabilizing effect of the latter on the p53.	ebna-5	4-10	MDM2 proto-oncogene	Homo sapiens	22-26
21291561-5	2011	PS also inhibits N-methyl-D-aspartate (NMDA) excitotoxicity by phosphorylating Bad and Mdm2 which blocks the downstream steps in the intrinsic apoptotic cascade.	N-Methylaspartate	17-37	MDM2 proto-oncogene	Homo sapiens	87-91
21291561-5	2011	PS also inhibits N-methyl-D-aspartate (NMDA) excitotoxicity by phosphorylating Bad and Mdm2 which blocks the downstream steps in the intrinsic apoptotic cascade.	N-Methylaspartate	39-43	MDM2 proto-oncogene	Homo sapiens	87-91
21229604-0	2011	Role of the MDM2 SNP309 polymorphism in the initiation and early age of onset of nasopharyngeal carcinoma.	snp309	17-23	MDM2 proto-oncogene	Homo sapiens	12-16
21205074-11	2011	An in vivo antitumor effect of nutlin-3 alone and its additive augmentation by 5-fluorouracil were confirmed in an MDM2 overexpressed xenograft tumor model.	Fluorouracil	79-93	MDM2 proto-oncogene	Homo sapiens	115-119
21091766-7	2011	Taken together, these results indicate that cytostatic effects triggered by melatonin and D3 are likely related to a complex TGFbeta-1-dependent mechanism, involving down-regulation of both MDM2 and Akt-phosphorylation.	Melatonin	76-85	MDM2 proto-oncogene	Homo sapiens	190-194
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	MDM2 proto-oncogene	Homo sapiens	128-132
20876686-7	2011	Despite the absence of internal ribosome entry site activity we demonstrate, using a dual reporter assay, that both the reported mdm2 5"-UTRs confer resistance to rapamycin relative to the 5"-UTR of beta-actin.	Sirolimus	163-172	MDM2 proto-oncogene	Homo sapiens	129-133
20876686-9	2011	Furthermore, extended exposure to rapamycin in the presence of serum increased the steady-state level of the endogenous MDM2 protein.	Sirolimus	34-43	MDM2 proto-oncogene	Homo sapiens	120-124
21091766-0	2011	Melatonin and vitamin D3 synergistically down-regulate Akt and MDM2 leading to TGFbeta-1-dependent growth inhibition of breast cancer cells.	Cholecalciferol	14-24	MDM2 proto-oncogene	Homo sapiens	63-67
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	MDM2 proto-oncogene	Homo sapiens	116-120
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	MDM2 proto-oncogene	Homo sapiens	163-167
21081496-6	2011	Upon agonist stimulation, beta-arrestins-mediated phosphorylation of GRK2 at serine 670 by MAPK facilitates Mdm2-mediated GRK2 degradation, whereas c-Src-dependent phosphorylation would support the action of an undetermined beta-arrestin-recruited ligase in the absence of GPCR activation.	Serine	77-83	MDM2 proto-oncogene	Homo sapiens	108-112
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	MDM2 proto-oncogene	Homo sapiens	100-104
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	MDM2 proto-oncogene	Homo sapiens	100-104
21146529-2	2011	We previously reported that protoporphyrin IX (PpIX) disrupts the p53/murine double minute 2 (MDM2) complex and leads to p53 accumulation and activation of apoptosis in HCT 116 cells.	protoporphyrin IX	28-45	MDM2 proto-oncogene	Homo sapiens	66-92
21146529-2	2011	We previously reported that protoporphyrin IX (PpIX) disrupts the p53/murine double minute 2 (MDM2) complex and leads to p53 accumulation and activation of apoptosis in HCT 116 cells.	protoporphyrin IX	47-51	MDM2 proto-oncogene	Homo sapiens	66-92
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	MDM2 proto-oncogene	Homo sapiens	38-42
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	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	61-65
20812030-5	2011	However, the Mdm2 antagonist Nutlin-3 induced apoptosis in a dose dependent manner by activating caspases-9 and -3.	nutlin 3	29-37	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	116-120
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	MDM2 proto-oncogene	Homo sapiens	116-120
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	MDM2 proto-oncogene	Homo sapiens	164-168
20850924-0	2010	MDM2 antagonist Nutlin-3 enhances bortezomib-mediated mitochondrial apoptosis in TP53-mutated mantle cell lymphoma.	Bortezomib	34-44	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	182-186
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	MDM2 proto-oncogene	Homo sapiens	182-186
20850924-1	2010	This study demonstrated a pronounced synergistic growth-inhibitory effect of an MDM2 inhibitor Nutlin-3 and a proteasome inhibitor bortezomib in mantle cell lymphoma (MCL) cells regardless of TP53 mutant status and innate bortezomib sensitivity.	nutlin	95-101	MDM2 proto-oncogene	Homo sapiens	80-84
21034728-1	2010	Insulin-like growth factor-I and insulin induce the production of phospho-Ser-166 MDM2, a target of Akt, and influence the formation of the MDM2 complex.	Serine	74-77	MDM2 proto-oncogene	Homo sapiens	140-144
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	MDM2 proto-oncogene	Homo sapiens	129-133
21093410-5	2010	MDM2-mediated degradation of p73 was inhibited by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	MDM2 proto-oncogene	Homo sapiens	0-4
20935220-0	2010	Degradation of MDM2 by the interaction between berberine and DAXX leads to potent apoptosis in MDM2-overexpressing cancer cells.	Berberine	47-56	MDM2 proto-oncogene	Homo sapiens	15-19
20935220-0	2010	Degradation of MDM2 by the interaction between berberine and DAXX leads to potent apoptosis in MDM2-overexpressing cancer cells.	Berberine	47-56	MDM2 proto-oncogene	Homo sapiens	95-99
20935220-2	2010	Herein, we demonstrate that berberine induces apoptosis in acute lymphoblastic leukemia (ALL) cells by downregulating the MDM2 oncoprotein.	Berberine	28-37	MDM2 proto-oncogene	Homo sapiens	122-126
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	MDM2 proto-oncogene	Homo sapiens	76-80
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	MDM2 proto-oncogene	Homo sapiens	74-78
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	MDM2 proto-oncogene	Homo sapiens	129-133
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	MDM2 proto-oncogene	Homo sapiens	129-133
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	MDM2 proto-oncogene	Homo sapiens	191-195
20935220-6	2010	We discovered that downregulation of MDM2 in ALL cells by berberine occurred at a posttranslational level through modulation of death domain-associated protein (DAXX), which disrupted the MDM2-DAXX-HAUSP interactions and thereby promoted MDM2 self-ubiquitination and degradation.	Berberine	58-67	MDM2 proto-oncogene	Homo sapiens	37-41
20935220-6	2010	We discovered that downregulation of MDM2 in ALL cells by berberine occurred at a posttranslational level through modulation of death domain-associated protein (DAXX), which disrupted the MDM2-DAXX-HAUSP interactions and thereby promoted MDM2 self-ubiquitination and degradation.	Berberine	58-67	MDM2 proto-oncogene	Homo sapiens	188-192
20935220-6	2010	We discovered that downregulation of MDM2 in ALL cells by berberine occurred at a posttranslational level through modulation of death domain-associated protein (DAXX), which disrupted the MDM2-DAXX-HAUSP interactions and thereby promoted MDM2 self-ubiquitination and degradation.	Berberine	58-67	MDM2 proto-oncogene	Homo sapiens	188-192
21034728-1	2010	Insulin-like growth factor-I and insulin induce the production of phospho-Ser-166 MDM2, a target of Akt, and influence the formation of the MDM2 complex.	Serine	74-77	MDM2 proto-oncogene	Homo sapiens	82-86
21034728-9	2010	This low concentration of wortmannin completely blocked the induction of phospho-MDM2 by rewarming.	Wortmannin	26-36	MDM2 proto-oncogene	Homo sapiens	81-85
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	MDM2 proto-oncogene	Homo sapiens	111-115
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	MDM2 proto-oncogene	Homo sapiens	111-115
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	90-92	MDM2 proto-oncogene	Homo sapiens	111-115
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	90-92	MDM2 proto-oncogene	Homo sapiens	111-115
20962272-4	2010	Phosphorylation at Thr18 functions as an on/off switch to regulate binding to the N-terminal domain of HDM2.	UNII-PYZ33YLR8A	19-24	MDM2 proto-oncogene	Homo sapiens	103-107
20956468-0	2010	Molecular imaging of MDM2 messenger RNA with 99mTc-labeled antisense oligonucleotides in experimental human breast cancer xenografts.	Oligonucleotides	69-85	MDM2 proto-oncogene	Homo sapiens	21-25
20956468-3	2010	The overall aim of this study was to evaluate whether liposome-coated (99m)Tc-radiolabeled antisense oligonucleotides (ASONs) targeting MDM2 messenger RNA (mRNA) could be used for imaging of MDM2 expression in vivo.	Technetium	75-77	MDM2 proto-oncogene	Homo sapiens	136-140
20956468-3	2010	The overall aim of this study was to evaluate whether liposome-coated (99m)Tc-radiolabeled antisense oligonucleotides (ASONs) targeting MDM2 messenger RNA (mRNA) could be used for imaging of MDM2 expression in vivo.	Technetium	75-77	MDM2 proto-oncogene	Homo sapiens	191-195
20956468-3	2010	The overall aim of this study was to evaluate whether liposome-coated (99m)Tc-radiolabeled antisense oligonucleotides (ASONs) targeting MDM2 messenger RNA (mRNA) could be used for imaging of MDM2 expression in vivo.	Oligonucleotides	101-117	MDM2 proto-oncogene	Homo sapiens	136-140
20956468-3	2010	The overall aim of this study was to evaluate whether liposome-coated (99m)Tc-radiolabeled antisense oligonucleotides (ASONs) targeting MDM2 messenger RNA (mRNA) could be used for imaging of MDM2 expression in vivo.	Oligonucleotides	101-117	MDM2 proto-oncogene	Homo sapiens	191-195
20956468-4	2010	METHODS: ASON and mismatch oligonucleotide (ASONM) targeted to MDM2 mRNA were synthesized and radiolabeled with (99m)Tc using the bifunctional chelator hydrazinonicotinamide (HYNIC).	Oligonucleotides	27-42	MDM2 proto-oncogene	Homo sapiens	63-67
20956468-4	2010	METHODS: ASON and mismatch oligonucleotide (ASONM) targeted to MDM2 mRNA were synthesized and radiolabeled with (99m)Tc using the bifunctional chelator hydrazinonicotinamide (HYNIC).	asonm	44-49	MDM2 proto-oncogene	Homo sapiens	63-67
20956468-16	2010	The antisense imaging with liposome-coated (99m)Tc-HYNIC-ASON may be a promising method for visualization of MDM2 expression in human breast cancer.	tc-hynic-ason	48-61	MDM2 proto-oncogene	Homo sapiens	109-113
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	MDM2 proto-oncogene	Homo sapiens	55-59
20594980-8	2010	Moreover, LPA induced increased mdm2 phosphorylation, a negative regulator of p53.	lysophosphatidic acid	10-13	MDM2 proto-oncogene	Homo sapiens	32-36
20619429-7	2010	Moreover, MDM2 knockdown decreased the sensitivity of N-MLV infection to treatment with MG132 and As(2)O(3), two known TRIM5alpha pharmacological inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	MDM2 proto-oncogene	Homo sapiens	10-14
21051655-3	2010	The minor allele of MDM2 that includes a 309T&gt;G transversion (single-nucleotide polymorphism rs2279744) in the MDM2 promoter is known to enhance MDM2 expression.	single-nucleotide	65-82	MDM2 proto-oncogene	Homo sapiens	20-24
21051655-3	2010	The minor allele of MDM2 that includes a 309T&gt;G transversion (single-nucleotide polymorphism rs2279744) in the MDM2 promoter is known to enhance MDM2 expression.	single-nucleotide	65-82	MDM2 proto-oncogene	Homo sapiens	114-118
21051655-3	2010	The minor allele of MDM2 that includes a 309T&gt;G transversion (single-nucleotide polymorphism rs2279744) in the MDM2 promoter is known to enhance MDM2 expression.	single-nucleotide	65-82	MDM2 proto-oncogene	Homo sapiens	114-118
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	MDM2 proto-oncogene	Homo sapiens	82-86
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	MDM2 proto-oncogene	Homo sapiens	82-86
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	MDM2 proto-oncogene	Homo sapiens	65-69
21041384-8	2010	This review highlights the significance of the network and systems biology-based strategy and presents a proof of concept recently validated in our laboratory using the example of a combination treatment of oxaliplatin and the MDM2 inhibitor MI-219 in genetically complex and incurable pancreatic adenocarcinoma.	MI-219	242-248	MDM2 proto-oncogene	Homo sapiens	227-231
20840854-5	2010	This treatment also resulted in the attenuation of BP-induced Mdm2 phosphorylation at Ser166 and amplification of the p53 Ser15 response.	Benzo(a)pyrene	51-53	MDM2 proto-oncogene	Homo sapiens	62-66
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	MDM2 proto-oncogene	Homo sapiens	174-178
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	MDM2 proto-oncogene	Homo sapiens	324-328
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	MDM2 proto-oncogene	Homo sapiens	174-178
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	MDM2 proto-oncogene	Homo sapiens	324-328
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	MDM2 proto-oncogene	Homo sapiens	174-178
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	MDM2 proto-oncogene	Homo sapiens	324-328
20878097-7	2010	In addition, treatment by resveratrol also resulted in attenuated expression of bcl-xl, fibronectin-1, HIP, mdm2, PIG3 and WSB1/SWIP-1 in HAECs, and CDX1, engrailed homolog 1, FASN, fibronectin-1, forkhead box A2, Hoxa-1, hsp27, PIG3, ELAM-1/E-selectin and WSB1/SWIP-1 in HPAECs.	Resveratrol	26-37	MDM2 proto-oncogene	Homo sapiens	108-112
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	MDM2 proto-oncogene	Homo sapiens	75-80
20671028-2	2010	In addition to E3 ubiquitin ligase activity, the Mdm2 RING preferentially binds adenine base nucleotides, and such binding leads to a conformational change in the Mdm2 C-terminus.	adenine base nucleotides	80-104	MDM2 proto-oncogene	Homo sapiens	49-53
20671028-2	2010	In addition to E3 ubiquitin ligase activity, the Mdm2 RING preferentially binds adenine base nucleotides, and such binding leads to a conformational change in the Mdm2 C-terminus.	adenine base nucleotides	80-104	MDM2 proto-oncogene	Homo sapiens	163-167
20671028-4	2010	We have found that MdmX, an Mdm2 family member with high sequence homology, binds adenine nucleotides with similar affinity and specificity as Mdm2, suggesting that residues involved in nucleotide binding may be conserved between the two proteins and adenosine triphosphate (ATP) binding may have similar functional consequences for both Mdm family members.	Adenine Nucleotides	82-101	MDM2 proto-oncogene	Homo sapiens	28-32
20671028-5	2010	By generating and testing a series of proteins with deletions and substitution mutations within the Mdm2 RING, we mapped the specific adenine nucleotide binding region of Mdm2 to residues 429-484, encompassing the minimal RING domain.	Adenine Nucleotides	134-152	MDM2 proto-oncogene	Homo sapiens	100-104
20671028-5	2010	By generating and testing a series of proteins with deletions and substitution mutations within the Mdm2 RING, we mapped the specific adenine nucleotide binding region of Mdm2 to residues 429-484, encompassing the minimal RING domain.	Adenine Nucleotides	134-152	MDM2 proto-oncogene	Homo sapiens	171-175
20671028-6	2010	Using a series of ATP derivatives, we demonstrate that phosphate coordination by the Mdm2 P-loop contributes to, but is not primarily responsible for, ATP binding.	Adenosine Triphosphate	18-21	MDM2 proto-oncogene	Homo sapiens	85-89
20671028-6	2010	Using a series of ATP derivatives, we demonstrate that phosphate coordination by the Mdm2 P-loop contributes to, but is not primarily responsible for, ATP binding.	Phosphates	55-64	MDM2 proto-oncogene	Homo sapiens	85-89
20671028-6	2010	Using a series of ATP derivatives, we demonstrate that phosphate coordination by the Mdm2 P-loop contributes to, but is not primarily responsible for, ATP binding.	Adenosine Triphosphate	151-154	MDM2 proto-oncogene	Homo sapiens	85-89
20821791-0	2010	High specificity in protein recognition by hydrogen-bond-surrogate alpha-helices: selective inhibition of the p53/MDM2 complex.	Hydrogen	43-51	MDM2 proto-oncogene	Homo sapiens	114-118
20472715-0	2010	HDMX regulates p53 activity and confers chemoresistance to 3-bis(2-chloroethyl)-1-nitrosourea.	3-bis(2-chloroethyl)-1-nitrosourea	59-93	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	104-108
20447891-5	2010	METHODS: MDM2 SNP309 polymorphism was investigated in 110 confirmed subjects with HCC and 110 cancer-free control subjects matched on age, gender, smoking and alcohol consumption by using a polymerase chain reaction-restriction fragment length polymorphism assay.	Alcohols	159-166	MDM2 proto-oncogene	Homo sapiens	9-13
20591651-3	2010	HDM2 plays an important role in the expression of Noxa, a pro-apoptotic molecule of the Bcl-2 family, which induces NB cell apoptotic death after doxorubcin (Doxo) treatment.	doxorubcin	146-156	MDM2 proto-oncogene	Homo sapiens	0-4
20591651-3	2010	HDM2 plays an important role in the expression of Noxa, a pro-apoptotic molecule of the Bcl-2 family, which induces NB cell apoptotic death after doxorubcin (Doxo) treatment.	Desoxycorticosterone Acetate	158-162	MDM2 proto-oncogene	Homo sapiens	0-4
20591651-4	2010	Knockdown of HDM2 by siRNA resulted in the upregulation of Noxa at mRNA/protein levels and improved the sensitivity of Doxo-resistant NB cells, although these were not observed in p53-mutant NB cells.	Desoxycorticosterone Acetate	119-123	MDM2 proto-oncogene	Homo sapiens	13-17
20591651-5	2010	Noxa-knockdown abolished the recovered Doxo-induced cell death by HDM2 reduction.	Desoxycorticosterone Acetate	39-43	MDM2 proto-oncogene	Homo sapiens	66-70
20591651-6	2010	Intriguingly, resistance to Doxo was up-regulated by over-expression of HDM2 in Doxo-sensitive NB cells.	Desoxycorticosterone Acetate	28-32	MDM2 proto-oncogene	Homo sapiens	72-76
20591651-6	2010	Intriguingly, resistance to Doxo was up-regulated by over-expression of HDM2 in Doxo-sensitive NB cells.	Desoxycorticosterone Acetate	80-84	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	77-81
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	MDM2 proto-oncogene	Homo sapiens	63-67
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	MDM2 proto-oncogene	Homo sapiens	114-118
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	MDM2 proto-oncogene	Homo sapiens	200-204
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	MDM2 proto-oncogene	Homo sapiens	200-204
20422343-9	2010	Nutlin-3 induces apoptosis and potentiates the cytotoxic effect of gemcitabine through disrupting the binding of p73 with MDM2.	gemcitabine	67-78	MDM2 proto-oncogene	Homo sapiens	122-126
20422343-13	2010	Nutlin-3 acts through the inhibition of p73-MDM2 with subsequent activation of the apoptotic pathway signaling, which leads to the increase in chemosensitivity to gemcitabine.	gemcitabine	163-174	MDM2 proto-oncogene	Homo sapiens	44-48
20540933-10	2010	We also found that hispolon induced increased association of Hsp70, Hsc70, Hsp90 and LAMP2A with MDM2.	hispolon	19-27	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	171-175
20540933-12	2010	GA also attenuated hispolon-induced MDM2 downregulation.	geldanamycin	0-2	MDM2 proto-oncogene	Homo sapiens	36-40
20540933-13	2010	Meanwhile, inhibition of Hsc70 using siRNA attenuated hispolon-induced MDM2 downregulation.	hispolon	54-62	MDM2 proto-oncogene	Homo sapiens	71-75
20453884-8	2010	An hTERT mutant with all five lysine residues at the N-terminus of hTERT that mutated to arginine became resistant to Hdm2-mediated ubiquitination and degradation.	Lysine	30-36	MDM2 proto-oncogene	Homo sapiens	118-122
20571051-8	2010	Furthermore, we show that MDM2 or Fbw7 depletion inhibits degradation of endogenous DeltaNp63alpha in cells exposed to UV irradiation, adriamycin and upon keratinocyte differentiation.	Doxorubicin	135-145	MDM2 proto-oncogene	Homo sapiens	26-30
20453884-8	2010	An hTERT mutant with all five lysine residues at the N-terminus of hTERT that mutated to arginine became resistant to Hdm2-mediated ubiquitination and degradation.	Arginine	89-97	MDM2 proto-oncogene	Homo sapiens	118-122
20375080-5	2010	In arsenite-exposed cells, the levels of phospho-p53, p21, and mdm2 increase at early times after exposure.	arsenite	3-11	MDM2 proto-oncogene	Homo sapiens	63-67
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	MDM2 proto-oncogene	Homo sapiens	71-75
20591158-0	2010	Modulation of mdm2 pre-mRNA splicing by 9-aminoacridine-PNA (peptide nucleic acid) conjugates targeting intron-exon junctions.	9-aminoacridine-pna	40-59	MDM2 proto-oncogene	Homo sapiens	14-18
20591158-2	2010	In this study, we have examined the potential of peptide nucleic acid (PNA) 9-aminoacridine conjugates to modulate the pre-mRNA splicing of the mdm2 human cancer gene in JAR cells.	Aminacrine	76-91	MDM2 proto-oncogene	Homo sapiens	144-148
20331637-7	2010	Mithramycin temporally decreased transcription of both the mdm2-P1 and -P2 promoters.	Plicamycin	0-11	MDM2 proto-oncogene	Homo sapiens	59-74
19711344-11	2010	Bleomycin-induced upregulation of BCL-XL/BCLXL1 and MDM2 suggests that it is the ratio of proapoptotic and antiapoptotic proteins that regulates the apoptosis response of HCC cells toward chemotherapy, thereby playing a decisive role between treatment sensitivity vs. drug resistance.	Bleomycin	0-9	MDM2 proto-oncogene	Homo sapiens	52-56
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	MDM2 proto-oncogene	Homo sapiens	131-135
20418664-0	2010	MDM2 antagonist nutlin plus proteasome inhibitor velcade combination displays a synergistic anti-myeloma activity.	Bortezomib	49-56	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	60-64
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	MDM2 proto-oncogene	Homo sapiens	58-62
20019189-0	2010	Iron-dependent regulation of MDM2 influences p53 activity and hepatic carcinogenesis.	Iron	0-4	MDM2 proto-oncogene	Homo sapiens	29-33
20080970-9	2010	The effect of SJ-172550 is additive when combined with an MDM2 inhibitor.	SJ 172550	14-23	MDM2 proto-oncogene	Homo sapiens	58-62
20124408-8	2010	In addition to reactivating mutant p53, SCH529074 binding inhibits ubiquitination of p53 by HDM2.	SCH 529074	40-49	MDM2 proto-oncogene	Homo sapiens	92-96
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	MDM2 proto-oncogene	Homo sapiens	138-142
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	MDM2 proto-oncogene	Homo sapiens	41-45
20156675-0	2010	MDM2 inhibitor MI-319 in combination with cisplatin is an effective treatment for pancreatic cancer independent of p53 function.	MI 319	15-21	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	211-215
20215498-3	2010	Simultaneous blockade of MEK and MDM2 signaling by AZD6244 and Nutlin-3a triggered synergistic proapoptotic responses in AML cell lines [combination index (CI) = 0.06 +/- 0.03 and 0.43 +/- 0.03 in OCI/AML3 and MOLM13 cells, respectively] and in primary AML cells (CI = 0.52 +/- 0.01).	AZD 6244	51-58	MDM2 proto-oncogene	Homo sapiens	33-37
20215498-3	2010	Simultaneous blockade of MEK and MDM2 signaling by AZD6244 and Nutlin-3a triggered synergistic proapoptotic responses in AML cell lines [combination index (CI) = 0.06 +/- 0.03 and 0.43 +/- 0.03 in OCI/AML3 and MOLM13 cells, respectively] and in primary AML cells (CI = 0.52 +/- 0.01).	nutlin 3	63-72	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	120-124
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	MDM2 proto-oncogene	Homo sapiens	270-274
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	MDM2 proto-oncogene	Homo sapiens	110-115
19788889-0	2010	DNA damage response to the Mdm2 inhibitor nutlin-3.	nutlin 3	42-50	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	161-165
20237429-2	2010	We present here the structures of the most potent inhibitors bound to MDM2 and MDMX that are based on the new imidazo-indole scaffold.	imidazo-indole	110-124	MDM2 proto-oncogene	Homo sapiens	70-74
20237429-3	2010	In addition, the structure of the recently reported spiro-oxindole inhibitor bound to MDM2 is described.	spiro-oxindole	52-66	MDM2 proto-oncogene	Homo sapiens	86-90
20237429-5	2010	While the spiro-oxindole inhibitor triggers significant ligand-induced changes in MDM2, the imidazo-indoles share similar binding modes for MDMX and MDM2, but cause only minimal induced-fit changes in the structures of both proteins.	spiro-oxindole	10-24	MDM2 proto-oncogene	Homo sapiens	82-86
20237429-5	2010	While the spiro-oxindole inhibitor triggers significant ligand-induced changes in MDM2, the imidazo-indoles share similar binding modes for MDMX and MDM2, but cause only minimal induced-fit changes in the structures of both proteins.	imidazo-indoles	92-107	MDM2 proto-oncogene	Homo sapiens	149-153
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	MDM2 proto-oncogene	Homo sapiens	151-155
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	MDM2 proto-oncogene	Homo sapiens	151-155
19954744-4	2010	MDM2 SNP309 is also associated with HCC.	snp309	5-11	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	29-33
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	MDM2 proto-oncogene	Homo sapiens	29-33
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	4-8
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	MDM2 proto-oncogene	Homo sapiens	67-71
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	MDM2 proto-oncogene	Homo sapiens	67-71
20019189-8	2010	In conclusion, iron status influences p53 activity and antioxidant response by modulating MDM2 expression.	Iron	15-19	MDM2 proto-oncogene	Homo sapiens	90-94
20019189-9	2010	MDM2 inhibitors may enhance the antiproliferative activity of iron chelators.	Iron	62-66	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	104-108
19927155-8	2010	The same lysines are also targets of MDM2-mediated ubiquitination.	Lysine	9-16	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	129-133
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	MDM2 proto-oncogene	Homo sapiens	104-108
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	MDM2 proto-oncogene	Homo sapiens	129-133
19918798-8	2010	PTX/LPC treatment induced a weakness of Akt-MDM2-p53 complex and increased nuclear p53 levels.	Paclitaxel	0-3	MDM2 proto-oncogene	Homo sapiens	44-48
19918798-8	2010	PTX/LPC treatment induced a weakness of Akt-MDM2-p53 complex and increased nuclear p53 levels.	beta-lapachone	4-7	MDM2 proto-oncogene	Homo sapiens	44-48
20043868-4	2010	Interestingly, the simvastatin-induced apoptosis was accompanied by p53 stabilization involving Mdm2 degradation.	Simvastatin	19-30	MDM2 proto-oncogene	Homo sapiens	96-100
20080757-7	2010	We also show that 53BP1-deficient CH12F3-2 cells are protected from apoptosis mediated by the MDM2 inhibitor Nutlin-3.	nutlin 3	109-117	MDM2 proto-oncogene	Homo sapiens	94-98
19897582-4	2010	This is supported by data showing that inhibition of both MDM2 and XIAP by their respective ASOs induced significantly more cell death than either ASO alone.	Oligonucleotides, Antisense	92-95	MDM2 proto-oncogene	Homo sapiens	58-62
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	MDM2 proto-oncogene	Homo sapiens	105-109
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	MDM2 proto-oncogene	Homo sapiens	180-185
19946262-4	2010	We investigated the interaction of FLT3 and p53 pathways after their simultaneous blockade using the selective FLT3 inhibitor FI-700 and the MDM2 inhibitor Nutlin-3 in AML.	nutlin 3	156-164	MDM2 proto-oncogene	Homo sapiens	141-145
19752772-4	2010	RESULTS: Interestingly, the G-allele of MDM2 SNP309 is shown to associate with a 9-year earlier age of PDAC onset (P = 0.021).	pdac	103-107	MDM2 proto-oncogene	Homo sapiens	40-44
19934289-9	2009	Concurrent Hdm2 inhibition with bortezomib may extend the spectrum of bortezomib applications to malignancies with currently limited sensitivity to single-agent bortezomib or, in the future, to MM patients with decreased clinical responsiveness to bortezomib-based therapy.	Bortezomib	70-80	MDM2 proto-oncogene	Homo sapiens	11-15
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	MDM2 proto-oncogene	Homo sapiens	35-39
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	MDM2 proto-oncogene	Homo sapiens	43-47
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	MDM2 proto-oncogene	Homo sapiens	9-13
19751709-0	2009	Non-dioxin-like-PCBs phosphorylate Mdm2 at Ser166 and attenuate the p53 response in HepG2 cells.	Dioxins	4-10	MDM2 proto-oncogene	Homo sapiens	35-39
19751709-0	2009	Non-dioxin-like-PCBs phosphorylate Mdm2 at Ser166 and attenuate the p53 response in HepG2 cells.	Polychlorinated Biphenyls	15-20	MDM2 proto-oncogene	Homo sapiens	35-39
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	MDM2 proto-oncogene	Homo sapiens	3-7
19958544-1	2009	BACKGROUND: MI-319 is a synthetic small molecule designed to target the MDM2-P53 interaction.	MI 319	12-18	MDM2 proto-oncogene	Homo sapiens	72-76
19958544-2	2009	It is closely related to MDM2 antagonists MI-219 and Nutlin-3 in terms of the expected working mechanisms.	MI-219	42-48	MDM2 proto-oncogene	Homo sapiens	25-29
19958544-5	2009	RESULTS: MI-319 was shown to bind to MDM2 protein with an affinity slightly higher than that of MI-219 and Nutlin-3.	2-methyl-4-isothiazolin-3-one	9-11	MDM2 proto-oncogene	Homo sapiens	37-41
19920202-3	2009	Primary CCRCC specimens exhibiting strong hypoxic signatures show increased levels of activated nuclear phospho-Hdm2(Ser(166)), which is concomitant with low p53 expression.	Serine	117-120	MDM2 proto-oncogene	Homo sapiens	112-116
19934289-0	2009	Interactions of the Hdm2/p53 and proteasome pathways may enhance the antitumor activity of bortezomib.	Bortezomib	91-101	MDM2 proto-oncogene	Homo sapiens	20-24
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	MDM2 proto-oncogene	Homo sapiens	49-53
19934289-9	2009	Concurrent Hdm2 inhibition with bortezomib may extend the spectrum of bortezomib applications to malignancies with currently limited sensitivity to single-agent bortezomib or, in the future, to MM patients with decreased clinical responsiveness to bortezomib-based therapy.	Bortezomib	70-80	MDM2 proto-oncogene	Homo sapiens	11-15
19934289-9	2009	Concurrent Hdm2 inhibition with bortezomib may extend the spectrum of bortezomib applications to malignancies with currently limited sensitivity to single-agent bortezomib or, in the future, to MM patients with decreased clinical responsiveness to bortezomib-based therapy.	Bortezomib	70-80	MDM2 proto-oncogene	Homo sapiens	11-15
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	MDM2 proto-oncogene	Homo sapiens	122-126
19880322-0	2009	N-acylpolyamine inhibitors of HDM2 and HDMX binding to p53.	n-acylpolyamine	0-15	MDM2 proto-oncogene	Homo sapiens	30-34
19880322-0	2009	N-acylpolyamine inhibitors of HDM2 and HDMX binding to p53.	n-acylpolyamine	0-15	MDM2 proto-oncogene	Homo sapiens	39-43
19824037-0	2009	Convergent solid-phase and solution approaches in the synthesis of the cysteine-rich Mdm2 RING finger domain.	Cysteine	71-79	MDM2 proto-oncogene	Homo sapiens	85-89
19946100-5	2009	METHODS: IHC for MDM2/CDK4 was carried out on a series of 129 paraffin-embedded lipomatous and non-lipomatous soft tissue tumours.	Paraffin	62-70	MDM2 proto-oncogene	Homo sapiens	17-21
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	MDM2 proto-oncogene	Homo sapiens	142-146
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	MDM2 proto-oncogene	Homo sapiens	174-178
19428175-0	2009	Gambogic acid down-regulates MDM2 oncogene and induces p21(Waf1/CIP1) expression independent of p53.	gambogic acid	0-13	MDM2 proto-oncogene	Homo sapiens	29-33
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	MDM2 proto-oncogene	Homo sapiens	52-56
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	MDM2 proto-oncogene	Homo sapiens	181-185
19732750-3	2009	A chromatin immunoprecipitation assay showed that Jmjd2c was recruited to the P2 promoter region of Mdm2 gene resulting in demethylation of histone H3 lysine 9, as typically found in actively transcribed genes.	Lysine	151-157	MDM2 proto-oncogene	Homo sapiens	100-104
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	MDM2 proto-oncogene	Homo sapiens	217-221
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	MDM2 proto-oncogene	Homo sapiens	223-227
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	MDM2 proto-oncogene	Homo sapiens	223-227
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	43-47
19855165-0	2009	Cellular quiescence caused by the Mdm2 inhibitor nutlin-3A.	nutlin 3	49-58	MDM2 proto-oncogene	Homo sapiens	34-38
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	MDM2 proto-oncogene	Homo sapiens	215-219
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	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	80-84
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	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	158-162
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	MDM2 proto-oncogene	Homo sapiens	132-136
19581590-7	2009	Here, we show that shorter-tailed Ubs, such as UBB(+1), bind to the proteasome but because they cannot be efficiently degraded, they inhibit the degradation of other Ub system"s substrates such as Myc, p21, Mdm2, and MyoD.	N-[(S)-({[(Benzyloxy)carbonyl]amino}methyl)(Hydroxy)phosphoryl]-L-Leucyl-L-Valine	34-37	MDM2 proto-oncogene	Homo sapiens	207-211
19596022-0	2009	Association of genetic polymorphisms in GADD45A, MDM2, and p14 ARF with the risk of chronic benzene poisoning in a Chinese occupational population.	Benzene	92-99	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	128-133
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	MDM2 proto-oncogene	Homo sapiens	128-133
20157557-0	2009	Reduced transcriptional activity in the p53 pathway of senescent cells revealed by the MDM2 antagonist nutlin-3.	nutlin 3	103-111	MDM2 proto-oncogene	Homo sapiens	87-91
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	MDM2 proto-oncogene	Homo sapiens	95-99
19455066-0	2009	Germline analysis of thymidine/guanidine polymorphism at position 309 of the Mdm2 promoter in malignant melanoma patients.	Thymidine	21-30	MDM2 proto-oncogene	Homo sapiens	77-81
19455066-0	2009	Germline analysis of thymidine/guanidine polymorphism at position 309 of the Mdm2 promoter in malignant melanoma patients.	Guanidine	31-40	MDM2 proto-oncogene	Homo sapiens	77-81
19455066-4	2009	We speculated that guanine at position 309 (G309) of the Mdm2 promoter might be a cause of Mdm2 overexpression in MM patients, and associated with increased risk of MM.	Guanine	19-26	MDM2 proto-oncogene	Homo sapiens	57-61
19455066-4	2009	We speculated that guanine at position 309 (G309) of the Mdm2 promoter might be a cause of Mdm2 overexpression in MM patients, and associated with increased risk of MM.	Guanine	19-26	MDM2 proto-oncogene	Homo sapiens	91-95
19455066-7	2009	The relevant DNA stretch was sequenced and thymidine/guanidine polymorphism at position 309 of Mdm2 promoter was examined.	Thymidine	43-52	MDM2 proto-oncogene	Homo sapiens	95-99
19455066-7	2009	The relevant DNA stretch was sequenced and thymidine/guanidine polymorphism at position 309 of Mdm2 promoter was examined.	Guanidine	53-62	MDM2 proto-oncogene	Homo sapiens	95-99
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	MDM2 proto-oncogene	Homo sapiens	109-113
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	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	45-49
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	MDM2 proto-oncogene	Homo sapiens	220-224
19548636-4	2009	Arrays of amides were synthesized with improved hydrophilicity and retainment and/or improvement of p53/mdm2 inhibitory activity.	Amides	10-16	MDM2 proto-oncogene	Homo sapiens	104-108
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	MDM2 proto-oncogene	Homo sapiens	117-121
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	MDM2 proto-oncogene	Homo sapiens	100-104
19414261-0	2009	Stereochemical studies of hexylitaconic acid, an inhibitor of p53-HDM2 interaction.	2-methylene-3-hexylbutanedioic acid	26-44	MDM2 proto-oncogene	Homo sapiens	66-70
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	MDM2 proto-oncogene	Homo sapiens	114-118
19509161-10	2009	The effect of nutlin-3 was almost the same in terms of half maximal inhibitory concentration and apoptosis whether or not MDM2 was overexpressed.	nutlin 3	14-22	MDM2 proto-oncogene	Homo sapiens	122-126
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	MDM2 proto-oncogene	Homo sapiens	181-185
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	137-141
18804411-0	2009	MDM2 SNP309 does not confer an increased risk to oral squamous cell carcinoma but may modulate the age of disease onset.	snp309	5-11	MDM2 proto-oncogene	Homo sapiens	0-4
19408261-10	2009	The calculations reveal that significant stabilizing van der Waals interactions and polarization effects occur between the Trp side chain in each ligand and aromatic and aliphatic residues in HDM2.	Tryptophan	123-126	MDM2 proto-oncogene	Homo sapiens	192-196
19408261-12	2009	In addition, the calculations suggest that at least one stabilizing hydrogen bond is formed, between the Trp indole-NH in both ligands and HDM2.	Hydrogen	68-76	MDM2 proto-oncogene	Homo sapiens	139-143
19408261-12	2009	In addition, the calculations suggest that at least one stabilizing hydrogen bond is formed, between the Trp indole-NH in both ligands and HDM2.	trp indole-nh	105-118	MDM2 proto-oncogene	Homo sapiens	139-143
19363523-8	2009	Binding of Mdm2 to TAD was reduced significantly only on phosphorylation of Thr18 (sevenfold) or by hepta-phosphorylation (24-fold).	UNII-PYZ33YLR8A	76-81	MDM2 proto-oncogene	Homo sapiens	11-15
19363523-8	2009	Binding of Mdm2 to TAD was reduced significantly only on phosphorylation of Thr18 (sevenfold) or by hepta-phosphorylation (24-fold).	Heptachlor	100-105	MDM2 proto-oncogene	Homo sapiens	11-15
19408261-13	2009	Other hydrogen-bonding interactions also arise, however, along the alpha-helical backbone of the linear peptide upon binding to HDM2, but are not mimicked in the constrained inhibitor-HDM2 complex.	Hydrogen	6-14	MDM2 proto-oncogene	Homo sapiens	128-132
19408261-14	2009	The formation of these hydrogen bonds upon helix folding could contribute significantly to the enhanced enthalpy observed in binding of the linear peptide to HDM2.	Hydrogen	23-31	MDM2 proto-oncogene	Homo sapiens	158-162
19360352-0	2009	The MDM2 antagonist nutlin-3 sensitizes p53-null neuroblastoma cells to doxorubicin via E2F1 and TAp73.	Doxorubicin	72-83	MDM2 proto-oncogene	Homo sapiens	4-8
19441944-0	2009	MDM2/MDMX inhibitor peptide: WO2008106507.	wo2008106507	29-41	MDM2 proto-oncogene	Homo sapiens	0-4
19188367-3	2009	The domain structure includes: (i) a hydrophobic pocket at the N terminus of MDM2 that is involved in both its transrepressor and E3-ubiqutin ligase functions, (ii) a central acid domain that recognizes a ubiquitination signal in the core DNA binding domain of p53, and (iii) a C-terminal C2H2C4 RING finger domain that is required for E2 enzyme-binding and ATP-dependent molecular chaperone activity.	Adenosine Triphosphate	358-361	MDM2 proto-oncogene	Homo sapiens	77-81
19318567-0	2009	Depletion of guanine nucleotides leads to the Mdm2-dependent proteasomal degradation of nucleostemin.	Guanine Nucleotides	13-32	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	80-84
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	MDM2 proto-oncogene	Homo sapiens	133-137
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	MDM2 proto-oncogene	Homo sapiens	89-93
19153082-4	2009	We have determined the crystal structures at 1.3 A of the N-terminal domain of HdmX bound to two p53 peptidomimetics without and with a 6-chlorine substituent on the indole (which binds in the same subpocket as Trp(23) of p53).	6-chlorine	136-146	MDM2 proto-oncogene	Homo sapiens	79-83
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	MDM2 proto-oncogene	Homo sapiens	29-33
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	MDM2 proto-oncogene	Homo sapiens	35-39
19153082-6	2009	The x-ray structures revealed surprising conformational changes of the binding cleft of HdmX, including an "open conformation" of Tyr(99) and unexpected "cross-talk" between the Trp and Leu pockets.	Tyrosine	130-133	MDM2 proto-oncogene	Homo sapiens	88-92
19153082-6	2009	The x-ray structures revealed surprising conformational changes of the binding cleft of HdmX, including an "open conformation" of Tyr(99) and unexpected "cross-talk" between the Trp and Leu pockets.	Tryptophan	178-181	MDM2 proto-oncogene	Homo sapiens	88-92
19153082-4	2009	We have determined the crystal structures at 1.3 A of the N-terminal domain of HdmX bound to two p53 peptidomimetics without and with a 6-chlorine substituent on the indole (which binds in the same subpocket as Trp(23) of p53).	indole	166-172	MDM2 proto-oncogene	Homo sapiens	79-83
19153082-6	2009	The x-ray structures revealed surprising conformational changes of the binding cleft of HdmX, including an "open conformation" of Tyr(99) and unexpected "cross-talk" between the Trp and Leu pockets.	Leucine	186-189	MDM2 proto-oncogene	Homo sapiens	88-92
19153082-4	2009	We have determined the crystal structures at 1.3 A of the N-terminal domain of HdmX bound to two p53 peptidomimetics without and with a 6-chlorine substituent on the indole (which binds in the same subpocket as Trp(23) of p53).	Tryptophan	211-214	MDM2 proto-oncogene	Homo sapiens	79-83
19323829-4	2009	EBNA-5 associates with p53-hMDM2-p14ARF complexes.	N-tert-Butyl-N-ethylnitrosamine	0-4	MDM2 proto-oncogene	Homo sapiens	27-32
18814047-9	2009	For SCC, the trend of increased risk across the three genotypes of MDM2 was stronger among p53 Pro carriers (p, trend, 0.05) than p53 Arg/Arg wild-type group (p, trend, 0.99; p, interaction, 0.07).	Arginine	134-137	MDM2 proto-oncogene	Homo sapiens	67-71
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	MDM2 proto-oncogene	Homo sapiens	73-77
18814047-9	2009	For SCC, the trend of increased risk across the three genotypes of MDM2 was stronger among p53 Pro carriers (p, trend, 0.05) than p53 Arg/Arg wild-type group (p, trend, 0.99; p, interaction, 0.07).	Arginine	138-141	MDM2 proto-oncogene	Homo sapiens	67-71
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	MDM2 proto-oncogene	Homo sapiens	44-48
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	MDM2 proto-oncogene	Homo sapiens	207-211
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	MDM2 proto-oncogene	Homo sapiens	207-211
19075013-9	2009	One of these phosphorylations, on tyrosine 99, inhibited Hdmx interaction with p53.	Tyrosine	34-42	MDM2 proto-oncogene	Homo sapiens	57-61
19091570-7	2009	There was stable down-regulation of MDM2 and UGB as well as overexpression of SOD2, CSTB, and G3BP when RA-treated SHG-44 was compared with normal SHG-44.	Tretinoin	104-106	MDM2 proto-oncogene	Homo sapiens	36-40
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	MDM2 proto-oncogene	Homo sapiens	139-143
19008219-3	2009	Silencing Spry2 in this context resulted in increased apoptosis, associated with decreased Akt activation and decreased phosphorylation of HDM2 at Ser-166, which has been shown to stabilize HDM2.	Serine	147-150	MDM2 proto-oncogene	Homo sapiens	139-143
18828159-9	2009	Collectively, our results identify HMGA2 and MDM2 as amplification targets in PA and Ca-ex-PA and suggest that amplification of 12q genes (in particular MDM2), deletions of 5q23.2-q31.2, gains of 8q12.1 (PLAG1) and 8q22.1-q24.1 (MYC), and amplification of ERBB2 may be of importance for malignant transformation of benign PA.	ca-ex-pa	85-93	MDM2 proto-oncogene	Homo sapiens	45-49
18948082-7	2008	In addition, MDM2, an E3 ubiquitin ligase, binds Galphas and promotes its degradation.	galphas	49-56	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	140-144
18959403-0	2008	Analysis of chemical shift changes reveals the binding modes of isoindolinone inhibitors of the MDM2-p53 interaction.	phthalimidine	64-77	MDM2 proto-oncogene	Homo sapiens	96-100
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	MDM2 proto-oncogene	Homo sapiens	100-104
19015526-0	2008	ATM-mediated serine 72 phosphorylation stabilizes ribonucleotide reductase small subunit p53R2 protein against MDM2 to DNA damage.	Serine	13-19	MDM2 proto-oncogene	Homo sapiens	111-115
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	MDM2 proto-oncogene	Homo sapiens	130-134
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	MDM2 proto-oncogene	Homo sapiens	207-211
18959403-4	2008	Isoindolinones are a novel class of MDM2-antagonists of moderate affinity, which still require the development of more potent candidates for clinical applications.	phthalimidine	0-14	MDM2 proto-oncogene	Homo sapiens	36-40
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	MDM2 proto-oncogene	Homo sapiens	51-55
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	MDM2 proto-oncogene	Homo sapiens	116-120
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	113-117
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	MDM2 proto-oncogene	Homo sapiens	193-197
18976073-10	2008	CONCLUSIONS: Although the MDM2 SNP309 does not portend decreased survival, the increased incidence of the mutant G allele in patients with GBM and its influence on age of onset suggest a potential role in the molecular pathogenesis of GBM, and may be a therapeutic target.	snp309	31-37	MDM2 proto-oncogene	Homo sapiens	26-30
18813780-7	2008	Consistently, PTX increased p21WAF1, bax and MDM2 levels, suggesting that p53 is transcriptionally active.	Paclitaxel	14-17	MDM2 proto-oncogene	Homo sapiens	45-49
18839023-0	2008	Inhibition of all-trans retinoic acid on MDM2 gene expression in astrocytoma cell line SHG-44.	2-octenal	18-23	MDM2 proto-oncogene	Homo sapiens	41-45
18839023-0	2008	Inhibition of all-trans retinoic acid on MDM2 gene expression in astrocytoma cell line SHG-44.	Tretinoin	24-37	MDM2 proto-oncogene	Homo sapiens	41-45
18839023-1	2008	OBJECTIVE: To investigate the impact of all-trans retinoic acid (ATRA) on MDM2 gene expression in astrocytoma cell line SHG-44, and to provide basic data for further research on the progression mechanism and gene therapy of human astrocytoma.	Tretinoin	40-63	MDM2 proto-oncogene	Homo sapiens	74-78
18839023-1	2008	OBJECTIVE: To investigate the impact of all-trans retinoic acid (ATRA) on MDM2 gene expression in astrocytoma cell line SHG-44, and to provide basic data for further research on the progression mechanism and gene therapy of human astrocytoma.	Tretinoin	65-69	MDM2 proto-oncogene	Homo sapiens	74-78
18839023-2	2008	METHODS: The differential expressions of MDM2 gene and protein in SHG-44 cells were detected by cDNA microarray and Western blot, respectively, before and after treatment of ATRA.	Tretinoin	174-178	MDM2 proto-oncogene	Homo sapiens	41-45
18839023-5	2008	RESULTS: The intensity ratio of ATRA-treated to untreated SHG-44 cell was 0.37 in the cDNA microarray, suggesting that the expression of MDM2 gene was down-regulated in SHG-44 cells after treatment with ATRA.	Tretinoin	32-36	MDM2 proto-oncogene	Homo sapiens	137-141
18839023-5	2008	RESULTS: The intensity ratio of ATRA-treated to untreated SHG-44 cell was 0.37 in the cDNA microarray, suggesting that the expression of MDM2 gene was down-regulated in SHG-44 cells after treatment with ATRA.	Tretinoin	203-207	MDM2 proto-oncogene	Homo sapiens	137-141
18839023-7	2008	Western blot demonstrated that the optical density ratios of MDM2 to beta-actin in ATRA-treated and untreated SHG-44 were 14.02+/-0.35 and 21.40+/-0.58 (t = 24.728, P = 0.000), respectively, suggesting that the expression of MDM2 protein was inhibited in ATRA-treated SHG-44 cells.	Tretinoin	83-87	MDM2 proto-oncogene	Homo sapiens	61-65
18839023-7	2008	Western blot demonstrated that the optical density ratios of MDM2 to beta-actin in ATRA-treated and untreated SHG-44 were 14.02+/-0.35 and 21.40+/-0.58 (t = 24.728, P = 0.000), respectively, suggesting that the expression of MDM2 protein was inhibited in ATRA-treated SHG-44 cells.	Tretinoin	83-87	MDM2 proto-oncogene	Homo sapiens	225-229
18839023-7	2008	Western blot demonstrated that the optical density ratios of MDM2 to beta-actin in ATRA-treated and untreated SHG-44 were 14.02+/-0.35 and 21.40+/-0.58 (t = 24.728, P = 0.000), respectively, suggesting that the expression of MDM2 protein was inhibited in ATRA-treated SHG-44 cells.	Tretinoin	255-259	MDM2 proto-oncogene	Homo sapiens	61-65
18839023-9	2008	CONCLUSION: ATRA can inhibit MDM2 gene expression in SHG-44 cells, and MDM2 is related to astrocytoma progression.	Tretinoin	12-16	MDM2 proto-oncogene	Homo sapiens	29-33
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	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	73-77
18952844-5	2008	We further show that MDM2 also promotes the CRM1-p53 association and Thr-55 phosphorylation is required for this process.	Threonine	69-72	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	193-197
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	MDM2 proto-oncogene	Homo sapiens	193-197
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	MDM2 proto-oncogene	Homo sapiens	193-197
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	MDM2 proto-oncogene	Homo sapiens	193-197
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	MDM2 proto-oncogene	Homo sapiens	25-29
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	MDM2 proto-oncogene	Homo sapiens	25-29
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	MDM2 proto-oncogene	Homo sapiens	25-29
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	MDM2 proto-oncogene	Homo sapiens	25-29
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	MDM2 proto-oncogene	Homo sapiens	25-29
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	MDM2 proto-oncogene	Homo sapiens	25-29
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	MDM2 proto-oncogene	Homo sapiens	25-29
18725577-0	2008	SNP309 as predictor for sensitivity of CLL cells to the MDM2 inhibitor nutlin-3a.	snp309	0-6	MDM2 proto-oncogene	Homo sapiens	56-60
18799043-5	2008	Most intriguingly, this alternative splice form, termed Mdm2(+108), is acutely induced by the chemotherapeutic agents Adriamycin and Actinomycin D, but not other DNA damaging agents.	Doxorubicin	118-128	MDM2 proto-oncogene	Homo sapiens	56-60
18799043-5	2008	Most intriguingly, this alternative splice form, termed Mdm2(+108), is acutely induced by the chemotherapeutic agents Adriamycin and Actinomycin D, but not other DNA damaging agents.	Dactinomycin	133-146	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	0-5
18725577-0	2008	SNP309 as predictor for sensitivity of CLL cells to the MDM2 inhibitor nutlin-3a.	nutlin 3	71-80	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	68-72
18618574-10	2008	The p53 overexpression was associated with MDM2 SNP309.	snp309	48-54	MDM2 proto-oncogene	Homo sapiens	43-47
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	MDM2 proto-oncogene	Homo sapiens	83-87
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	MDM2 proto-oncogene	Homo sapiens	126-130
18723490-0	2008	Targeting tumor cells expressing p53 with a water-soluble inhibitor of Hdm2.	Water	44-49	MDM2 proto-oncogene	Homo sapiens	71-75
18426989-0	2008	MDM2 SNP309 and TP53 Arg72Pro interact to alter therapy-related acute myeloid leukemia susceptibility.	snp309	5-11	MDM2 proto-oncogene	Homo sapiens	0-4
18490454-4	2008	Here, we demonstrate that hydrogen peroxide-induced oxidative stress elicits down-regulation of HDM2.	Hydrogen Peroxide	26-43	MDM2 proto-oncogene	Homo sapiens	96-100
18471438-3	2008	During adriamycin (ADR)-mediated apoptosis, expression levels of NFBD1 reduced in association with the down-regulation of MDM2.	Doxorubicin	7-17	MDM2 proto-oncogene	Homo sapiens	122-126
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	MDM2 proto-oncogene	Homo sapiens	126-130
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	MDM2 proto-oncogene	Homo sapiens	23-27
18665269-8	2008	Furthermore, in vivo co-expression of Mdm2 and FOXO induces FOXO mono-ubiquitination and consistent with this result, siRNA-mediated depletion of Mdm2 inhibits mono-ubiquitination of FOXO induced by hydrogen peroxide.	Hydrogen Peroxide	199-216	MDM2 proto-oncogene	Homo sapiens	38-42
18665269-8	2008	Furthermore, in vivo co-expression of Mdm2 and FOXO induces FOXO mono-ubiquitination and consistent with this result, siRNA-mediated depletion of Mdm2 inhibits mono-ubiquitination of FOXO induced by hydrogen peroxide.	Hydrogen Peroxide	199-216	MDM2 proto-oncogene	Homo sapiens	146-150
18428185-0	2008	Isoquinolin-1-one inhibitors of the MDM2-p53 interaction.	isocarbostyril	0-17	MDM2 proto-oncogene	Homo sapiens	36-40
18632619-6	2008	Whereas Mdm2 catalyzed lysine 63 (K63) chain ubiquitination, c-Cbl modified IGF-IR through K48 chains.	Lysine	23-29	MDM2 proto-oncogene	Homo sapiens	8-12
18632619-9	2008	Taken together, our results show that c-Cbl constitutes a new ligase responsible for the ubiquitination of IGF-IR and that it complements the action of Mdm2 on ubiquitin lysine residue specificity, responsiveness to IGF-I, and type of endocytic pathway used.	Lysine	170-176	MDM2 proto-oncogene	Homo sapiens	152-156
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	MDM2 proto-oncogene	Homo sapiens	71-75
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	MDM2 proto-oncogene	Homo sapiens	100-104
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	MDM2 proto-oncogene	Homo sapiens	147-151
18426907-5	2008	NS binds to the central acidic domain of MDM2 and inhibits MDM2-mediated p53 ubiquitylation and degradation.	ns	0-2	MDM2 proto-oncogene	Homo sapiens	41-45
18604177-0	2008	BH3 activation blocks Hdmx suppression of apoptosis and cooperates  with Nutlin to induce cell death.	BH 3	0-3	MDM2 proto-oncogene	Homo sapiens	22-26
18604177-4	2008	In this report, we demonstrate that this also applies to MI-219, another Hdm2 antagonist.	MI-219	57-63	MDM2 proto-oncogene	Homo sapiens	73-77
18426907-5	2008	NS binds to the central acidic domain of MDM2 and inhibits MDM2-mediated p53 ubiquitylation and degradation.	ns	0-2	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	126-130
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.	snp309	5-11	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	0-4
18332867-0	2008	Isosilybin B causes androgen receptor degradation in human prostate carcinoma cells via PI3K-Akt-Mdm2-mediated pathway.	isosilybin A	0-12	MDM2 proto-oncogene	Homo sapiens	97-101
19062713-0	2008	[Impact of PI3K /Akt /mdm2 signaling pathway on the sensitivity of gastric cancer cell line SGC7901 to doxorubicin].	Doxorubicin	103-114	MDM2 proto-oncogene	Homo sapiens	22-26
19062713-1	2008	OBJECTIVE: To explore whether PI3K/Akt/mdm2 signalling pathway affect the sensitivity of gastric cancer cell line SGC7901 cells to doxorubicin.	Doxorubicin	131-142	MDM2 proto-oncogene	Homo sapiens	39-43
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	MDM2 proto-oncogene	Homo sapiens	85-89
19062713-9	2008	CONCLUSION: PI3K/Akt/mdm2 signalling pathway can be activated by doxorubicin and suppress apoptosis by promoting phosphorylation of mdm2.	Doxorubicin	65-76	MDM2 proto-oncogene	Homo sapiens	21-25
19062713-9	2008	CONCLUSION: PI3K/Akt/mdm2 signalling pathway can be activated by doxorubicin and suppress apoptosis by promoting phosphorylation of mdm2.	Doxorubicin	65-76	MDM2 proto-oncogene	Homo sapiens	132-136
18467333-5	2008	Additionally, the Pim kinases phosphorylate Mdm2 in vitro and in cultured cells at Ser(166) and Ser(186), two previously identified targets of other signaling pathways, including Akt.	Serine	83-86	MDM2 proto-oncogene	Homo sapiens	44-48
18467333-5	2008	Additionally, the Pim kinases phosphorylate Mdm2 in vitro and in cultured cells at Ser(166) and Ser(186), two previously identified targets of other signaling pathways, including Akt.	Serine	96-99	MDM2 proto-oncogene	Homo sapiens	44-48
18332867-5	2008	In mechanistic studies identifying AR degradation, isosilybin B caused increased phosphorylation of Akt (Ser-473 and Thr-308) and Mdm2 (Ser-166), which was linked with AR degradation as pretreatment with PI3K inhibitor (LY294002)-restored AR level.	isosilybin A	51-63	MDM2 proto-oncogene	Homo sapiens	130-134
18332867-7	2008	Antibody pull-down results also indicated that isosilybin B treatment enhances the formation of complex between Akt, Mdm2 and AR, which promotes phosphorylation-dependent AR ubiquitination and its degradation by proteasome.	isosilybin A	47-59	MDM2 proto-oncogene	Homo sapiens	117-121
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	MDM2 proto-oncogene	Homo sapiens	54-58
18219319-7	2008	Here we report the crystal structure of the MDM2/MDMX RING domain heterodimer and map residues required for functional interaction with the E2 (UbcH5b).	Estradiol	140-142	MDM2 proto-oncogene	Homo sapiens	44-48
18451149-7	2008	We show that changes in MDM2 expression alter folate metabolism in cells as evidenced by MDM2-dependent alteration in the sensitivity of cells to the antifolate drug methotrexate.	Folic Acid	46-52	MDM2 proto-oncogene	Homo sapiens	24-28
18451149-7	2008	We show that changes in MDM2 expression alter folate metabolism in cells as evidenced by MDM2-dependent alteration in the sensitivity of cells to the antifolate drug methotrexate.	Folic Acid	46-52	MDM2 proto-oncogene	Homo sapiens	89-93
18451149-7	2008	We show that changes in MDM2 expression alter folate metabolism in cells as evidenced by MDM2-dependent alteration in the sensitivity of cells to the antifolate drug methotrexate.	Methotrexate	166-178	MDM2 proto-oncogene	Homo sapiens	24-28
18451149-7	2008	We show that changes in MDM2 expression alter folate metabolism in cells as evidenced by MDM2-dependent alteration in the sensitivity of cells to the antifolate drug methotrexate.	Methotrexate	166-178	MDM2 proto-oncogene	Homo sapiens	89-93
18451149-9	2008	Our studies provide for the first time a link between MDM2, an oncogene with a critical ubiquitin ligase activity and a vital one-carbon donor pathway involved in epigenetic regulation, and DNA metabolism, which has wide ranging implications for both cell biology and tumor development.	Carbon	130-136	MDM2 proto-oncogene	Homo sapiens	54-58
18423915-8	2008	The MDM2 SNP309 G/G polymorphism was associated with poor OS in advanced OSCC, and the OS and DSF of irradiated patients.	Osmium	58-60	MDM2 proto-oncogene	Homo sapiens	4-8
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.	snp309	24-30	MDM2 proto-oncogene	Homo sapiens	19-23
18646312-5	2008	RESULTS: While Mdm2-overexpressing G/G cells were resistant to p53 activation by DNA damage, they were sensitive to Nutlin-3.	nutlin 3	116-124	MDM2 proto-oncogene	Homo sapiens	15-19
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	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	71-75
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	MDM2 proto-oncogene	Homo sapiens	159-163
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	MDM2 proto-oncogene	Homo sapiens	60-64
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	MDM2 proto-oncogene	Homo sapiens	80-84
18294283-5	2008	In addition, doxorubicin caused a dramatic reduction of Hdm2 mRNA and protein levels in cells expressing HBx.	Doxorubicin	13-24	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	146-150
18483299-3	2008	We report that inhibition of PI3K/Akt, either by the PI3K inhibitor Ly294002 or by expression of PTEN, synergized the ability of the MDM2 antagonist nutlin-3 to induce apoptosis in acute lymphoblastic leukemia (ALL).	nutlin 3	149-157	MDM2 proto-oncogene	Homo sapiens	133-137
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	MDM2 proto-oncogene	Homo sapiens	54-58
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	MDM2 proto-oncogene	Homo sapiens	150-154
18359851-6	2008	Furthermore, Hh signaling induced the phosphorylation of human Mdm2 protein on serines 166 and 186, which are activating phosphorylation sites of Mdm2.	Serine	79-86	MDM2 proto-oncogene	Homo sapiens	63-67
18096571-0	2008	Mdm2 as a sensitive and mechanistically informative marker for genotoxicity induced by benzo[a]pyrene and dibenzo[a,l]pyrene.	Benzo(a)pyrene	87-101	MDM2 proto-oncogene	Homo sapiens	0-4
18096571-0	2008	Mdm2 as a sensitive and mechanistically informative marker for genotoxicity induced by benzo[a]pyrene and dibenzo[a,l]pyrene.	dibenzo(a,l)pyrene	106-124	MDM2 proto-oncogene	Homo sapiens	0-4
18096571-3	2008	Employing the Mdm2 2A10 antibody and phosphatase treatment we found that Mdm2 accumulated in HepG2 cells when exposed to low concentrations of genotoxic compounds such as mitomycin C, etoposide, 5-fluorouracil, and benzo[a]pyrene (BP).	Mitomycin	171-182	MDM2 proto-oncogene	Homo sapiens	73-77
18096571-3	2008	Employing the Mdm2 2A10 antibody and phosphatase treatment we found that Mdm2 accumulated in HepG2 cells when exposed to low concentrations of genotoxic compounds such as mitomycin C, etoposide, 5-fluorouracil, and benzo[a]pyrene (BP).	Etoposide	184-193	MDM2 proto-oncogene	Homo sapiens	73-77
18096571-3	2008	Employing the Mdm2 2A10 antibody and phosphatase treatment we found that Mdm2 accumulated in HepG2 cells when exposed to low concentrations of genotoxic compounds such as mitomycin C, etoposide, 5-fluorouracil, and benzo[a]pyrene (BP).	Fluorouracil	195-209	MDM2 proto-oncogene	Homo sapiens	73-77
18096571-3	2008	Employing the Mdm2 2A10 antibody and phosphatase treatment we found that Mdm2 accumulated in HepG2 cells when exposed to low concentrations of genotoxic compounds such as mitomycin C, etoposide, 5-fluorouracil, and benzo[a]pyrene (BP).	Benzo(a)pyrene	215-229	MDM2 proto-oncogene	Homo sapiens	73-77
18096571-3	2008	Employing the Mdm2 2A10 antibody and phosphatase treatment we found that Mdm2 accumulated in HepG2 cells when exposed to low concentrations of genotoxic compounds such as mitomycin C, etoposide, 5-fluorouracil, and benzo[a]pyrene (BP).	Benzo(a)pyrene	231-233	MDM2 proto-oncogene	Homo sapiens	73-77
18096571-4	2008	The low-dose responses were not accompanied by p53 accumulation and the effect of low concentrations of BP on Mdm2 was not affected by small interfering RNA for p53.	Benzo(a)pyrene	104-106	MDM2 proto-oncogene	Homo sapiens	110-114
18096571-5	2008	In human lymphoblasts 10nM BP induced an Mdm2 response.	Benzo(a)pyrene	27-29	MDM2 proto-oncogene	Homo sapiens	41-45
18096571-6	2008	Low concentrations of BP also induced binding of Mdm2 to chromatin in HepG2 cells, but no p53 binding or H2AX phosphorylation.	Benzo(a)pyrene	22-24	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	44-48
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	MDM2 proto-oncogene	Homo sapiens	163-167
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.	gammah2ax	260-269	MDM2 proto-oncogene	Homo sapiens	163-167
18359851-6	2008	Furthermore, Hh signaling induced the phosphorylation of human Mdm2 protein on serines 166 and 186, which are activating phosphorylation sites of Mdm2.	Serine	79-86	MDM2 proto-oncogene	Homo sapiens	146-150
17828296-0	2008	Picropodophyllin induces downregulation of the insulin-like growth factor 1 receptor: potential mechanistic involvement of Mdm2 and beta-arrestin1.	picropodophyllin	0-16	MDM2 proto-oncogene	Homo sapiens	123-127
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	MDM2 proto-oncogene	Homo sapiens	31-35
18262501-0	2008	Influence of MDM2 SNP309 alone or in combination with the TP53 R72P polymorphism in oligodendroglial tumors.	snp309	18-24	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	111-115
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	MDM2 proto-oncogene	Homo sapiens	242-246
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	MDM2 proto-oncogene	Homo sapiens	113-117
32038776-0	2008	Elevated Levels of PDGF Receptor and MDM2 as Potential Biomarkers for Formaldehyde Intoxication.	Formaldehyde	70-82	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	71-75
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	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	257-261
17935137-7	2008	In addition, pretreatment of wortmannin blocked etoposide and doxorubicin induced IkappaB-alpha degradation, NFkappaB activation, phosphorylation of Akt, MDM-2 and forkhead transcription factors.	Wortmannin	29-39	MDM2 proto-oncogene	Homo sapiens	154-159
17935137-7	2008	In addition, pretreatment of wortmannin blocked etoposide and doxorubicin induced IkappaB-alpha degradation, NFkappaB activation, phosphorylation of Akt, MDM-2 and forkhead transcription factors.	Doxorubicin	62-73	MDM2 proto-oncogene	Homo sapiens	154-159
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	MDM2 proto-oncogene	Homo sapiens	41-45
17931661-5	2007	Furthermore, when different types of cell lines were treated with a HDM2 gene specific antisense phosphorothioate oligodeoxynucleotide (HDMAS5), the expression of VEGF mRNA as well as the levels of VEGF protein was found to be decreased.	Parathion	97-113	MDM2 proto-oncogene	Homo sapiens	68-72
17721920-7	2007	Cellular accumulation of phosphorylated-AKT was observed in 66% (82/125) of ASCCs and an association demonstrated between nuclear accumulation of MDM2 and activated AKT (p &lt; 0.001).	asccs	76-81	MDM2 proto-oncogene	Homo sapiens	146-150
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	MDM2 proto-oncogene	Homo sapiens	82-86
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	MDM2 proto-oncogene	Homo sapiens	108-112
17897804-0	2007	Exploration of liquid and supercritical fluid chromatographic chiral separation and purification of Nutlin-3--a small molecule antagonist of MDM2.	nutlin 3	100-111	MDM2 proto-oncogene	Homo sapiens	141-145
17897804-2	2007	The imidazoline compound (Nutlin-3) is a promising small molecule antagonist of the MDM2-p53 interaction.	Imidazolines	4-15	MDM2 proto-oncogene	Homo sapiens	84-88
17897804-2	2007	The imidazoline compound (Nutlin-3) is a promising small molecule antagonist of the MDM2-p53 interaction.	nutlin 3	26-34	MDM2 proto-oncogene	Homo sapiens	84-88
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	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	117-121
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	MDM2 proto-oncogene	Homo sapiens	11-15
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	MDM2 proto-oncogene	Homo sapiens	40-44
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	MDM2 proto-oncogene	Homo sapiens	98-102
17848574-6	2007	The ATP binding mutant MDM2 protein (K454A) lacks the chaperone activity both in vivo and in vitro.	Adenosine Triphosphate	4-7	MDM2 proto-oncogene	Homo sapiens	23-27
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	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	139-143
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	MDM2 proto-oncogene	Homo sapiens	40-44
17957142-0	2007	Modulation of the p53-MDM2 interaction by phosphorylation of Thr18: a computational study.	UNII-PYZ33YLR8A	61-66	MDM2 proto-oncogene	Homo sapiens	22-26
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	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	97-101
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	MDM2 proto-oncogene	Homo sapiens	200-204
17957142-8	2007	Electrostatics of MDM2 reveal local anionic patches in the region where Thr18 docks.	UNII-PYZ33YLR8A	72-77	MDM2 proto-oncogene	Homo sapiens	18-22
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	MDM2 proto-oncogene	Homo sapiens	53-57
17931661-5	2007	Furthermore, when different types of cell lines were treated with a HDM2 gene specific antisense phosphorothioate oligodeoxynucleotide (HDMAS5), the expression of VEGF mRNA as well as the levels of VEGF protein was found to be decreased.	Oligodeoxyribonucleotides	114-134	MDM2 proto-oncogene	Homo sapiens	68-72
17895758-5	2007	In 48 cases, the amplification status of MDM2 and CDK4 could be evaluated with quantitative polymerase chain reaction on paraffin-embedded tissues extracted DNAs.	Paraffin	121-129	MDM2 proto-oncogene	Homo sapiens	41-45
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	MDM2 proto-oncogene	Homo sapiens	0-4
17627285-0	2007	Ceramide-induced G2 arrest in rhabdomyosarcoma (RMS) cells requires p21Cip1/Waf1 induction and is prevented by MDM2 overexpression.	Ceramides	0-8	MDM2 proto-oncogene	Homo sapiens	111-115
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	MDM2 proto-oncogene	Homo sapiens	148-152
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	MDM2 proto-oncogene	Homo sapiens	66-70
17627285-9	2007	Additionally, these observations highlight MDM2 expression and proteasomal activity as key determinants of the cellular response to ceramide accumulation.	Ceramides	132-140	MDM2 proto-oncogene	Homo sapiens	43-47
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	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	44-48
17080308-8	2007	Overall, our data suggest that MDM2 SNP309 accelerates familial breast carcinogenesis, but that this acceleration is not influenced by estrogen signaling.	snp309	36-42	MDM2 proto-oncogene	Homo sapiens	31-35
17297446-0	2007	Dose-response transition from cell cycle arrest to apoptosis with selective degradation of Mdm2 and p21WAF1/CIP1 in response to the novel anticancer agent, aminoflavone (NSC 686,288).	aminoflavone	156-168	MDM2 proto-oncogene	Homo sapiens	91-95
17297446-7	2007	Proteasomal degradation appears responsible for the decrease of both Mdm2 and p21(CIP1/WAF1), as MG-132 prevented their degradation and revealed AF-induced Mdm2 polyubiquitylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-103	MDM2 proto-oncogene	Homo sapiens	69-73
17699852-5	2007	As a known PDK-1 inhibitor, OSU-03012 inhibited the PI3K/Akt pathway with downstream effects on BAD, GSK-3beta, FoxO1a, p70S6K, and MDM-2.	OSU 03012	28-37	MDM2 proto-oncogene	Homo sapiens	132-137
17634539-10	2007	Positive staining for MDM2 was detected in 2 of 15 (13%) TT genotype, 4 of 15 (26%) TG genotype, and 5 of 10 (50%) GG genotype carriers.	Thioguanine	84-86	MDM2 proto-oncogene	Homo sapiens	22-26
17354236-0	2007	Potential for treatment of liposarcomas with the MDM2 antagonist Nutlin-3A.	nutlin 3	65-74	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	166-170
17490733-10	2007	MDM2 phosphorylation is only partially blocked by gefitinib, and high MDM2 expression may relate to drug resistance.	Gefitinib	50-59	MDM2 proto-oncogene	Homo sapiens	0-4
17371838-4	2007	In contrast, downregulation of Mdm2 by a small interfering RNA (siRNA) approach led to increased levels of p53 lacking phosphorylation at serine 15 and acetylation at lysine 382.	Serine	138-144	MDM2 proto-oncogene	Homo sapiens	31-35
17527046-8	2007	In our study population, SNP309 affected MDM2 protein level, but had no significant involvement in glioma tumorigenesis.	snp309	25-31	MDM2 proto-oncogene	Homo sapiens	41-45
17371838-4	2007	In contrast, downregulation of Mdm2 by a small interfering RNA (siRNA) approach led to increased levels of p53 lacking phosphorylation at serine 15 and acetylation at lysine 382.	Lysine	167-173	MDM2 proto-oncogene	Homo sapiens	31-35
17440969-1	2007	BACKGROUND: Small molecule MDM2 antagonists including nutlin-3 have been shown to be effective against a range of cancer cell types and nutlin-3 can inhibit growth of LNCaP xenografts.	nutlin 3	54-62	MDM2 proto-oncogene	Homo sapiens	27-31
17440969-1	2007	BACKGROUND: Small molecule MDM2 antagonists including nutlin-3 have been shown to be effective against a range of cancer cell types and nutlin-3 can inhibit growth of LNCaP xenografts.	nutlin 3	136-144	MDM2 proto-oncogene	Homo sapiens	27-31
17498302-9	2007	Daunorubicin (DNR) induced continuing down regulation of Hdm2 and Mcl-1 in both cell lines followed by apoptosis.	Daunorubicin	0-12	MDM2 proto-oncogene	Homo sapiens	57-61
17498302-9	2007	Daunorubicin (DNR) induced continuing down regulation of Hdm2 and Mcl-1 in both cell lines followed by apoptosis.	Daunorubicin	14-17	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	34-38
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	MDM2 proto-oncogene	Homo sapiens	227-231
17242401-0	2007	5-fluorouracil activation of p53 involves an MDM2-ribosomal protein interaction.	Fluorouracil	0-14	MDM2 proto-oncogene	Homo sapiens	45-49
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	MDM2 proto-oncogene	Homo sapiens	89-93
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	MDM2 proto-oncogene	Homo sapiens	118-122
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	MDM2 proto-oncogene	Homo sapiens	186-190
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	MDM2 proto-oncogene	Homo sapiens	114-118
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	MDM2 proto-oncogene	Homo sapiens	255-259
17308077-12	2007	Our results support the role of MDM2-SNP309 as a genetic modifier in LFS.	snp309	37-43	MDM2 proto-oncogene	Homo sapiens	32-36
17332326-0	2007	Curcumin, a dietary component, has anticancer, chemosensitization, and radiosensitization effects by down-regulating the MDM2 oncogene through the PI3K/mTOR/ETS2 pathway.	Curcumin	0-8	MDM2 proto-oncogene	Homo sapiens	121-125
17332326-2	2007	We have identified curcumin, which has previously been shown to have anticancer activity, as an inhibitor of MDM2 expression.	Curcumin	19-27	MDM2 proto-oncogene	Homo sapiens	109-113
17332326-3	2007	Curcumin down-regulates MDM2, independent of p53.	Curcumin	0-8	MDM2 proto-oncogene	Homo sapiens	24-28
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	MDM2 proto-oncogene	Homo sapiens	72-76
17332326-9	2007	In these tumors, curcumin reduced the expression of MDM2.	Curcumin	17-25	MDM2 proto-oncogene	Homo sapiens	52-56
17332326-10	2007	Down-regulation of the MDM2 oncogene by curcumin is a novel mechanism of action that may be essential for its chemopreventive and chemotherapeutic effects.	Curcumin	40-48	MDM2 proto-oncogene	Homo sapiens	23-27
17332326-11	2007	Our observations help to elucidate the process by which mitogens up-regulate MDM2, independent of p53, and identify a mechanism by which curcumin functions as an anticancer agent.	Curcumin	137-145	MDM2 proto-oncogene	Homo sapiens	77-81
18038763-0	2007	The effect of Tc-99m-labeled MDM2 antisense oligonucleotide on gene expression in human breast cancer MCF-7 cells.	Technetium	14-20	MDM2 proto-oncogene	Homo sapiens	29-33
17107963-0	2007	MEK-ERK-mediated phosphorylation of Mdm2 at Ser-166 in hepatocytes.	Serine	44-47	MDM2 proto-oncogene	Homo sapiens	36-40
17107963-4	2007	We found that growth factor-induced Ser-166 phosphorylation of Mdm2 was inhibited by the MEK inhibitors U0126 and PD98059 in HepG2 cells and in a rat liver cell line, TRL 1215.	Serine	36-39	MDM2 proto-oncogene	Homo sapiens	63-67
17107963-4	2007	We found that growth factor-induced Ser-166 phosphorylation of Mdm2 was inhibited by the MEK inhibitors U0126 and PD98059 in HepG2 cells and in a rat liver cell line, TRL 1215.	U 0126	104-109	MDM2 proto-oncogene	Homo sapiens	63-67
17107963-4	2007	We found that growth factor-induced Ser-166 phosphorylation of Mdm2 was inhibited by the MEK inhibitors U0126 and PD98059 in HepG2 cells and in a rat liver cell line, TRL 1215.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	114-121	MDM2 proto-oncogene	Homo sapiens	63-67
17107963-5	2007	Also, bile acids and oxidative stress induced phosphorylation of Mdm2 at Ser-166 by an apparently MEK-ERK-dependent mechanism.	Bile Acids and Salts	6-16	MDM2 proto-oncogene	Homo sapiens	65-69
17107963-5	2007	Also, bile acids and oxidative stress induced phosphorylation of Mdm2 at Ser-166 by an apparently MEK-ERK-dependent mechanism.	Serine	73-76	MDM2 proto-oncogene	Homo sapiens	65-69
17107963-6	2007	In contrast, Ser-166 phosphorylation of Mdm2 in lung cells was mediated by Akt.	Serine	13-16	MDM2 proto-oncogene	Homo sapiens	40-44
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	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	27-31
17565390-10	2007	At the time of phosphorylation of p53, we found simultaneous phosphorylation of the oncoprotein Mdm2 on Ser-166.	Serine	104-107	MDM2 proto-oncogene	Homo sapiens	84-100
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	MDM2 proto-oncogene	Homo sapiens	114-118
17138942-0	2007	Antiangiogenic activity of the MDM2 antagonist nutlin-3.	nutlin 3	47-55	MDM2 proto-oncogene	Homo sapiens	31-35
18038763-1	2007	To investigate the effect of radiolabed mouse double minute 2 (MDM2) antisense oligonucleotide on gene expression in human breast cancer MCF-7 cells, an antisense oligonucleotide (ASON) targeting MDM2 mRNA was synthesized and radiolabeled with 99Tcm.	Oligonucleotides	163-178	MDM2 proto-oncogene	Homo sapiens	196-200
18038763-1	2007	To investigate the effect of radiolabed mouse double minute 2 (MDM2) antisense oligonucleotide on gene expression in human breast cancer MCF-7 cells, an antisense oligonucleotide (ASON) targeting MDM2 mRNA was synthesized and radiolabeled with 99Tcm.	Oligonucleotides, Antisense	180-184	MDM2 proto-oncogene	Homo sapiens	196-200
18038763-8	2007	The oligonucleotide can be successfully radiolabeled, and specially hybridized to the MDM2 mRNA and inhibit gene expression intensively as compared to mismatch oligonucleotide.	Oligonucleotides	4-19	MDM2 proto-oncogene	Homo sapiens	86-90
17056014-5	2006	Treatment with actinomycin D, but not with camptothecin, augmented the interaction of p53 with Mdm2 and KAP1.	Dactinomycin	15-28	MDM2 proto-oncogene	Homo sapiens	95-99
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	MDM2 proto-oncogene	Homo sapiens	208-212
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	216-222	MDM2 proto-oncogene	Homo sapiens	208-212
16883576-4	2006	In this study, we have shown that the phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, and the mammalian target of rapamycin (mTOR) inhibitor, rapamycin, have similar effects on the inhibition of HDM2 phosphorylation and protein turnover.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	86-94	MDM2 proto-oncogene	Homo sapiens	205-209
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	MDM2 proto-oncogene	Homo sapiens	323-327
17172851-4	2006	We here investigate the potential therapeutic utility of combined targeting of Mdm2 by Nutlin-3a and Bcl-2 by ABT-737, recently developed inhibitors of protein-protein interactions.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	110-113	MDM2 proto-oncogene	Homo sapiens	79-83
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	MDM2 proto-oncogene	Homo sapiens	112-120
17010455-10	2006	Examining the binding sites of such targets and new protein sequence searches provided additional potential target proteins for S100B including Hdm2 and Hdm4, which were both found to bind S100B in a calcium-dependent manner.	Calcium	200-207	MDM2 proto-oncogene	Homo sapiens	144-148
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	MDM2 proto-oncogene	Homo sapiens	323-327
16883576-5	2006	Rapamycin inhibited p70S6K1, but not AKT activation, indicating that rapamycin affects HDM2 phosphorylation via an AKT-independent mechanism.	Sirolimus	0-9	MDM2 proto-oncogene	Homo sapiens	87-91
16883576-5	2006	Rapamycin inhibited p70S6K1, but not AKT activation, indicating that rapamycin affects HDM2 phosphorylation via an AKT-independent mechanism.	Sirolimus	69-78	MDM2 proto-oncogene	Homo sapiens	87-91
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	MDM2 proto-oncogene	Homo sapiens	31-35
17034127-0	2006	Small-molecule inhibitors of the MDM2-p53 protein-protein interaction based on an isoindolinone scaffold.	phthalimidine	82-95	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	190-194
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	MDM2 proto-oncogene	Homo sapiens	351-355
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	MDM2 proto-oncogene	Homo sapiens	227-231
16702947-0	2006	c-Abl phosphorylates Hdm2 at tyrosine 276 in response to DNA damage and regulates interaction with ARF.	Tyrosine	29-37	MDM2 proto-oncogene	Homo sapiens	21-25
16702947-3	2006	As part of this mechanism ATM itself, and the ATM-activated protein tyrosine kinase, c-Abl, inhibit Hdm2 function through phosphorylation of serine 395 and tyrosine 394 (Y394), respectively.	Serine	141-147	MDM2 proto-oncogene	Homo sapiens	100-104
16702947-3	2006	As part of this mechanism ATM itself, and the ATM-activated protein tyrosine kinase, c-Abl, inhibit Hdm2 function through phosphorylation of serine 395 and tyrosine 394 (Y394), respectively.	Tyrosine	68-76	MDM2 proto-oncogene	Homo sapiens	100-104
16702947-4	2006	In the present study, we have identified a novel target of c-Abl in the Hdm2 protein, tyrosine 276 (Y276).	Tyrosine	86-94	MDM2 proto-oncogene	Homo sapiens	72-76
16702947-4	2006	In the present study, we have identified a novel target of c-Abl in the Hdm2 protein, tyrosine 276 (Y276).	y276	100-104	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	117-121
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	MDM2 proto-oncogene	Homo sapiens	102-106
17002294-5	2006	Specificity for binding MDM2 via FXX phi phi motifs derives almost entirely from Trp23 of p53, with a 3.0 kcal mol(-1) loss of binding energy when Trp23 is changed to p65-derived Leu.	Leucine	179-182	MDM2 proto-oncogene	Homo sapiens	24-28
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	MDM2 proto-oncogene	Homo sapiens	132-136
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	MDM2 proto-oncogene	Homo sapiens	209-213
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	MDM2 proto-oncogene	Homo sapiens	195-199
17064483-0	2006	[Targeting the MDM2 gene using antisense oligonucleotide to induce cell apoptosis in human hepatoblastoma cell line HepG2].	Oligonucleotides	41-56	MDM2 proto-oncogene	Homo sapiens	15-19
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	145-155	MDM2 proto-oncogene	Homo sapiens	195-199
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	MDM2 proto-oncogene	Homo sapiens	236-240
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	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	37-41
16877339-0	2006	MDM2: a novel mineralocorticoid-responsive gene involved in aldosterone-induced human vascular structural remodeling.	Aldosterone	60-71	MDM2 proto-oncogene	Homo sapiens	0-4
16877339-4	2006	Results of these studies eventually demonstrated that MDM2, one of the genes involved in anti-apoptosis and cell growth, was markedly increased in mineralocorticoid receptor (MR)-positive VSMCs by aldosterone in all microarray, reverse transcriptase-polymerase chain reaction, immunoblotting, and immunofluorescence analyses.	Aldosterone	197-208	MDM2 proto-oncogene	Homo sapiens	54-58
16877339-8	2006	MDM2 is therefore considered one of the mineralocorticoid-responsive genes that regulates cell proliferation of VSMCs induced by MR-mediated aldosterone stimulation, possibly playing an important role in aldosterone-induced vascular structural remodeling.	Aldosterone	141-152	MDM2 proto-oncogene	Homo sapiens	0-4
16815295-0	2006	p73 and MDM2 confer the resistance of epidermoid carcinoma to cisplatin by blocking p53.	Cisplatin	62-71	MDM2 proto-oncogene	Homo sapiens	8-12
16815295-3	2006	In this study, we found that p73 and MDM2 correlate with cisplatin-resistant phenotype of human epidermoid carcinoma-derived cells.	Cisplatin	57-66	MDM2 proto-oncogene	Homo sapiens	37-41
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	44-53	MDM2 proto-oncogene	Homo sapiens	8-12
16678843-0	2006	The inhibition of calcium carbonate crystal growth by the cysteine-rich Mdm2 peptide.	Calcium Carbonate	18-35	MDM2 proto-oncogene	Homo sapiens	72-76
16678843-1	2006	The crystal growth of calcite, the most stable calcium carbonate polymorph, in the presence of the cysteine-rich Mdm2 peptide (containing 48 amino acids in the ring finger configuration), has been investigated by the constant composition technique.	Cysteine	99-107	MDM2 proto-oncogene	Homo sapiens	113-117
16543464-0	2006	Mdm2 inhibitor Nutlin-3a induces p53-mediated apoptosis by transcription-dependent and transcription-independent mechanisms and may overcome Atm-mediated resistance to fludarabine in chronic lymphocytic leukemia.	fludarabine	168-179	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	236-240
16647257-0	2006	Novel 1,4-benzodiazepine-2,5-diones as Hdm2 antagonists with improved cellular activity.	Bz-423	6-35	MDM2 proto-oncogene	Homo sapiens	39-43
16647257-2	2006	We have identified the 1,4-benzodiazepine-2,5-dione scaffold as a suitable template for inhibiting this interaction by binding to the Hdm2 protein.	Bz-423	23-51	MDM2 proto-oncogene	Homo sapiens	134-138
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	MDM2 proto-oncogene	Homo sapiens	234-238
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	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	87-91
21172150-3	2006	METHODS: Plasmid targeting MDM2 was constructed with pPUR/U6 vector and oligonucleotide designed according to the sequence of effective antisense oligonucleotides and principles of siRNA design.	Oligonucleotides	72-87	MDM2 proto-oncogene	Homo sapiens	27-31
21172150-3	2006	METHODS: Plasmid targeting MDM2 was constructed with pPUR/U6 vector and oligonucleotide designed according to the sequence of effective antisense oligonucleotides and principles of siRNA design.	Oligonucleotides	146-162	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	187-191
16707433-0	2006	MDM2 SNP309 accelerates tumor formation in a gender-specific and hormone-dependent manner.	snp309	5-11	MDM2 proto-oncogene	Homo sapiens	0-4
16759082-0	2006	Structure-based design of spiro-oxindoles as potent, specific small-molecule inhibitors of the MDM2-p53 interaction.	spiro-oxindoles	26-41	MDM2 proto-oncogene	Homo sapiens	95-99
16571800-3	2006	Here we report that, in contrast to uninfected cells, mdm2 was undetectable upon treatment of infected fibroblasts with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	MDM2 proto-oncogene	Homo sapiens	54-58
16331255-4	2006	Here, we have cloned several of these transcripts, including the previously described HDM2-A, -B and -C (which encode the COOH terminus of HDM2), and two novel variants (HDM2-HL1 and -HL2) containing a complete p53 interaction domain.	Carbonic Acid	122-126	MDM2 proto-oncogene	Homo sapiens	139-143
16331255-4	2006	Here, we have cloned several of these transcripts, including the previously described HDM2-A, -B and -C (which encode the COOH terminus of HDM2), and two novel variants (HDM2-HL1 and -HL2) containing a complete p53 interaction domain.	Carbonic Acid	122-126	MDM2 proto-oncogene	Homo sapiens	139-143
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	MDM2 proto-oncogene	Homo sapiens	83-87
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	MDM2 proto-oncogene	Homo sapiens	84-88
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	MDM2 proto-oncogene	Homo sapiens	258-262
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	MDM2 proto-oncogene	Homo sapiens	8-12
16180010-7	2006	Elevation of MDM2 was also abolished by U0126.	U 0126	40-45	MDM2 proto-oncogene	Homo sapiens	13-17
16478747-2	2006	SNP309 induces an increase in the level of Mdm2 protein, which causes attenuation of the p53 pathway.	snp309	0-6	MDM2 proto-oncogene	Homo sapiens	43-47
16412023-6	2006	LY209002 induced cell cycle arrest in the G0/G1 phase and apoptosis, which were associated with upregulation of MDM2, downregulation of cyclin D1, activation of caspase 9 and poly-ADP-ribose polymerase cleavage.	ly209002	0-8	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	32-36
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	MDM2 proto-oncogene	Homo sapiens	83-87
16671545-5	2006	The cells treated with R8-liposomal hdm2-siRNA significantly enhanced the cellular uptake of hdm2-siRNA and facilitated the functions of hdm2-siRNA through silencing of target gene which, in turn, inhibited tumor cell growth, compared with lipofectamine 2000.	Lipofectamine	240-258	MDM2 proto-oncogene	Homo sapiens	36-40
16671545-5	2006	The cells treated with R8-liposomal hdm2-siRNA significantly enhanced the cellular uptake of hdm2-siRNA and facilitated the functions of hdm2-siRNA through silencing of target gene which, in turn, inhibited tumor cell growth, compared with lipofectamine 2000.	Lipofectamine	240-258	MDM2 proto-oncogene	Homo sapiens	93-97
16671545-5	2006	The cells treated with R8-liposomal hdm2-siRNA significantly enhanced the cellular uptake of hdm2-siRNA and facilitated the functions of hdm2-siRNA through silencing of target gene which, in turn, inhibited tumor cell growth, compared with lipofectamine 2000.	Lipofectamine	240-258	MDM2 proto-oncogene	Homo sapiens	93-97
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	MDM2 proto-oncogene	Homo sapiens	60-64
16297858-3	2006	It was found that depletion of MDM2 in this pattern promoted apoptosis of LoVo cells and Cisplatin (DDP) treated in the mdm2siRNA3 transfected cell population would result in a substantial decrease by MTT colorimetry.	Cisplatin	89-98	MDM2 proto-oncogene	Homo sapiens	31-35
16297858-3	2006	It was found that depletion of MDM2 in this pattern promoted apoptosis of LoVo cells and Cisplatin (DDP) treated in the mdm2siRNA3 transfected cell population would result in a substantial decrease by MTT colorimetry.	monooxyethylene trimethylolpropane tristearate	201-204	MDM2 proto-oncogene	Homo sapiens	31-35
17120736-0	2006	P53 regulation of leukemia cells with the blockage of MDM2 by antisense oligonucleotides.	Oligonucleotides	72-88	MDM2 proto-oncogene	Homo sapiens	54-58
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	MDM2 proto-oncogene	Homo sapiens	437-441
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	MDM2 proto-oncogene	Homo sapiens	42-46
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	MDM2 proto-oncogene	Homo sapiens	58-62
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	MDM2 proto-oncogene	Homo sapiens	44-48
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	MDM2 proto-oncogene	Homo sapiens	105-109
17120736-5	2006	Apoptosis rate were reduced by MDM2 specific antisense oligonucletides and cisplatin (P &lt; 0.01).	oligonucletides	55-70	MDM2 proto-oncogene	Homo sapiens	31-35
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	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	91-95
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	MDM2 proto-oncogene	Homo sapiens	157-161
17357486-4	2006	Immunohistochemical method (SABC) was used to detect expression of MDM2 and CD6.	sabc	28-32	MDM2 proto-oncogene	Homo sapiens	67-71
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	MDM2 proto-oncogene	Homo sapiens	38-42
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	MDM2 proto-oncogene	Homo sapiens	38-42
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	MDM2 proto-oncogene	Homo sapiens	62-66
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	MDM2 proto-oncogene	Homo sapiens	5-9
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.	Phenylalanine	140-143	MDM2 proto-oncogene	Homo sapiens	5-9
16394138-2	2005	Many published in vitro and in vivo investigations have demonstrated that various MDM2 inhibitors including antisense oligonucleotides, siRNA, and small molecule MDM2 inhibitors have antitumor activity in in vitro and in vivo human cancer models, used alone or in combination with cancer chemotherapeutics and radiation therapy.	Oligonucleotides	118-134	MDM2 proto-oncogene	Homo sapiens	82-86
16394138-3	2005	For example, the mixed backbone antisense oligonucleotide developed in our laboratory specifically inhibited MDM2 expression in a dose- and time-dependent manner, resulting in significant antitumor activity in vitro and in vivo.	Oligonucleotides	42-57	MDM2 proto-oncogene	Homo sapiens	109-113
16227609-0	2005	DNA damage-induced phosphorylation of MdmX at serine 367 activates p53 by targeting MdmX for Mdm2-dependent degradation.	Serine	46-52	MDM2 proto-oncogene	Homo sapiens	93-97
16081268-6	2005	Resveratrol increased (+) and decreased (-) gene expression associated with apoptosis (Birc5+, Cash+, Mcl-1+, Mdm2+, Rpa-like+), cellular proliferation (Ctsd+, Mdm2+, Egr1+, ODC+) and cell cycle (cyclin D+, cyclin g+, Gadd45a-, Mad2l-, Mdm2+).	Resveratrol	0-11	MDM2 proto-oncogene	Homo sapiens	110-114
16081268-6	2005	Resveratrol increased (+) and decreased (-) gene expression associated with apoptosis (Birc5+, Cash+, Mcl-1+, Mdm2+, Rpa-like+), cellular proliferation (Ctsd+, Mdm2+, Egr1+, ODC+) and cell cycle (cyclin D+, cyclin g+, Gadd45a-, Mad2l-, Mdm2+).	Resveratrol	0-11	MDM2 proto-oncogene	Homo sapiens	160-164
16081268-6	2005	Resveratrol increased (+) and decreased (-) gene expression associated with apoptosis (Birc5+, Cash+, Mcl-1+, Mdm2+, Rpa-like+), cellular proliferation (Ctsd+, Mdm2+, Egr1+, ODC+) and cell cycle (cyclin D+, cyclin g+, Gadd45a-, Mad2l-, Mdm2+).	Resveratrol	0-11	MDM2 proto-oncogene	Homo sapiens	160-164
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	MDM2 proto-oncogene	Homo sapiens	54-58
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	MDM2 proto-oncogene	Homo sapiens	43-47
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	MDM2 proto-oncogene	Homo sapiens	88-92
16166295-0	2005	Genistein, a dietary isoflavone, down-regulates the MDM2 oncogene at both transcriptional and posttranslational levels.	Genistein	0-9	MDM2 proto-oncogene	Homo sapiens	52-56
16166295-8	2005	We further showed that MDM2 overexpression abrogated genistein-induced apoptosis in vitro and that genistein inhibited MDM2 expression and tumor growth in PC3 xenografts.	Genistein	53-62	MDM2 proto-oncogene	Homo sapiens	23-27
16166295-0	2005	Genistein, a dietary isoflavone, down-regulates the MDM2 oncogene at both transcriptional and posttranslational levels.	Isoflavones	21-31	MDM2 proto-oncogene	Homo sapiens	52-56
16166295-8	2005	We further showed that MDM2 overexpression abrogated genistein-induced apoptosis in vitro and that genistein inhibited MDM2 expression and tumor growth in PC3 xenografts.	Genistein	99-108	MDM2 proto-oncogene	Homo sapiens	119-123
16166295-9	2005	In conclusion, genistein directly down-regulates the MDM2 oncogene, representing a novel mechanism of its action that may have implications for its chemopreventive and chemotherapeutic effects.	Genistein	15-24	MDM2 proto-oncogene	Homo sapiens	53-57
16166295-5	2005	We found that the NFAT transcription site in the region between -132 and +33 in the MDM2 P2 promoter was responsive to genistein.	Genistein	119-128	MDM2 proto-oncogene	Homo sapiens	84-88
15985438-0	2005	Secretase-dependent tyrosine phosphorylation of Mdm2 by the ErbB-4 intracellular domain fragment.	Tyrosine	20-28	MDM2 proto-oncogene	Homo sapiens	48-52
15985438-1	2005	Heregulin activation of the endogenous receptor tyrosine kinase ErbB-4 in ZR-75-1 breast cancer cells provokes tyrosine phosphorylation of Hdm2 in a manner that is sensitive to inhibition of alpha- or gamma-secretase activity, indicating that liberation of the tyrosine kinase intracellular domain (ICD) fragment is required.	Tyrosine	48-56	MDM2 proto-oncogene	Homo sapiens	139-143
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	MDM2 proto-oncogene	Homo sapiens	118-122
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	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	92-96
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	MDM2 proto-oncogene	Homo sapiens	152-156
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	MDM2 proto-oncogene	Homo sapiens	27-31
19565011-6	2005	When MCF-7 cells were treated with 100 nM of progesterone, MDM2 p90 was inhibited but the highly expressed MDM2 p57 isoform was not.	Progesterone	45-57	MDM2 proto-oncogene	Homo sapiens	59-63
19565011-6	2005	When MCF-7 cells were treated with 100 nM of progesterone, MDM2 p90 was inhibited but the highly expressed MDM2 p57 isoform was not.	Progesterone	45-57	MDM2 proto-oncogene	Homo sapiens	107-111
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	MDM2 proto-oncogene	Homo sapiens	18-22
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	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	143-147
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	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	92-96
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	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	188-192
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	MDM2 proto-oncogene	Homo sapiens	152-156
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	MDM2 proto-oncogene	Homo sapiens	188-192
16093429-6	2005	Quantification of apoptotic cells by 7-aminoactinomycin D staining and of senescent cells by X-gal staining showed that both processes were significantly increased in H460 cells treated with MDM2-specific ASODN and radiation.	7-aminoactinomycin D	37-57	MDM2 proto-oncogene	Homo sapiens	191-195
16093429-6	2005	Quantification of apoptotic cells by 7-aminoactinomycin D staining and of senescent cells by X-gal staining showed that both processes were significantly increased in H460 cells treated with MDM2-specific ASODN and radiation.	5-bromo-4-chloro-3-indolyl beta-galactoside	93-98	MDM2 proto-oncogene	Homo sapiens	191-195
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	MDM2 proto-oncogene	Homo sapiens	39-43
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	MDM2 proto-oncogene	Homo sapiens	39-43
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	MDM2 proto-oncogene	Homo sapiens	39-43
15725629-7	2005	Nested-PCR showed that BPDE-induced MDM2 splicing had occurred in the H1355 cell line but not in normal MRC-5 cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	23-27	MDM2 proto-oncogene	Homo sapiens	36-40
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	MDM2 proto-oncogene	Homo sapiens	206-210
15714438-10	2005	Finally, with the use of several specific inhibitors, we found that BPDE-induced MDM2 mRNA alternative splicing in H1355 cells may occur through the PI3K or MAPK pathway.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	68-72	MDM2 proto-oncogene	Homo sapiens	81-85
16002925-10	2005	The 57-kD MDM2 isoform plasma concentration was very high in LCW and LCT samples (75,696.4 +/- 11,979 DU and 78,551.7 +/- 11,548 DU, respectively).	du	102-104	MDM2 proto-oncogene	Homo sapiens	10-14
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	MDM2 proto-oncogene	Homo sapiens	87-91
15746249-9	2005	Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake.	Glucose	220-227	MDM2 proto-oncogene	Homo sapiens	168-172
15780621-0	2005	Structure-based design, synthesis, and biological evaluation of novel 1,4-diazepines as HDM2 antagonists.	1,4-diazepines	70-84	MDM2 proto-oncogene	Homo sapiens	88-92
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	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	198-202
15625077-3	2005	It was found that pravastatin induced Mdm2 phosphorylation at Ser166 and at 2A10 antibody-specific epitopes in HepG2 cells, while mRNA levels were unchanged.	Pravastatin	18-29	MDM2 proto-oncogene	Homo sapiens	38-42
15713419-0	2005	Isoindolinone-based inhibitors of the MDM2-p53 protein-protein interaction.	phthalimidine	0-13	MDM2 proto-oncogene	Homo sapiens	38-42
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	MDM2 proto-oncogene	Homo sapiens	108-112
15703839-0	2005	Phosphorylation of mdm2 at serine 269 impairs its interaction with the retinoblastoma protein.	Serine	27-33	MDM2 proto-oncogene	Homo sapiens	19-23
15703839-1	2005	We previously reported that protein kinase CK2 phosphorylates the human mdm2 (hdm2) protein at serine residue 269.	Serine	95-101	MDM2 proto-oncogene	Homo sapiens	72-76
15703839-1	2005	We previously reported that protein kinase CK2 phosphorylates the human mdm2 (hdm2) protein at serine residue 269.	Serine	95-101	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	165-169
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	MDM2 proto-oncogene	Homo sapiens	67-71
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	MDM2 proto-oncogene	Homo sapiens	97-101
15720185-6	2005	Moreover, anti-MDM2 antisense oligonucleotides have in vitro and in vivo antitumor activity and chemosensitizing and radiosensitizing effects in several human cancer models, regardless of their p53 status.	Oligonucleotides	30-46	MDM2 proto-oncogene	Homo sapiens	15-19
15720188-0	2005	Novel antisense anti-MDM2 mixed-backbone oligonucleotides: proof of principle, in vitro and in vivo activities, and mechanisms.	Oligonucleotides	41-57	MDM2 proto-oncogene	Homo sapiens	21-25
15720188-5	2005	Antisense mixed-backbone oligonucleotides (MBO) specifically inhibit MDM2 expression in a dose- and time-dependent manner, resulting in significant anti-tumor activity in vitro and in vivo.	Oligonucleotides	25-41	MDM2 proto-oncogene	Homo sapiens	69-73
15375377-5	2004	In addition, hdm2-siRNA displayed in vivo antitumor activity and increased therapeutic effectiveness of mitomycin in MCF-7 xenografts.	Mitomycin	104-113	MDM2 proto-oncogene	Homo sapiens	13-17
15720188-7	2005	These results provide a basis for clinical evaluation of antisense anti-MDM2 oligonucleotides as chemosensitizers and radiosensitizers.	Oligonucleotides	77-93	MDM2 proto-oncogene	Homo sapiens	72-76
15720189-0	2005	Chemosensitization by antisense oligonucleotides targeting MDM2.	Oligonucleotides	32-48	MDM2 proto-oncogene	Homo sapiens	59-63
15720189-4	2005	Different generations of anti-human-MDM2 oligonucleotides have been tested in in vitro and in vivo human cancer models, revealing specific inhibition of MDM2 expression and significant antitumor activity.	Oligonucleotides	41-57	MDM2 proto-oncogene	Homo sapiens	36-40
15720189-4	2005	Different generations of anti-human-MDM2 oligonucleotides have been tested in in vitro and in vivo human cancer models, revealing specific inhibition of MDM2 expression and significant antitumor activity.	Oligonucleotides	41-57	MDM2 proto-oncogene	Homo sapiens	153-157
15720189-8	2005	Moreover, MDM2 antisense oligonucleotides potentiate the effect of epidermal growth factor receptor (EGFR) inhibitors by affecting in vitro and in vivo proliferation, apoptosis and protein expression in hormone-refractory and hormone-dependent human prostate cancer cells.	Oligonucleotides	25-41	MDM2 proto-oncogene	Homo sapiens	10-14
15720189-9	2005	These data support the development, among other MDM2 inhibitors, of anti-MDM2 antisense oligonucleotides as a novel class of anticancer agents, and suggest a potentially relevant role for the oligonucleotides when integrated with conventional treatments and/or other signaling inhibitors in novel therapeutic strategies.	Oligonucleotides	88-104	MDM2 proto-oncogene	Homo sapiens	48-52
15720189-9	2005	These data support the development, among other MDM2 inhibitors, of anti-MDM2 antisense oligonucleotides as a novel class of anticancer agents, and suggest a potentially relevant role for the oligonucleotides when integrated with conventional treatments and/or other signaling inhibitors in novel therapeutic strategies.	Oligonucleotides	88-104	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	59-63
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.	Norbornanes	177-187	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	59-63
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	MDM2 proto-oncogene	Homo sapiens	59-63
15505803-9	2005	We have also applied alanine scanning to the mimic-MDM2 complex and reveal which mutations are most likely to alter the binding affinity, possibly giving rise to escape mutants.	Alanine	21-28	MDM2 proto-oncogene	Homo sapiens	51-55
15600307-2	2004	A retroinverso isomer of the natural N-terminal helical peptide was found to interact with MDM2 using the same hydrophobic residues, Phe, Trp, and Leu.	Phenylalanine	133-136	MDM2 proto-oncogene	Homo sapiens	91-95
15600307-2	2004	A retroinverso isomer of the natural N-terminal helical peptide was found to interact with MDM2 using the same hydrophobic residues, Phe, Trp, and Leu.	Tryptophan	138-141	MDM2 proto-oncogene	Homo sapiens	91-95
15600307-2	2004	A retroinverso isomer of the natural N-terminal helical peptide was found to interact with MDM2 using the same hydrophobic residues, Phe, Trp, and Leu.	Leucine	147-150	MDM2 proto-oncogene	Homo sapiens	91-95
15527798-3	2004	In the present study, we identify Ser-166, a site previously reported as an AKT target, and Ser-188, a novel site which is the major site of phosphorylation of MDM2 by AKT in vitro.	Serine	34-37	MDM2 proto-oncogene	Homo sapiens	160-164
15527798-3	2004	In the present study, we identify Ser-166, a site previously reported as an AKT target, and Ser-188, a novel site which is the major site of phosphorylation of MDM2 by AKT in vitro.	Serine	92-95	MDM2 proto-oncogene	Homo sapiens	160-164
15527798-4	2004	Analysis of MDM2 in cultured cells confirms that Ser-166 and Ser-188 are phosphorylated by AKT in a physiological context.	Serine	49-52	MDM2 proto-oncogene	Homo sapiens	12-16
15527798-4	2004	Analysis of MDM2 in cultured cells confirms that Ser-166 and Ser-188 are phosphorylated by AKT in a physiological context.	Serine	61-64	MDM2 proto-oncogene	Homo sapiens	12-16
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	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	148-152
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	MDM2 proto-oncogene	Homo sapiens	28-32
15337760-6	2004	The inhibition of PI3K by LY294002 inhibited p70S6K1 and HDM2 activity in the cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	26-34	MDM2 proto-oncogene	Homo sapiens	57-61
15337760-7	2004	Forced expression of p70S6K1 or HDM2 reversed LY294002-inhibited VEGF transcriptional activation and HIF-1alpha expression.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	46-54	MDM2 proto-oncogene	Homo sapiens	32-36
15308643-7	2004	The interaction of L5 with MDM2 was also enhanced by treatment with a low dose of actinomycin D.	Dactinomycin	82-95	MDM2 proto-oncogene	Homo sapiens	27-31
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	MDM2 proto-oncogene	Homo sapiens	58-62
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	MDM2 proto-oncogene	Homo sapiens	165-169
15172967-8	2004	Here we show that bleeding into a joint in vivo and iron in vitro result in increased expression of the p53-binding protein, mdm2.	Iron	52-56	MDM2 proto-oncogene	Homo sapiens	125-129
15172967-9	2004	Iron induced the expression of mdm2 by normal human synovial cells approximately 8-fold.	Iron	0-4	MDM2 proto-oncogene	Homo sapiens	31-35
15172967-11	2004	Iron, in vitro, induced the expression of mdm2.	Iron	0-4	MDM2 proto-oncogene	Homo sapiens	42-46
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	MDM2 proto-oncogene	Homo sapiens	91-95
15217838-7	2004	Overexpressing STAT1beta reversed the negative regulation of Mdm2 expression observed after treatment with interferon-gamma (IFN-gamma), which activates STAT1, or with fludarabine.	fludarabine	168-179	MDM2 proto-oncogene	Homo sapiens	61-65
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	MDM2 proto-oncogene	Homo sapiens	19-23
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	MDM2 proto-oncogene	Homo sapiens	176-180
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	MDM2 proto-oncogene	Homo sapiens	176-180
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	MDM2 proto-oncogene	Homo sapiens	321-325
15169778-3	2004	Here we show that PKB inhibits Mdm2 self-ubiquitination via phosphorylation of Mdm2 on Ser(166) and Ser(188).	Serine	87-90	MDM2 proto-oncogene	Homo sapiens	31-35
15169778-3	2004	Here we show that PKB inhibits Mdm2 self-ubiquitination via phosphorylation of Mdm2 on Ser(166) and Ser(188).	Serine	87-90	MDM2 proto-oncogene	Homo sapiens	79-83
15169778-3	2004	Here we show that PKB inhibits Mdm2 self-ubiquitination via phosphorylation of Mdm2 on Ser(166) and Ser(188).	Serine	100-103	MDM2 proto-oncogene	Homo sapiens	31-35
15169778-4	2004	Stimulation of human embryonic kidney 293 cells with insulin-like growth factor-1 increased Mdm2 phosphorylation on Ser(166) and Ser(188) in a phosphatidylinositide 3"-OH kinase-dependent manner, and the treatment of both human embryonic kidney 293 and COS-1 cells with phosphatidylinositide 3"-OH kinase inhibitor LY-294002 led to proteasome-mediated Mdm2 degradation.	Serine	116-119	MDM2 proto-oncogene	Homo sapiens	92-96
15169778-4	2004	Stimulation of human embryonic kidney 293 cells with insulin-like growth factor-1 increased Mdm2 phosphorylation on Ser(166) and Ser(188) in a phosphatidylinositide 3"-OH kinase-dependent manner, and the treatment of both human embryonic kidney 293 and COS-1 cells with phosphatidylinositide 3"-OH kinase inhibitor LY-294002 led to proteasome-mediated Mdm2 degradation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	315-324	MDM2 proto-oncogene	Homo sapiens	92-96
15169778-5	2004	Introduction of a constitutively active form of PKB together with Mdm2 into cells induced phosphorylation of Mdm2 at Ser(166) and Ser(188) and stabilized Mdm2 protein.	Serine	117-120	MDM2 proto-oncogene	Homo sapiens	66-70
15169778-5	2004	Introduction of a constitutively active form of PKB together with Mdm2 into cells induced phosphorylation of Mdm2 at Ser(166) and Ser(188) and stabilized Mdm2 protein.	Serine	117-120	MDM2 proto-oncogene	Homo sapiens	109-113
15169778-5	2004	Introduction of a constitutively active form of PKB together with Mdm2 into cells induced phosphorylation of Mdm2 at Ser(166) and Ser(188) and stabilized Mdm2 protein.	Serine	117-120	MDM2 proto-oncogene	Homo sapiens	109-113
15169778-5	2004	Introduction of a constitutively active form of PKB together with Mdm2 into cells induced phosphorylation of Mdm2 at Ser(166) and Ser(188) and stabilized Mdm2 protein.	Serine	130-133	MDM2 proto-oncogene	Homo sapiens	66-70
15293988-0	2004	A nonpeptidic sulfonamide inhibits the p53-mdm2 interaction and activates p53-dependent transcription in mdm2-overexpressing cells.	Sulfonamides	14-25	MDM2 proto-oncogene	Homo sapiens	43-47
15293988-0	2004	A nonpeptidic sulfonamide inhibits the p53-mdm2 interaction and activates p53-dependent transcription in mdm2-overexpressing cells.	Sulfonamides	14-25	MDM2 proto-oncogene	Homo sapiens	105-109
15293988-1	2004	The evaluation of a sulfonamide inhibitor of the p53-mdm2 interaction is presented.	Sulfonamides	20-31	MDM2 proto-oncogene	Homo sapiens	53-57
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	MDM2 proto-oncogene	Homo sapiens	63-67
15176048-2	2004	In this study, we tested whether interruption of MDM2 function using antisense MDM2 oligonucleotide (AS) affects the apoptotic response of prostate cancer cells to AD.	Oligonucleotides	84-99	MDM2 proto-oncogene	Homo sapiens	79-83
15254743-6	2004	Furthermore, we show that SU5416-induced apoptosis is associated with a decrease in the expression of the apoptosis inhibitors, MDM2 and Bcl-2, and an increase in the level of NF-kappaB inhibitor, IkappaBalpha.	Semaxinib	26-32	MDM2 proto-oncogene	Homo sapiens	128-132
15176048-2	2004	In this study, we tested whether interruption of MDM2 function using antisense MDM2 oligonucleotide (AS) affects the apoptotic response of prostate cancer cells to AD.	Arsenic	101-103	MDM2 proto-oncogene	Homo sapiens	49-53
15176048-2	2004	In this study, we tested whether interruption of MDM2 function using antisense MDM2 oligonucleotide (AS) affects the apoptotic response of prostate cancer cells to AD.	Arsenic	101-103	MDM2 proto-oncogene	Homo sapiens	79-83
15176048-3	2004	METHODS: Wild type LNCaP cells and MDM2-overexpressing (LNCaP-MST) cells were treated with AS alone or in combination with AD.	Arsenic	91-93	MDM2 proto-oncogene	Homo sapiens	35-39
15269162-4	2004	For this purpose, we have used the EGFR tyrosine kinase inhibitor gefitinib (ZD1839, Iressa) and a second generation hybrid oligonucleotide antisense MDM2 (AS-MDM2), respectively.	Oligonucleotides	124-139	MDM2 proto-oncogene	Homo sapiens	150-154
15269162-10	2004	CONCLUSIONS: This study shows that EGFR and MDM2 play a critical role in the growth of prostate cancer, especially hormone-dependent, and that their combined blockade by gefitinib and AS-MDM2 causes a cooperative antitumor effect, supporting the clinical development of this therapeutic strategy.	Gefitinib	170-179	MDM2 proto-oncogene	Homo sapiens	44-48
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	MDM2 proto-oncogene	Homo sapiens	299-303
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	MDM2 proto-oncogene	Homo sapiens	154-158
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	MDM2 proto-oncogene	Homo sapiens	299-303
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	MDM2 proto-oncogene	Homo sapiens	40-44
15269162-0	2004	Combined targeting of epidermal growth factor receptor and MDM2 by gefitinib and antisense MDM2 cooperatively inhibit hormone-independent prostate cancer.	Gefitinib	67-76	MDM2 proto-oncogene	Homo sapiens	59-63
15064747-5	2004	However, the increase of p21 and mdm2 mRNAs was indistinguishable following treatment with adriamycin or induction of p14ARF.	Doxorubicin	91-101	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	192-196
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	MDM2 proto-oncogene	Homo sapiens	82-86
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	MDM2 proto-oncogene	Homo sapiens	51-55
14977824-0	2004	Radiosensitization by antisense anti-MDM2 mixed-backbone oligonucleotide in in vitro and in vivo human cancer models.	Oligonucleotides	57-72	MDM2 proto-oncogene	Homo sapiens	37-41
14761977-10	2004	The inhibition of MDM2 with anti-MDM2 antisense oligonucleotide or Short Interference RNA targeting MDM2 significantly elevated p21 protein levels in PC3 cells (p53 null).	Oligonucleotides	48-63	MDM2 proto-oncogene	Homo sapiens	18-22
14761977-10	2004	The inhibition of MDM2 with anti-MDM2 antisense oligonucleotide or Short Interference RNA targeting MDM2 significantly elevated p21 protein levels in PC3 cells (p53 null).	Oligonucleotides	48-63	MDM2 proto-oncogene	Homo sapiens	33-37
14761977-10	2004	The inhibition of MDM2 with anti-MDM2 antisense oligonucleotide or Short Interference RNA targeting MDM2 significantly elevated p21 protein levels in PC3 cells (p53 null).	Oligonucleotides	48-63	MDM2 proto-oncogene	Homo sapiens	33-37
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	MDM2 proto-oncogene	Homo sapiens	168-172
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	MDM2 proto-oncogene	Homo sapiens	168-172
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	MDM2 proto-oncogene	Homo sapiens	109-113
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	MDM2 proto-oncogene	Homo sapiens	215-220
14977824-2	2004	We have demonstrated a second-generation antisense antihuman-MDM2 oligonucleotide to have antitumor activity when administered alone or in combination with cancer chemotherapeutic agents.	Oligonucleotides	66-81	MDM2 proto-oncogene	Homo sapiens	61-65
14977824-10	2004	CONCLUSIONS: These results suggest that MDM2 has a role in radiation therapy of human cancers, regardless of p53 status, providing a basis for future development of MDM2 inhibitors, such as antisense oligonucleotides, as radiosensitizers.	Oligonucleotides	200-216	MDM2 proto-oncogene	Homo sapiens	40-44
14977824-10	2004	CONCLUSIONS: These results suggest that MDM2 has a role in radiation therapy of human cancers, regardless of p53 status, providing a basis for future development of MDM2 inhibitors, such as antisense oligonucleotides, as radiosensitizers.	Oligonucleotides	200-216	MDM2 proto-oncogene	Homo sapiens	165-169
14682762-0	2003	Solid-phase synthesis of the cyclic peptide portion of chlorofusin, an inhibitor of p53-MDM2 interactions.	Peptides, Cyclic	29-43	MDM2 proto-oncogene	Homo sapiens	88-92
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	MDM2 proto-oncogene	Homo sapiens	172-176
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	MDM2 proto-oncogene	Homo sapiens	214-218
14757843-0	2004	MDM2 and its splice variant messenger RNAs: expression in tumors and down-regulation using antisense oligonucleotides.	Oligonucleotides	101-117	MDM2 proto-oncogene	Homo sapiens	0-4
14757843-5	2004	We also discuss the progress that has been made in the development of antisense oligonucleotides targeted to MDM2 for use as a potential cancer therapy.	Oligonucleotides	80-96	MDM2 proto-oncogene	Homo sapiens	109-113
14682762-0	2003	Solid-phase synthesis of the cyclic peptide portion of chlorofusin, an inhibitor of p53-MDM2 interactions.	chlorofusin	55-66	MDM2 proto-oncogene	Homo sapiens	88-92
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	MDM2 proto-oncogene	Homo sapiens	256-260
14654783-2	2003	Here, we investigate phosphorylation of Mdm2 at serine 407 (S407).	Serine	48-54	MDM2 proto-oncogene	Homo sapiens	40-44
14513366-7	2003	Similarly, inductions of p21(WAF1/CIP1) and Mdm2 were observed in sensitive cells exposed to cisplatin.	Cisplatin	93-102	MDM2 proto-oncogene	Homo sapiens	44-48
14633995-4	2003	This decrease was reversed by the proteasome inhibitors MG132 and lactacystin, by p19(arf), and by small interfering RNA (siRNA) against MDM2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	MDM2 proto-oncogene	Homo sapiens	137-141
14633995-7	2003	MDM2 shortened the half-life of both exogenous and endogenous p21waf1/cip1 by 50% and led to the degradation of its lysine-free mutant.	Lysine	116-122	MDM2 proto-oncogene	Homo sapiens	0-4
14751837-0	2003	Chemosensitization and radiosensitization of human cancer by antisense anti-MDM2 oligonucleotides: in vitro and in vivo activities and mechanisms.	Oligonucleotides	81-97	MDM2 proto-oncogene	Homo sapiens	76-80
14751837-5	2003	The antisense oligonucleotide specifically inhibited MDM2 expression in a dose- and time-dependent manner, resulting in significant antitumor activity in vitro and in vivo.	Oligonucleotides	14-29	MDM2 proto-oncogene	Homo sapiens	53-57
14751837-9	2003	These results provide a basis for clinical evaluation of antisense anti-MDM2 oligonucleotides as chemosensitizer and radiosensitizer.	Oligonucleotides	77-93	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	115-119
14723816-14	2003	MTT results showed that the survival rate of MDM2 transfected EU-4 cells was higher than that of parental cells.	monooxyethylene trimethylolpropane tristearate	0-3	MDM2 proto-oncogene	Homo sapiens	45-49
13130078-2	2003	An antisense anti-human-MDM2 mixed-backbone oligonucleotide was tested in human prostate cancer models with various p53 statuses, LNCaP (p53wt/wt), DU145 (p53mt/mt), and PC3 (p53null).	Oligonucleotides	44-59	MDM2 proto-oncogene	Homo sapiens	24-28
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	MDM2 proto-oncogene	Homo sapiens	118-122
13130078-7	2003	In all three cell lines, MDM2 inhibition reduced cell proliferation, induced apoptosis, and potentiated the effects of the chemotherapeutic agents 10-hydroxycamptothecin and paclitaxel.	Paclitaxel	174-184	MDM2 proto-oncogene	Homo sapiens	25-29
13130078-8	2003	The anti-MDM2 oligonucleotide showed antitumor activity and increased therapeutic effectiveness of paclitaxel in both LNCaP and PC3 xenografts, causing changes in gene expression similar to those seen in vitro.	Oligonucleotides	14-29	MDM2 proto-oncogene	Homo sapiens	9-13
13130078-8	2003	The anti-MDM2 oligonucleotide showed antitumor activity and increased therapeutic effectiveness of paclitaxel in both LNCaP and PC3 xenografts, causing changes in gene expression similar to those seen in vitro.	Paclitaxel	99-109	MDM2 proto-oncogene	Homo sapiens	9-13
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	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	150-154
14559824-5	2003	Examining the cellular localization of MDM2, we confirmed that the majority of MDM2 is localized in the nucleus in PTEN-negative doxorubicin-sensitive ALL cells, whereas MDM2 is expressed predominantly in the cytoplasm in either PTEN-positive or PTEN-transfected cells.	Doxorubicin	129-140	MDM2 proto-oncogene	Homo sapiens	79-83
14559824-5	2003	Examining the cellular localization of MDM2, we confirmed that the majority of MDM2 is localized in the nucleus in PTEN-negative doxorubicin-sensitive ALL cells, whereas MDM2 is expressed predominantly in the cytoplasm in either PTEN-positive or PTEN-transfected cells.	Doxorubicin	129-140	MDM2 proto-oncogene	Homo sapiens	79-83
14580339-2	2003	We found that Mdm2 binds adenine-containing nucleotides preferentially and that nucleotide binding leads to a conformational change in the Mdm2 C terminus.	Adenine	25-32	MDM2 proto-oncogene	Homo sapiens	14-18
14580339-4	2003	Consistent with this, ATP-bound Mdm2 is preferentially localized to the nucleolus.	Adenosine Triphosphate	22-25	MDM2 proto-oncogene	Homo sapiens	32-36
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	MDM2 proto-oncogene	Homo sapiens	204-208
13130078-7	2003	In all three cell lines, MDM2 inhibition reduced cell proliferation, induced apoptosis, and potentiated the effects of the chemotherapeutic agents 10-hydroxycamptothecin and paclitaxel.	10-hydroxycamptothecin	147-169	MDM2 proto-oncogene	Homo sapiens	25-29
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	MDM2 proto-oncogene	Homo sapiens	74-78
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	MDM2 proto-oncogene	Homo sapiens	193-197
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	MDM2 proto-oncogene	Homo sapiens	42-46
12926050-6	2003	We found that expression of Mdm2 mutants were tightly regulated by doxycycline.	Doxycycline	67-78	MDM2 proto-oncogene	Homo sapiens	28-32
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	MDM2 proto-oncogene	Homo sapiens	81-85
12893182-7	2003	After cisplatin treatment, A2780-MDM2 cells showed a pronounced S-phase arrest; however, A2780 cells with intact wild-type p53 arrested primarily in G2/M phase.	Cisplatin	6-15	MDM2 proto-oncogene	Homo sapiens	33-37
12893182-8	2003	CONCLUSIONS: MDM2 overexpression can increase cisplatin cytotoxicity in A2780, with loss of G1/S checkpoint control and decreased cisplatin-DNA adduct repair.	Cisplatin	46-55	MDM2 proto-oncogene	Homo sapiens	13-17
12893182-8	2003	CONCLUSIONS: MDM2 overexpression can increase cisplatin cytotoxicity in A2780, with loss of G1/S checkpoint control and decreased cisplatin-DNA adduct repair.	Cisplatin	130-139	MDM2 proto-oncogene	Homo sapiens	13-17
12893182-9	2003	This suggests that ovarian cancers that overexpress MDM2 may be amenable to treatment with platinum compounds.	Platinum	91-99	MDM2 proto-oncogene	Homo sapiens	52-56
12759344-9	2003	Interestingly, PML mutants in which sumoylation at lysine 160 was inhibited displayed an increased association with MDM2, suggesting that sumoylation at this site may be a determinant of PML-MDM2 binding.	Lysine	51-57	MDM2 proto-oncogene	Homo sapiens	116-120
12759344-9	2003	Interestingly, PML mutants in which sumoylation at lysine 160 was inhibited displayed an increased association with MDM2, suggesting that sumoylation at this site may be a determinant of PML-MDM2 binding.	Lysine	51-57	MDM2 proto-oncogene	Homo sapiens	191-195
12867035-7	2003	CtBP proteins can undergo an NADH-induced conformational change, which we show here results in a loss of their Hdm2 binding ability.	NAD	29-33	MDM2 proto-oncogene	Homo sapiens	111-115
12926050-7	2003	Withdrawal of doxycycline in culture medium triggered overexpression of Mdm2 mutants.	Doxycycline	14-25	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	138-143
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	MDM2 proto-oncogene	Homo sapiens	153-157
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	MDM2 proto-oncogene	Homo sapiens	117-121
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	MDM2 proto-oncogene	Homo sapiens	218-222
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	MDM2 proto-oncogene	Homo sapiens	316-320
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	MDM2 proto-oncogene	Homo sapiens	118-122
12592381-0	2003	Nuclear export inhibitor leptomycin B induces the appearance of novel forms of human Mdm2 protein.	leptomycin B	25-37	MDM2 proto-oncogene	Homo sapiens	85-89
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	MDM2 proto-oncogene	Homo sapiens	133-137
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	MDM2 proto-oncogene	Homo sapiens	133-137
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	MDM2 proto-oncogene	Homo sapiens	102-106
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	MDM2 proto-oncogene	Homo sapiens	45-49
12518324-0	2003	Experimental therapy of human prostate cancer by inhibiting MDM2 expression with novel mixed-backbone antisense oligonucleotides: in vitro and in vivo activities and mechanisms.	Oligonucleotides	112-128	MDM2 proto-oncogene	Homo sapiens	60-64
12518324-3	2003	METHODS: Antisense anti-human-MDM2 mixed-backbone oligonucleotide and its mismatch control were tested in in vitro and in vivo human prostate cancer models (LNCaP, DU 145, and PC-3) for anti-tumor activity.	Oligonucleotides	50-65	MDM2 proto-oncogene	Homo sapiens	30-34
12518324-5	2003	RESULTS: The antisense oligonucleotide specifically inhibited MDM2 expression in a dose- and time-dependent manner, resulting in significant anti-tumor activity in vitro and in vivo.	Oligonucleotides	23-38	MDM2 proto-oncogene	Homo sapiens	62-66
12710210-0	2003	Antisense oligonucleotide inhibitors of MDM2 oncogene expression.	Oligonucleotides	10-25	MDM2 proto-oncogene	Homo sapiens	40-44
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	MDM2 proto-oncogene	Homo sapiens	110-114
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	MDM2 proto-oncogene	Homo sapiens	168-172
12824538-4	2003	Fluorescence-activated cell sorter (FACS) analysis following bromodeoxyuridine (BrdU) incorporation can be used to determine whether MDM2-expressing cells are synthesizing DNA.	Bromodeoxyuridine	61-78	MDM2 proto-oncogene	Homo sapiens	133-137
12824538-4	2003	Fluorescence-activated cell sorter (FACS) analysis following bromodeoxyuridine (BrdU) incorporation can be used to determine whether MDM2-expressing cells are synthesizing DNA.	Bromodeoxyuridine	80-84	MDM2 proto-oncogene	Homo sapiens	133-137
12393906-6	2002	Lysine residues 182 and 185 map within the nuclear localization signal of Mdm2.	Lysine	0-6	MDM2 proto-oncogene	Homo sapiens	74-78
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	MDM2 proto-oncogene	Homo sapiens	59-64
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	MDM2 proto-oncogene	Homo sapiens	24-28
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	MDM2 proto-oncogene	Homo sapiens	186-190
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	MDM2 proto-oncogene	Homo sapiens	247-251
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	MDM2 proto-oncogene	Homo sapiens	117-121
12393902-7	2002	This study also suggests that ubiquitination of Mdm2 and MdmX may not serve as a signal for degradation, as we show that each are capable of synthesizing non-lysine 48 polyubiquitin chains and, in fact, utilize multiple lysine linkages.	Lysine	158-164	MDM2 proto-oncogene	Homo sapiens	48-52
12393906-5	2002	When several lysine residues of Mdm2 were sequentially mutated to arginine, the K182R mutant was not sumoylated in intact cells; however, in the in vitro system this mutant was sumoylated by PIAS1, PIASxbeta, and RanBP2 as efficiently as the wild-type Mdm2 protein.	Lysine	13-19	MDM2 proto-oncogene	Homo sapiens	32-36
12427017-0	2002	Nitric oxide-mediated inhibition of Hdm2-p53 binding.	Nitric Oxide	0-12	MDM2 proto-oncogene	Homo sapiens	36-40
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	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	53-57
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	MDM2 proto-oncogene	Homo sapiens	53-57
12427017-5	2002	Moreover, nitric oxide inhibition of Hdm2-p53 binding was found to be reversible.	Nitric Oxide	10-22	MDM2 proto-oncogene	Homo sapiens	37-41
12427017-7	2002	Finally, we have identified a critical cysteine residue that nitric oxide modifies to disrupt Hdm2-p53 binding.	Cysteine	39-47	MDM2 proto-oncogene	Homo sapiens	94-98
12427017-7	2002	Finally, we have identified a critical cysteine residue that nitric oxide modifies to disrupt Hdm2-p53 binding.	Nitric Oxide	61-73	MDM2 proto-oncogene	Homo sapiens	94-98
12427017-8	2002	This cysteine is proximal to the Hdm2-p53 binding interface and is conserved across species from zebrafish to humans.	Cysteine	5-13	MDM2 proto-oncogene	Homo sapiens	33-37
12427017-9	2002	Mutation of this residue from a cysteine to an alanine does not interfere with binding but rather eliminates the sensitivity of Hdm2 to nitric oxide inactivation.	Cysteine	32-40	MDM2 proto-oncogene	Homo sapiens	128-132
12427017-9	2002	Mutation of this residue from a cysteine to an alanine does not interfere with binding but rather eliminates the sensitivity of Hdm2 to nitric oxide inactivation.	Alanine	47-54	MDM2 proto-oncogene	Homo sapiens	128-132
12427017-9	2002	Mutation of this residue from a cysteine to an alanine does not interfere with binding but rather eliminates the sensitivity of Hdm2 to nitric oxide inactivation.	Nitric Oxide	136-148	MDM2 proto-oncogene	Homo sapiens	128-132
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	MDM2 proto-oncogene	Homo sapiens	0-5
12487430-2	2002	Fluorescence polarization analysis revealed that phosphorylation at Thr18 decreased binding to recombinant Mdm2 protein compared with the unphosphorylated and the two other single phosphorylated analogues.	UNII-PYZ33YLR8A	68-73	MDM2 proto-oncogene	Homo sapiens	107-111
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	MDM2 proto-oncogene	Homo sapiens	116-121
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	MDM2 proto-oncogene	Homo sapiens	0-5
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	MDM2 proto-oncogene	Homo sapiens	114-119
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	MDM2 proto-oncogene	Homo sapiens	125-130
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	MDM2 proto-oncogene	Homo sapiens	125-130
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	MDM2 proto-oncogene	Homo sapiens	51-56
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	MDM2 proto-oncogene	Homo sapiens	151-155
12231395-2	2002	Here, the expression of mdm2 mRNA subsequent to phorbol 12,13-dibutyrate (PDB) or diethylstilbestrol (DES) treatment was analyzed in human breast tumor-derived GI-101A cell line.	Phorbol 12,13-Dibutyrate	48-72	MDM2 proto-oncogene	Homo sapiens	24-28
12231395-2	2002	Here, the expression of mdm2 mRNA subsequent to phorbol 12,13-dibutyrate (PDB) or diethylstilbestrol (DES) treatment was analyzed in human breast tumor-derived GI-101A cell line.	Phorbol 12,13-Dibutyrate	74-77	MDM2 proto-oncogene	Homo sapiens	24-28
12231395-2	2002	Here, the expression of mdm2 mRNA subsequent to phorbol 12,13-dibutyrate (PDB) or diethylstilbestrol (DES) treatment was analyzed in human breast tumor-derived GI-101A cell line.	Diethylstilbestrol	82-100	MDM2 proto-oncogene	Homo sapiens	24-28
12231395-2	2002	Here, the expression of mdm2 mRNA subsequent to phorbol 12,13-dibutyrate (PDB) or diethylstilbestrol (DES) treatment was analyzed in human breast tumor-derived GI-101A cell line.	Diethylstilbestrol	102-105	MDM2 proto-oncogene	Homo sapiens	24-28
12231395-8	2002	Tamoxifen and chelerythrine co-treatments inhibited DES and PDB stimulated increases of mdm2 transcription respectively, in GI-101A cells.	Tamoxifen	0-9	MDM2 proto-oncogene	Homo sapiens	88-92
12231395-8	2002	Tamoxifen and chelerythrine co-treatments inhibited DES and PDB stimulated increases of mdm2 transcription respectively, in GI-101A cells.	chelerythrine	14-27	MDM2 proto-oncogene	Homo sapiens	88-92
12224024-3	2002	By sequestering mdm2, ARF may promote growth suppression through the Rb pathway as well because mdm2 can bind to Rb and attenuate its function.	Rubidium	69-71	MDM2 proto-oncogene	Homo sapiens	16-20
12091392-8	2002	Moreover, the induction of p21/WAF1 and Mdm2 by doxorubicin was abrogated by simultaneous treatment with Bis IX.	Doxorubicin	48-59	MDM2 proto-oncogene	Homo sapiens	40-44
12091392-8	2002	Moreover, the induction of p21/WAF1 and Mdm2 by doxorubicin was abrogated by simultaneous treatment with Bis IX.	bisindolylmaleimide IX	105-111	MDM2 proto-oncogene	Homo sapiens	40-44
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	MDM2 proto-oncogene	Homo sapiens	174-178
12359050-4	2002	PAb240 reacted with a low percentage of cells at 37 degrees C and no reaction was observed at 31 degrees C. PAb421 antibody stained a significantly lower percentage of cells at 37 degrees C than at 31 degrees C. Cells were not stained with PAb1620 antibody and were negative for antibodies against p21(WAF1) and MDM2 proteins independently of the temperature.	pab421	108-114	MDM2 proto-oncogene	Homo sapiens	312-316
12058035-8	2002	In addition, gene expression analysis revealed that EGCG prevented both the 6-OHDA-induced expression of several mRNAs, such as Bax, Bad, and Mdm2, and the decrease in Bcl-2, Bcl-w, and Bcl-x(L).	epigallocatechin gallate	52-56	MDM2 proto-oncogene	Homo sapiens	142-146
12058035-8	2002	In addition, gene expression analysis revealed that EGCG prevented both the 6-OHDA-induced expression of several mRNAs, such as Bax, Bad, and Mdm2, and the decrease in Bcl-2, Bcl-w, and Bcl-x(L).	Oxidopamine	76-82	MDM2 proto-oncogene	Homo sapiens	142-146
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	MDM2 proto-oncogene	Homo sapiens	120-124
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	MDM2 proto-oncogene	Homo sapiens	120-124
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	MDM2 proto-oncogene	Homo sapiens	174-178
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	MDM2 proto-oncogene	Homo sapiens	131-135
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	MDM2 proto-oncogene	Homo sapiens	79-83
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	MDM2 proto-oncogene	Homo sapiens	208-212
12432259-5	2002	High concentrations of FL (500 nM) decreased levels of p21 and Mdm-2 but dramatically induced p53.	alvocidib	23-25	MDM2 proto-oncogene	Homo sapiens	63-68
12110584-0	2002	Tyrosine phosphorylation of Mdm2 by c-Abl: implications for p53 regulation.	Tyrosine	0-8	MDM2 proto-oncogene	Homo sapiens	28-32
12085228-3	2002	Here we relate physical interactions between p14ARF and MDM2, as determined using synthetic peptides and systematic deletions of p14ARF, with consequential effects on p53 stabilization and transcriptional activity.	Peptides	92-100	MDM2 proto-oncogene	Homo sapiens	56-60
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	MDM2 proto-oncogene	Homo sapiens	87-91
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	MDM2 proto-oncogene	Homo sapiens	86-90
12168835-0	2002	Detection of MDM2 alterations in cultured human hepatocytes treated with 17beta-estradiol or 17alpha-ethinylestradiol.	Estradiol	73-89	MDM2 proto-oncogene	Homo sapiens	13-17
11992615-9	2002	In addition, combined TRAIL and wortmannin treatment resulted in cleavage of several proteins: PARP, Akt, p21/WAF1, and MDM2 as well as dephosphorylation of Akt.	Wortmannin	32-42	MDM2 proto-oncogene	Homo sapiens	120-124
12168835-0	2002	Detection of MDM2 alterations in cultured human hepatocytes treated with 17beta-estradiol or 17alpha-ethinylestradiol.	Ethinyl Estradiol	93-117	MDM2 proto-oncogene	Homo sapiens	13-17
12168835-2	2002	Here we present the first report on the modulational effects of the steroids 17beta-estradiol (E2) and 17alpha-ethinylestradiol (EE2) on oncogene MDM2 in human hepatocytes.	Steroids	68-76	MDM2 proto-oncogene	Homo sapiens	146-150
12168835-2	2002	Here we present the first report on the modulational effects of the steroids 17beta-estradiol (E2) and 17alpha-ethinylestradiol (EE2) on oncogene MDM2 in human hepatocytes.	Estradiol	77-93	MDM2 proto-oncogene	Homo sapiens	146-150
12168835-2	2002	Here we present the first report on the modulational effects of the steroids 17beta-estradiol (E2) and 17alpha-ethinylestradiol (EE2) on oncogene MDM2 in human hepatocytes.	Estradiol	95-97	MDM2 proto-oncogene	Homo sapiens	146-150
12168835-2	2002	Here we present the first report on the modulational effects of the steroids 17beta-estradiol (E2) and 17alpha-ethinylestradiol (EE2) on oncogene MDM2 in human hepatocytes.	Ethinyl Estradiol	103-127	MDM2 proto-oncogene	Homo sapiens	146-150
12168835-2	2002	Here we present the first report on the modulational effects of the steroids 17beta-estradiol (E2) and 17alpha-ethinylestradiol (EE2) on oncogene MDM2 in human hepatocytes.	Ethinyl Estradiol	129-132	MDM2 proto-oncogene	Homo sapiens	146-150
12168835-4	2002	RESULTS: The hepatocytes responded to stimulation with steroid E2/EE2 concentrations from 1-100 nmol/l with the overexpression of MDM2 protein while non-stimulated cells were negative.	Steroids	55-62	MDM2 proto-oncogene	Homo sapiens	130-134
12168835-8	2002	CONCLUSION: The data show that steroid hormones are involved in the induction of MDM2 alterations in benign human hepatocytes.	Steroids	31-47	MDM2 proto-oncogene	Homo sapiens	81-85
12747748-7	2002	Interestingly, the synthetic wild type sequence p53 (264-272) and MDM-2 (53-61) peptides were able to drive in vitro generation of tumor-specific CTLs from the PBMCs of normal HLA-A2+ donors.	Peptides	80-88	MDM2 proto-oncogene	Homo sapiens	66-71
11964305-0	2002	MDM2 induces NF-kappaB/p65 expression transcriptionally through Sp1-binding sites: a novel, p53-independent role of MDM2 in doxorubicin resistance in acute lymphoblastic leukemia.	Doxorubicin	124-135	MDM2 proto-oncogene	Homo sapiens	0-4
11964305-4	2002	Initially, we noted that the overexpression of MDM2 protein in leukemic bone marrow cells of patients with B-cell precursor acute lymphoblastic leukemia (BCP-ALL), and an ALL cell line (EU-4) transfected with the MDM2 gene was associated with elevated expression of p65 and in vitro resistance to doxorubicin (Adriamycin).	Doxorubicin	297-308	MDM2 proto-oncogene	Homo sapiens	47-51
11964305-4	2002	Initially, we noted that the overexpression of MDM2 protein in leukemic bone marrow cells of patients with B-cell precursor acute lymphoblastic leukemia (BCP-ALL), and an ALL cell line (EU-4) transfected with the MDM2 gene was associated with elevated expression of p65 and in vitro resistance to doxorubicin (Adriamycin).	Doxorubicin	310-320	MDM2 proto-oncogene	Homo sapiens	47-51
11956627-6	2002	Treatment of 17beta-estradiol (E2) significantly enhanced the expression of S-mdm2 but not that of L-mdm2 in MCF-7.	Estradiol	13-29	MDM2 proto-oncogene	Homo sapiens	78-82
11953887-7	2002	MDM2 splicing variants were present in tissues from alcohol- and autoimmune disorder-induced cirrhoses.	Alcohols	52-59	MDM2 proto-oncogene	Homo sapiens	0-4
11953887-8	2002	Sequencing of full-size mRNA revealed a MDM2 mis-sense mutation in an alcohol-induced cirrhosis.	Alcohols	70-77	MDM2 proto-oncogene	Homo sapiens	40-44
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	MDM2 proto-oncogene	Homo sapiens	161-165
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	MDM2 proto-oncogene	Homo sapiens	96-100
11960368-4	2002	This association was concurrent with phosphorylation of Akt (at Ser 473), and resulted in elevated expression of HDM2 and enhanced nuclear localization.	Serine	64-67	MDM2 proto-oncogene	Homo sapiens	113-117
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	MDM2 proto-oncogene	Homo sapiens	168-172
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	MDM2 proto-oncogene	Homo sapiens	109-113
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.	Irinotecan	125-135	MDM2 proto-oncogene	Homo sapiens	69-73
11948421-2	2002	We show that the product of the mdm2 proto-oncogene is able to sensitize MTT cells to ionizing radiation.	monooxyethylene trimethylolpropane tristearate	73-76	MDM2 proto-oncogene	Homo sapiens	32-36
11948421-4	2002	MTT cells expressing MDM2 (MTT-mdm2) are unable to respond to DNA damage with G2M arrest, and display a high percentage of apoptosis.	monooxyethylene trimethylolpropane tristearate	0-3	MDM2 proto-oncogene	Homo sapiens	21-25
11948421-4	2002	MTT cells expressing MDM2 (MTT-mdm2) are unable to respond to DNA damage with G2M arrest, and display a high percentage of apoptosis.	monooxyethylene trimethylolpropane tristearate	0-3	MDM2 proto-oncogene	Homo sapiens	27-35
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	MDM2 proto-oncogene	Homo sapiens	69-73
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	MDM2 proto-oncogene	Homo sapiens	46-50
12149568-3	2002	This study investigates the functions of the MDM2 oncogene in colon cancer growth and the potential value of MDM2 as a drug target for cancer therapy, by inhibiting MDM2 expression with an antisense anti-human-MDM2 oligonucleotide.	Oligonucleotides	215-230	MDM2 proto-oncogene	Homo sapiens	45-49
12149568-3	2002	This study investigates the functions of the MDM2 oncogene in colon cancer growth and the potential value of MDM2 as a drug target for cancer therapy, by inhibiting MDM2 expression with an antisense anti-human-MDM2 oligonucleotide.	Oligonucleotides	215-230	MDM2 proto-oncogene	Homo sapiens	109-113
12149568-3	2002	This study investigates the functions of the MDM2 oncogene in colon cancer growth and the potential value of MDM2 as a drug target for cancer therapy, by inhibiting MDM2 expression with an antisense anti-human-MDM2 oligonucleotide.	Oligonucleotides	215-230	MDM2 proto-oncogene	Homo sapiens	109-113
12149568-3	2002	This study investigates the functions of the MDM2 oncogene in colon cancer growth and the potential value of MDM2 as a drug target for cancer therapy, by inhibiting MDM2 expression with an antisense anti-human-MDM2 oligonucleotide.	Oligonucleotides	215-230	MDM2 proto-oncogene	Homo sapiens	109-113
12149568-7	2002	In vivo antitumor activity of the oligonucleotide occurred in a dose-dependent manner in both models and synergistically or additive therapeutic effects of MDM2 inhibition and the cancer chemotherapeutic agents 10-hydroxycamptothecin and 5-fluorouracil were also observed.	Oligonucleotides	34-49	MDM2 proto-oncogene	Homo sapiens	156-160
12149568-7	2002	In vivo antitumor activity of the oligonucleotide occurred in a dose-dependent manner in both models and synergistically or additive therapeutic effects of MDM2 inhibition and the cancer chemotherapeutic agents 10-hydroxycamptothecin and 5-fluorouracil were also observed.	Fluorouracil	238-252	MDM2 proto-oncogene	Homo sapiens	156-160
11960368-6	2002	Tryptic peptide and mutational analyses revealed evidence for an Akt phosphorylation site in HDM2 additional to the two consensus sites.	Peptides	8-15	MDM2 proto-oncogene	Homo sapiens	93-97
12149568-10	2002	This study should provide a basis for future development of anti-MDM2 antisense oligonucleotides as cancer therapeutic agents used alone or in combination with conventional chemotherapeutics.	Oligonucleotides	80-96	MDM2 proto-oncogene	Homo sapiens	65-69
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	MDM2 proto-oncogene	Homo sapiens	166-170
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	MDM2 proto-oncogene	Homo sapiens	71-75
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	MDM2 proto-oncogene	Homo sapiens	13-17
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	MDM2 proto-oncogene	Homo sapiens	110-114
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	MDM2 proto-oncogene	Homo sapiens	110-114
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	MDM2 proto-oncogene	Homo sapiens	36-41
12017271-2	2002	In this study we determined the therapeutic effects of an antisense anti-MDM2 oligonucleotide administered alone or in combination with the clinically used chemotherapeutic agents Paclitaxel and Irinotecan.	Oligonucleotides	78-93	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	74-78
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	MDM2 proto-oncogene	Homo sapiens	147-151
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	MDM2 proto-oncogene	Homo sapiens	175-179
12017271-2	2002	In this study we determined the therapeutic effects of an antisense anti-MDM2 oligonucleotide administered alone or in combination with the clinically used chemotherapeutic agents Paclitaxel and Irinotecan.	Irinotecan	195-205	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	35-39
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	MDM2 proto-oncogene	Homo sapiens	35-39
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	MDM2 proto-oncogene	Homo sapiens	14-18
11761456-6	2001	Inhibition of cisplatin-induced ERK activity by PD98059 resulted in decreased levels of p21WAF1, Gadd45 and Mdm2.	Cisplatin	14-23	MDM2 proto-oncogene	Homo sapiens	108-112
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	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	86-90
11705884-3	2001	In the present study, we investigated the functions of MDM2 oncogene in the growth of breast cancer and the potential value of MDM2 as a drug target for cancer therapy by inhibiting MDM2 expression with a specific antisense antihuman-MDM2 oligonucleotide (oligo).	Oligonucleotides	239-254	MDM2 proto-oncogene	Homo sapiens	127-131
11705884-3	2001	In the present study, we investigated the functions of MDM2 oncogene in the growth of breast cancer and the potential value of MDM2 as a drug target for cancer therapy by inhibiting MDM2 expression with a specific antisense antihuman-MDM2 oligonucleotide (oligo).	Oligonucleotides	239-254	MDM2 proto-oncogene	Homo sapiens	127-131
11705884-3	2001	In the present study, we investigated the functions of MDM2 oncogene in the growth of breast cancer and the potential value of MDM2 as a drug target for cancer therapy by inhibiting MDM2 expression with a specific antisense antihuman-MDM2 oligonucleotide (oligo).	Oligonucleotides	239-254	MDM2 proto-oncogene	Homo sapiens	127-131
11705884-3	2001	In the present study, we investigated the functions of MDM2 oncogene in the growth of breast cancer and the potential value of MDM2 as a drug target for cancer therapy by inhibiting MDM2 expression with a specific antisense antihuman-MDM2 oligonucleotide (oligo).	Oligonucleotides	239-244	MDM2 proto-oncogene	Homo sapiens	127-131
11705884-3	2001	In the present study, we investigated the functions of MDM2 oncogene in the growth of breast cancer and the potential value of MDM2 as a drug target for cancer therapy by inhibiting MDM2 expression with a specific antisense antihuman-MDM2 oligonucleotide (oligo).	Oligonucleotides	239-244	MDM2 proto-oncogene	Homo sapiens	127-131
11705884-3	2001	In the present study, we investigated the functions of MDM2 oncogene in the growth of breast cancer and the potential value of MDM2 as a drug target for cancer therapy by inhibiting MDM2 expression with a specific antisense antihuman-MDM2 oligonucleotide (oligo).	Oligonucleotides	239-244	MDM2 proto-oncogene	Homo sapiens	127-131
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	MDM2 proto-oncogene	Homo sapiens	35-39
11742497-5	2001	In 2 of the lines, SCMC and RD, the mdm2 gene caused between 2-fold and 61-fold increase in resistance to vincristine, etoposide and doxorubicin but not to cisplatin.	Vincristine	106-117	MDM2 proto-oncogene	Homo sapiens	36-40
11742497-5	2001	In 2 of the lines, SCMC and RD, the mdm2 gene caused between 2-fold and 61-fold increase in resistance to vincristine, etoposide and doxorubicin but not to cisplatin.	Etoposide	119-128	MDM2 proto-oncogene	Homo sapiens	36-40
11742497-5	2001	In 2 of the lines, SCMC and RD, the mdm2 gene caused between 2-fold and 61-fold increase in resistance to vincristine, etoposide and doxorubicin but not to cisplatin.	Doxorubicin	133-144	MDM2 proto-oncogene	Homo sapiens	36-40
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	MDM2 proto-oncogene	Homo sapiens	288-292
11761456-5	2001	In the ovarian carcinoma cell line A2780, cisplatin was shown to induce expression of p21WAF1, Gadd45 and Mdm2, but cisplatin had no effect on expression of Bax, Bcl-2, Bcl-x1, or Cyclin G.	Cisplatin	42-51	MDM2 proto-oncogene	Homo sapiens	106-110
11761456-6	2001	Inhibition of cisplatin-induced ERK activity by PD98059 resulted in decreased levels of p21WAF1, Gadd45 and Mdm2.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	48-55	MDM2 proto-oncogene	Homo sapiens	108-112
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	MDM2 proto-oncogene	Homo sapiens	194-198
11504915-3	2001	Mitogen-induced activation of phosphatidylinositol 3-kinase (PI3-kinase) and its downstream target, the Akt/PKB serine-threonine kinase, results in phosphorylation of Mdm2 on serine 166 and serine 186.	Serine	112-118	MDM2 proto-oncogene	Homo sapiens	167-171
11583595-5	2001	In contrast, replacement of serine 20 makes p53 highly sensitive to Mdm2-mediated turnover.	Serine	28-34	MDM2 proto-oncogene	Homo sapiens	68-72
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	MDM2 proto-oncogene	Homo sapiens	141-145
11504915-3	2001	Mitogen-induced activation of phosphatidylinositol 3-kinase (PI3-kinase) and its downstream target, the Akt/PKB serine-threonine kinase, results in phosphorylation of Mdm2 on serine 166 and serine 186.	Serine	175-181	MDM2 proto-oncogene	Homo sapiens	167-171
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	MDM2 proto-oncogene	Homo sapiens	64-68
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	MDM2 proto-oncogene	Homo sapiens	64-68
11562347-6	2001	Disruption of the p53-HDM2 interaction prevents Dex-induced ubiquitylation of GR and p53.	Dexamethasone	48-51	MDM2 proto-oncogene	Homo sapiens	22-26
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	MDM2 proto-oncogene	Homo sapiens	72-76
11526482-10	2001	In addition we show that like p14ARF, the proteasome inhibitor MG132 can promote the accumulation of Mdm2 in the nucleolus and that this can occur in the absence of p14ARF expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	MDM2 proto-oncogene	Homo sapiens	101-105
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	86-91
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	MDM2 proto-oncogene	Homo sapiens	152-156
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	MDM2 proto-oncogene	Homo sapiens	152-156
11279110-5	2001	Second, we examined the relationship between p53 and HDM2 in the adriamycin-mediated stabilization of p53 in NB.	Doxorubicin	65-75	MDM2 proto-oncogene	Homo sapiens	53-57
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	MDM2 proto-oncogene	Homo sapiens	123-127
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	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	112-116
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	MDM2 proto-oncogene	Homo sapiens	115-119
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	148-157	MDM2 proto-oncogene	Homo sapiens	115-119
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	148-157	MDM2 proto-oncogene	Homo sapiens	115-119
11327858-10	2001	The repeated motif contains Arg residues spaced by a hydrophobic segment that may be involved in Hdm2 recognition and binding.	Arginine	28-31	MDM2 proto-oncogene	Homo sapiens	97-101
11331603-0	2001	ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage.	Serine	41-47	MDM2 proto-oncogene	Homo sapiens	33-37
11331603-10	2001	Serine 395, residing within the carboxy-terminal 2A10 epitope, is the major target on Mdm2 for phosphorylation by ATM in vitro.	Serine	0-6	MDM2 proto-oncogene	Homo sapiens	86-90
11331603-11	2001	Mutational analysis supports the conclusion that Mdm2 undergoes ATM-dependent phosphorylation on serine 395 in vivo in response to DNA damage.	Serine	97-103	MDM2 proto-oncogene	Homo sapiens	49-53
11393276-1	2001	Recently, it has been demonstrated that Etoposide, a topoisomerase II inhibitor, can induce apoptosis in MDM2-overexpressing tumor cells by inhibition of MDM2 synthesis.	Etoposide	40-49	MDM2 proto-oncogene	Homo sapiens	105-109
11393276-1	2001	Recently, it has been demonstrated that Etoposide, a topoisomerase II inhibitor, can induce apoptosis in MDM2-overexpressing tumor cells by inhibition of MDM2 synthesis.	Etoposide	40-49	MDM2 proto-oncogene	Homo sapiens	154-158
11423970-0	2001	Activation of p53 by roscovitine-mediated suppression of MDM2 expression.	Roscovitine	21-32	MDM2 proto-oncogene	Homo sapiens	57-61
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	MDM2 proto-oncogene	Homo sapiens	204-208
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	MDM2 proto-oncogene	Homo sapiens	204-208
11423970-6	2001	Roscovitine induces down-regulation of MDM2 expression at both protein and mRNA levels.	Roscovitine	0-11	MDM2 proto-oncogene	Homo sapiens	39-43
11423970-7	2001	Ectopic expression of MDM2 can abrogate the ability of roscovitine to induce p53 stabilization.	Roscovitine	55-66	MDM2 proto-oncogene	Homo sapiens	22-26
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	MDM2 proto-oncogene	Homo sapiens	88-92
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	MDM2 proto-oncogene	Homo sapiens	52-56
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	MDM2 proto-oncogene	Homo sapiens	57-61
11306736-6	2001	However, the level of MDM2 was partially restored by proteasome inhibitors such as LLnL and lactacystin, even in the presence of etoposide.	lactacystin	92-103	MDM2 proto-oncogene	Homo sapiens	22-26
11306736-6	2001	However, the level of MDM2 was partially restored by proteasome inhibitors such as LLnL and lactacystin, even in the presence of etoposide.	Etoposide	129-138	MDM2 proto-oncogene	Homo sapiens	22-26
11178989-4	2001	MDM2 overexpressing clones derived from the breast cancer cell line, MCF-7 cells, showed a remarkable growth advantage only in estradiol supplemented conditions, and this profile coincided with increased transcriptional activity of ERalpha in these cells.	Estradiol	127-136	MDM2 proto-oncogene	Homo sapiens	0-4
11053443-0	2001	A role for the polyproline domain of p53 in its regulation by Mdm2.	polyproline	15-26	MDM2 proto-oncogene	Homo sapiens	62-66
11053443-5	2001	p53 lacking the polyproline region was identified to be more susceptible to inhibition by Mdm2.	polyproline	16-27	MDM2 proto-oncogene	Homo sapiens	90-94
11053443-7	2001	This increased sensitivity to Mdm2 results from an enhanced affinity of Mdm2 toward p53 lacking the polyproline region.	polyproline	100-111	MDM2 proto-oncogene	Homo sapiens	30-34
11053443-7	2001	This increased sensitivity to Mdm2 results from an enhanced affinity of Mdm2 toward p53 lacking the polyproline region.	polyproline	100-111	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	98-102
11148027-0	2001	Chalcone derivatives antagonize interactions between the human oncoprotein MDM2 and p53.	Chalcone	0-8	MDM2 proto-oncogene	Homo sapiens	63-79
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	MDM2 proto-oncogene	Homo sapiens	88-92
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	MDM2 proto-oncogene	Homo sapiens	88-92
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	MDM2 proto-oncogene	Homo sapiens	225-229
11178871-4	2001	Experimental blockade of Mdm2 expression with antisense oligodeoxynucleotides (ODN) results in neuronal death, suggesting an active role of Mdm2 in neuroprotection.	Oligodeoxyribonucleotides	56-77	MDM2 proto-oncogene	Homo sapiens	140-144
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	MDM2 proto-oncogene	Homo sapiens	174-178
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	MDM2 proto-oncogene	Homo sapiens	22-26
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	MDM2 proto-oncogene	Homo sapiens	121-125
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	MDM2 proto-oncogene	Homo sapiens	128-132
11178871-4	2001	Experimental blockade of Mdm2 expression with antisense oligodeoxynucleotides (ODN) results in neuronal death, suggesting an active role of Mdm2 in neuroprotection.	Oligodeoxyribonucleotides	56-77	MDM2 proto-oncogene	Homo sapiens	25-29
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	MDM2 proto-oncogene	Homo sapiens	101-105
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	MDM2 proto-oncogene	Homo sapiens	174-178
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	MDM2 proto-oncogene	Homo sapiens	101-105
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	MDM2 proto-oncogene	Homo sapiens	47-51
11140901-8	2001	Nevertheless, the high prevalence of MDM2 protein overexpression found in this study suggest that MDM2 may also participate in the carcinogenesis of AQ chewing-associated oral SCCs in Taiwan.	aq	149-151	MDM2 proto-oncogene	Homo sapiens	37-41
11140901-8	2001	Nevertheless, the high prevalence of MDM2 protein overexpression found in this study suggest that MDM2 may also participate in the carcinogenesis of AQ chewing-associated oral SCCs in Taiwan.	aq	149-151	MDM2 proto-oncogene	Homo sapiens	98-102
11094089-3	2000	Although the A4 mutant protein and the single lysine substitutions both bound MDM2 reasonably well, the single lysine substitutions underwent normal MDM2-dependent ubiquitination, whereas the A4 protein was inefficiently ubiquitinated.	Lysine	46-52	MDM2 proto-oncogene	Homo sapiens	78-82
11125034-0	2001	MDM2 mediated nuclear exclusion of p53 attenuates etoposide-induced apoptosis in neuroblastoma cells.	Etoposide	50-59	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	187-191
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	MDM2 proto-oncogene	Homo sapiens	14-18
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	MDM2 proto-oncogene	Homo sapiens	14-18
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	MDM2 proto-oncogene	Homo sapiens	14-18
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	MDM2 proto-oncogene	Homo sapiens	183-187
11716435-0	2000	Consequences of the inhibition of Hdm2 expression in human osteosarcoma cells using antisense oligonucleotides.	Oligonucleotides	94-110	MDM2 proto-oncogene	Homo sapiens	34-38
11716435-1	2000	The present study was performed to identify a potent and sequence-specific antisense oligonucleotide (ASO), to inhibit Hdm2 expression in human cancer cell lines and to study the downstream consequences.	Oligonucleotides	85-100	MDM2 proto-oncogene	Homo sapiens	119-123
11716435-1	2000	The present study was performed to identify a potent and sequence-specific antisense oligonucleotide (ASO), to inhibit Hdm2 expression in human cancer cell lines and to study the downstream consequences.	Oligonucleotides, Antisense	102-105	MDM2 proto-oncogene	Homo sapiens	119-123
11175332-2	2000	In X-irradiated human cells, HDM2 protein was rapidly phosphorylated in serine/threonine residues in a p53, p14ARF and p73-independent manner.	Serine	72-78	MDM2 proto-oncogene	Homo sapiens	29-33
11175332-2	2000	In X-irradiated human cells, HDM2 protein was rapidly phosphorylated in serine/threonine residues in a p53, p14ARF and p73-independent manner.	Threonine	79-88	MDM2 proto-oncogene	Homo sapiens	29-33
11175334-0	2000	DNA damage-induced phosphorylation of p53 at serine 20 correlates with p21 and Mdm-2 induction in vivo.	Serine	45-51	MDM2 proto-oncogene	Homo sapiens	79-84
11072252-0	2000	A novel MDM2 anti-sense oligonucleotide has anti-tumor activity and potentiates cytotoxic drugs acting by different mechanisms in human colon cancer.	Oligonucleotides	24-39	MDM2 proto-oncogene	Homo sapiens	8-12
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	MDM2 proto-oncogene	Homo sapiens	63-67
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	MDM2 proto-oncogene	Homo sapiens	144-148
11094089-0	2000	Multiple lysine mutations in the C-terminal domain of p53 interfere with MDM2-dependent protein degradation and ubiquitination.	Lysine	9-15	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	146-150
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	MDM2 proto-oncogene	Homo sapiens	22-26
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	MDM2 proto-oncogene	Homo sapiens	22-26
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	MDM2 proto-oncogene	Homo sapiens	195-199
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	MDM2 proto-oncogene	Homo sapiens	241-245
10995885-0	2000	Absence of p53-mediated G1 arrest with induction of MDM2 in sterigmatocystin-treated cells.	Sterigmatocystin	60-76	MDM2 proto-oncogene	Homo sapiens	52-56
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	MDM2 proto-oncogene	Homo sapiens	146-150
10723139-3	2000	We mutated the cysteine residue (C464) corresponding to the residue essential for the ubiquitin ligase activity of E6AP and this mutation diminished the ligase activity of MDM2.	Cysteine	15-23	MDM2 proto-oncogene	Homo sapiens	172-176
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	72-76
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	MDM2 proto-oncogene	Homo sapiens	94-98
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	MDM2 proto-oncogene	Homo sapiens	82-87
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	MDM2 proto-oncogene	Homo sapiens	135-140
10892746-2	2000	We demonstrate that Mdm2 is conjugated with SUMO-1 (sumoylated) at Lys-446, which is located within the RING finger domain and plays a critical role in Mdm2 self-ubiquitination.	Lysine	67-70	MDM2 proto-oncogene	Homo sapiens	20-24
10892746-2	2000	We demonstrate that Mdm2 is conjugated with SUMO-1 (sumoylated) at Lys-446, which is located within the RING finger domain and plays a critical role in Mdm2 self-ubiquitination.	Lysine	67-70	MDM2 proto-oncogene	Homo sapiens	152-156
10874665-6	2000	Mdm2 and p53 were demonstrated by immunohistology on formalin-fixed and paraffin-embedded tumor tissue.	Formaldehyde	53-61	MDM2 proto-oncogene	Homo sapiens	0-4
10874665-6	2000	Mdm2 and p53 were demonstrated by immunohistology on formalin-fixed and paraffin-embedded tumor tissue.	Paraffin	72-80	MDM2 proto-oncogene	Homo sapiens	0-4
10815906-4	2000	The overexpression of mdm2 and p53 proteins was investigated on paraffin-embedded material by using monoclonal antibodies.	Paraffin	64-72	MDM2 proto-oncogene	Homo sapiens	22-26
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	MDM2 proto-oncogene	Homo sapiens	84-100
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	MDM2 proto-oncogene	Homo sapiens	84-100
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	MDM2 proto-oncogene	Homo sapiens	84-100
10955790-12	2000	Interestingly, tumors with both negative mdm-2 and p21 expression, irrespective of p53 status, had a high response rate to docetaxel but no response to MF.	Docetaxel	123-132	MDM2 proto-oncogene	Homo sapiens	41-46
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	MDM2 proto-oncogene	Homo sapiens	13-17
10767389-0	2000	Prognostic value of simultaneous expression of p21 and mdm2 in breast carcinomas treated by adjuvant chemotherapy with antracyclin.	antracyclin	119-130	MDM2 proto-oncogene	Homo sapiens	55-59
10751633-0	2000	Absence of point mutations at codon 17 of the mdm2 gene (serine 17) in human primary tumors.	Serine	57-63	MDM2 proto-oncogene	Homo sapiens	46-50
10751633-2	2000	A serine located in position 17 of Mdm2, has been implicated in its phosphorylation process.	Serine	2-8	MDM2 proto-oncogene	Homo sapiens	35-39
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	MDM2 proto-oncogene	Homo sapiens	110-114
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	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	114-118
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	MDM2 proto-oncogene	Homo sapiens	114-118
10723139-4	2000	The cysteine residue described above is also one of the cysteine residues that form the RING finger domain of MDM2.	Cysteine	4-12	MDM2 proto-oncogene	Homo sapiens	110-114
10723139-4	2000	The cysteine residue described above is also one of the cysteine residues that form the RING finger domain of MDM2.	Cysteine	56-64	MDM2 proto-oncogene	Homo sapiens	110-114
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	MDM2 proto-oncogene	Homo sapiens	69-73
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	MDM2 proto-oncogene	Homo sapiens	205-209
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	MDM2 proto-oncogene	Homo sapiens	205-209
10737722-3	2000	The aim of the present study was to investigate whether mdm2-antisense oligodeoxyribonucleotides (AS-ODNs) can influence the growth characteristics of two MDM2-overexpressing STS cell lines (US8-93, LMS6-93) where both have heterozygous p53 non-missense mutations.	Oligodeoxyribonucleotides	71-96	MDM2 proto-oncogene	Homo sapiens	56-60
10810363-4	2000	This study investigated the effect of antisense oligodeoxynucleotides (ODNs), targeted against Mdm2 and p21WAF1/CIP1 on drug-mediated cell killing.	Oligodeoxyribonucleotides	48-69	MDM2 proto-oncogene	Homo sapiens	95-99
10810363-5	2000	Exposure of U2-OS osteosarcoma cells to DNA damaging agents, cisplatin or mitomycin C, caused upregulated expression of Mdm2 and p21WAF1/CIP1.	Cisplatin	61-70	MDM2 proto-oncogene	Homo sapiens	120-124
10810363-5	2000	Exposure of U2-OS osteosarcoma cells to DNA damaging agents, cisplatin or mitomycin C, caused upregulated expression of Mdm2 and p21WAF1/CIP1.	Mitomycin	74-85	MDM2 proto-oncogene	Homo sapiens	120-124
10788589-11	2000	Several approaches have now been tested using this strategy, including polypeptides targeted to MDM2-p53 binding domain and antisense oligonucleotides that specifically inhibit MDM2 expression.	Oligonucleotides	134-150	MDM2 proto-oncogene	Homo sapiens	177-181
10737722-3	2000	The aim of the present study was to investigate whether mdm2-antisense oligodeoxyribonucleotides (AS-ODNs) can influence the growth characteristics of two MDM2-overexpressing STS cell lines (US8-93, LMS6-93) where both have heterozygous p53 non-missense mutations.	Oligodeoxyribonucleotides	71-96	MDM2 proto-oncogene	Homo sapiens	155-159
10737722-4	2000	Cells were treated with lipofectamine-complexed mdm2 AS-ODNs complementary to a sequence of the mdm2 cDNA initiation site in comparison to sense control ODNs.	Lipofectamine	24-37	MDM2 proto-oncogene	Homo sapiens	48-52
10737722-4	2000	Cells were treated with lipofectamine-complexed mdm2 AS-ODNs complementary to a sequence of the mdm2 cDNA initiation site in comparison to sense control ODNs.	Lipofectamine	24-37	MDM2 proto-oncogene	Homo sapiens	96-100
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	MDM2 proto-oncogene	Homo sapiens	202-206
10656682-4	2000	Phosphorylation at serine 15 prevents the binding of HDM2, a negative regulator of p53.	Serine	19-25	MDM2 proto-oncogene	Homo sapiens	53-57
10656682-8	2000	Phosphorylation by DNA-PK, that modifies serines 15 and 37, inhibits HDM2 binding to p53 but does not induce the DNA-binding activity of p53.	Serine	41-48	MDM2 proto-oncogene	Homo sapiens	69-73
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	MDM2 proto-oncogene	Homo sapiens	26-30
10561590-5	1999	By using deletion mutants of mdm2 and a peptide library we identified the serine residue at position 269 which lies within a canonical CK2 consensus sequence (EGQELSDEDDE) as the most important CK2 phosphorylation site.	Serine	74-80	MDM2 proto-oncogene	Homo sapiens	29-33
10726657-8	2000	Furthermore, treatment with both E6-AP and MDM2 antisense oligonucleotides in HPV-positive cells does not lead to further induction of p53 over inhibition of E6-AP alone.	Oligonucleotides	58-74	MDM2 proto-oncogene	Homo sapiens	43-47
10775510-0	2000	P53-independent down-regulation of Mdm2 in human cancer cells treated with adriamycin.	Doxorubicin	75-85	MDM2 proto-oncogene	Homo sapiens	35-39
10775510-2	2000	In this study, we investigated the alteration of Mdm2 and p53 in three human cancer cell lines containing either a wild-type or mutant p53 gene after treatment with Adriamycin (doxorubicin, ADR), a DNA damaging agent.	Doxorubicin	165-175	MDM2 proto-oncogene	Homo sapiens	49-53
10775510-2	2000	In this study, we investigated the alteration of Mdm2 and p53 in three human cancer cell lines containing either a wild-type or mutant p53 gene after treatment with Adriamycin (doxorubicin, ADR), a DNA damaging agent.	Doxorubicin	177-188	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	14-18
10614665-6	2000	Cell cycle distribution of MDM2 transfectants [medullary thyroid tumor (MTT)-mdm2] revealed a fraction of the cell population in a hypodiploid status, suggesting that MDM2 is sufficient to promote apoptosis.	monooxyethylene trimethylolpropane tristearate	72-75	MDM2 proto-oncogene	Homo sapiens	27-31
10614665-6	2000	Cell cycle distribution of MDM2 transfectants [medullary thyroid tumor (MTT)-mdm2] revealed a fraction of the cell population in a hypodiploid status, suggesting that MDM2 is sufficient to promote apoptosis.	monooxyethylene trimethylolpropane tristearate	72-75	MDM2 proto-oncogene	Homo sapiens	167-171
10614665-12	2000	Protein levels of caspase-2, which are undetectable in the parental cell line, appear clearly elevated in MTT-mdm2 cells.	monooxyethylene trimethylolpropane tristearate	106-109	MDM2 proto-oncogene	Homo sapiens	110-114
10637478-2	2000	In the present study, we evaluated the incidence of MDM2 overexpression by ALL cells from pediatric patients at first relapse and compared MDM2 protein levels with in vitro response to adriamycin and with duration of initial complete remission (CR1).	Doxorubicin	185-195	MDM2 proto-oncogene	Homo sapiens	139-143
10637478-8	2000	Overexpression of MDM2 (&gt;/=10-fold) was significantly correlated with adriamycin resistance and decreased duration of CR1.	Doxorubicin	73-83	MDM2 proto-oncogene	Homo sapiens	18-22
10637478-12	2000	These results indicate that overexpression of MDM2 plays a significant role in refractory pediatric ALL and is associated with early relapse, adriamycin resistance, and failure to respond to re-induction therapy.	Doxorubicin	142-152	MDM2 proto-oncogene	Homo sapiens	46-50
10889922-3	2000	Formalin-fixed sections were submitted to monoclonal antibody anti-Mdm2 through use of the streptavidin-biotin method.	Formaldehyde	0-8	MDM2 proto-oncogene	Homo sapiens	67-71
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	MDM2 proto-oncogene	Homo sapiens	168-172
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	MDM2 proto-oncogene	Homo sapiens	202-206
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	MDM2 proto-oncogene	Homo sapiens	91-95
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	MDM2 proto-oncogene	Homo sapiens	194-198
10544021-8	1999	This p53 was co-immunoprecipitated with MDM2, but p53 activated by etoposide or doxorubicin barely complexed with MDM2.	Etoposide	67-76	MDM2 proto-oncogene	Homo sapiens	114-118
10544021-8	1999	This p53 was co-immunoprecipitated with MDM2, but p53 activated by etoposide or doxorubicin barely complexed with MDM2.	Doxorubicin	80-91	MDM2 proto-oncogene	Homo sapiens	114-118
10519756-4	1999	RESULTS: Positive immunostaining for MDM-2, proliferating cell nuclear antigen, cyclin D1, and cyclin A was occasionally observed in the large melanin-containing epithelioid cells.	Melanins	143-150	MDM2 proto-oncogene	Homo sapiens	37-42
10674873-0	1999	Mdm2 sensitizes MCF7 breast cancer cells to cisplatin or carboplatin.	Cisplatin	44-53	MDM2 proto-oncogene	Homo sapiens	0-4
10674873-0	1999	Mdm2 sensitizes MCF7 breast cancer cells to cisplatin or carboplatin.	Carboplatin	57-68	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	80-84
10674873-4	1999	MCF7-Mdm2 cells exhibited preferential sensitivity to cisplatin and carboplatin.	Cisplatin	54-63	MDM2 proto-oncogene	Homo sapiens	5-9
10674873-4	1999	MCF7-Mdm2 cells exhibited preferential sensitivity to cisplatin and carboplatin.	Carboplatin	68-79	MDM2 proto-oncogene	Homo sapiens	5-9
10674873-5	1999	MCF7-Mdm2 cells showed a pronounced S-phase arrest after cisplatin treatment, similar to that observed in mutant-p53 cells in the present and prior studies.	Cisplatin	57-66	MDM2 proto-oncogene	Homo sapiens	5-9
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	MDM2 proto-oncogene	Homo sapiens	29-33
10512695-1	1999	It is shown here that the N-terminal domain of MDM2, which is not thought to bind calcium ions, otherwise bears a striking resemblance to a cluster of four EF-hand modules like those found in the calmodulin family.	Calcium	82-89	MDM2 proto-oncogene	Homo sapiens	47-51
10493945-14	1999	This study should provide the basis for future development of anti-MDM2 antisense oligonucleotides as cancer therapeutic agents used alone or in combination with conventional chemotherapeutics.	Oligonucleotides	82-98	MDM2 proto-oncogene	Homo sapiens	67-71
11717960-0	1999	Interaction between gene p53 and oncogene mdm2 in human glandular lung cancer cell line GLC-82.	Glucose	88-91	MDM2 proto-oncogene	Homo sapiens	42-46
10491313-0	1999	Arsenic disrupts cellular levels of p53 and mdm2: a potential mechanism of carcinogenesis.	Arsenic	0-7	MDM2 proto-oncogene	Homo sapiens	44-48
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	MDM2 proto-oncogene	Homo sapiens	86-90
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	MDM2 proto-oncogene	Homo sapiens	37-41
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	MDM2 proto-oncogene	Homo sapiens	175-179
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	MDM2 proto-oncogene	Homo sapiens	126-131
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	MDM2 proto-oncogene	Homo sapiens	114-118
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	MDM2 proto-oncogene	Homo sapiens	49-53
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	MDM2 proto-oncogene	Homo sapiens	115-119
10397746-9	1999	Incubation of 3 different cell lines with DFO or 311 caused a pronounced concentration- and time-dependent increase in the expression of WAF1 and GADD45 mRNA, but not mdm-2 mRNA.	Deferoxamine	42-45	MDM2 proto-oncogene	Homo sapiens	167-172
10738909-7	1999	When the GI-101A cells were treated with DES (Diethylstilbestrol) the mdm-2 protein expression increased after 10 min treatment and reached a peak level at 40 min.	Diethylstilbestrol	41-44	MDM2 proto-oncogene	Homo sapiens	70-75
10738909-7	1999	When the GI-101A cells were treated with DES (Diethylstilbestrol) the mdm-2 protein expression increased after 10 min treatment and reached a peak level at 40 min.	Diethylstilbestrol	46-64	MDM2 proto-oncogene	Homo sapiens	70-75
10203582-2	1999	When transfected with a functional copy of the estrogen receptor, both ER and MDM2 expression are negatively regulated by the presence of increasing concentrations of estradiol, as previously reported.	Estradiol	167-176	MDM2 proto-oncogene	Homo sapiens	78-82
10222137-6	1999	Using a model cell line conditionally expressing MDM2, the murine analogue of HDM2, we present evidence indicating that leptomycin B abrogates MDM2"s role in p53 degradation and that the accumulation of p53 in distinct nuclear bodies is mediated by MDM2.	leptomycin B	120-132	MDM2 proto-oncogene	Homo sapiens	78-82
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	MDM2 proto-oncogene	Homo sapiens	6-10
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	MDM2 proto-oncogene	Homo sapiens	162-166
10078201-0	1999	RB regulates the stability and the apoptotic function of p53 via MDM2.	Rubidium	0-2	MDM2 proto-oncogene	Homo sapiens	65-69
10189892-7	1999	Moreover, mdm2 antisense oligonucleotides prevented E2-induced accumulation of p53.	Oligonucleotides	25-41	MDM2 proto-oncogene	Homo sapiens	10-14
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	MDM2 proto-oncogene	Homo sapiens	209-213
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	MDM2 proto-oncogene	Homo sapiens	123-127
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	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	92-96
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	MDM2 proto-oncogene	Homo sapiens	46-50
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	MDM2 proto-oncogene	Homo sapiens	92-96
10023685-3	1999	We show here that the topoisomerase poison etoposide, like ultra violet irradiation, inhibits Mdm2 synthesis.	Etoposide	43-52	MDM2 proto-oncogene	Homo sapiens	94-98
10023685-3	1999	We show here that the topoisomerase poison etoposide, like ultra violet irradiation, inhibits Mdm2 synthesis.	ultra violet	59-71	MDM2 proto-oncogene	Homo sapiens	94-98
10023685-4	1999	Cytotoxic concentrations of etoposide (IC90 for &gt; 3 h) result in inhibition of Mdm2 induction at both the RNA and protein level.	Etoposide	28-37	MDM2 proto-oncogene	Homo sapiens	82-86
10023685-7	1999	Inhibition of Mdm2 synthesis depends on the continuous presence of etoposide, suggesting the DNA damage may prevent transcription.	Etoposide	67-76	MDM2 proto-oncogene	Homo sapiens	14-18
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	MDM2 proto-oncogene	Homo sapiens	93-97
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	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	105-109
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	MDM2 proto-oncogene	Homo sapiens	105-109
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	MDM2 proto-oncogene	Homo sapiens	21-25
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	MDM2 proto-oncogene	Homo sapiens	105-109
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	MDM2 proto-oncogene	Homo sapiens	105-109
10072445-3	1999	MATERIALS AND METHODS: We have developed phosphorothioate antisense oligodeoxynucleotides optimized for inhibition of MDM2 expression and investigated the role of MDM2 in a large panel of tumor cell lines.	Parathion	41-57	MDM2 proto-oncogene	Homo sapiens	118-122
10072445-3	1999	MATERIALS AND METHODS: We have developed phosphorothioate antisense oligodeoxynucleotides optimized for inhibition of MDM2 expression and investigated the role of MDM2 in a large panel of tumor cell lines.	Oligodeoxyribonucleotides	68-89	MDM2 proto-oncogene	Homo sapiens	118-122
9836595-0	1998	Metal and RNA binding properties of the hdm2 RING finger domain.	Metals	0-5	MDM2 proto-oncogene	Homo sapiens	40-44
9836595-1	1998	The hdm2 oncoprotein contains a C-terminal domain that binds RNA and has been suggested to bind zinc(II) in an unusual RING finger domain in which Thr 455 was postulated as a ligand.	Zinc	96-104	MDM2 proto-oncogene	Homo sapiens	4-8
9836595-6	1998	Metal binding studies suggest that hdm2 indeed binds to two molecules of zinc in an intertwined motif similar to the BRCA1 RING finger peptide.	Metals	0-5	MDM2 proto-oncogene	Homo sapiens	35-39
9882094-0	1998	Metal and RNA binding properties of the hdm2 RING finger domain.	Metals	0-5	MDM2 proto-oncogene	Homo sapiens	40-44
9836595-1	1998	The hdm2 oncoprotein contains a C-terminal domain that binds RNA and has been suggested to bind zinc(II) in an unusual RING finger domain in which Thr 455 was postulated as a ligand.	Threonine	147-150	MDM2 proto-oncogene	Homo sapiens	4-8
9836595-9	1998	Studies of two mutant peptides confirm the assignment of binding residues in hdm2 and suggest that the coordination of Thr 455 previously proposed by sequence alignments is incorrect.	Threonine	119-122	MDM2 proto-oncogene	Homo sapiens	77-81
9836595-3	1998	We also tested the affinity of the hdm2 C-terminal peptide for metal binding, metal linkage to the folding of the C-terminal peptide, and the peptide"s affinity for RNA.	Metals	63-68	MDM2 proto-oncogene	Homo sapiens	35-39
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	MDM2 proto-oncogene	Homo sapiens	24-28
9836595-12	1998	However, distance measurement from fluorescence energy transfer indicated that the Tyr 489 residue was only approximately 14 A away from the first metal center, suggesting that the hdm2 protein exists in a compact form, at least in the presence of metal ion.	Tyrosine	83-86	MDM2 proto-oncogene	Homo sapiens	181-185
9836595-12	1998	However, distance measurement from fluorescence energy transfer indicated that the Tyr 489 residue was only approximately 14 A away from the first metal center, suggesting that the hdm2 protein exists in a compact form, at least in the presence of metal ion.	Metals	147-152	MDM2 proto-oncogene	Homo sapiens	181-185
9836595-12	1998	However, distance measurement from fluorescence energy transfer indicated that the Tyr 489 residue was only approximately 14 A away from the first metal center, suggesting that the hdm2 protein exists in a compact form, at least in the presence of metal ion.	Metals	248-253	MDM2 proto-oncogene	Homo sapiens	181-185
9836595-13	1998	In summary, hdm2 binds metal and RNA, but the RNA binding does not seem to occur in a zinc-dependent manner.	Metals	23-28	MDM2 proto-oncogene	Homo sapiens	12-16
9840926-2	1998	MDM2 is cleaved by Caspase 3 (CPP32) during apoptosis after aspartic acid-361, generating a 60 kd fragment.	Aspartic Acid	60-73	MDM2 proto-oncogene	Homo sapiens	0-4
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	MDM2 proto-oncogene	Homo sapiens	91-96
9819415-4	1998	It is predicted that LMB should inhibit nuclear-cytoplasmic shuttling by MDM2 and subsequently stabilize p53.	leptomycin B	21-24	MDM2 proto-oncogene	Homo sapiens	73-77
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	MDM2 proto-oncogene	Homo sapiens	47-51
9661637-7	1998	In BHT-101 cells, induction of p21 and Mdm-2 was evident 10 h after infection.	Butylated Hydroxytoluene	3-6	MDM2 proto-oncogene	Homo sapiens	39-44
11189516-11	1998	Two of 4 patients with MDM2+++ gained CR and then MDM2 turned negative.	Chromium	38-40	MDM2 proto-oncogene	Homo sapiens	23-27