PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset
33857626-0 2021 Sodium fluoride activates the extrinsic apoptosis via regulating NOX4/ROS-mediated p53/DR5 signaling pathway in lung cells both in vitro and in vivo. Reactive Oxygen Species 70-73 tumor protein p53 Homo sapiens 83-86
33857626-8 2021 Specifically, NOX4 knockdown inhibited NaF-induced the activation of p53/DR5 axis by reducing NOX4-derived ROS production. Reactive Oxygen Species 107-110 tumor protein p53 Homo sapiens 69-72
33325610-9 2021 Co-administration of the ROS inhibitor NAC largely abolished the up-regulated p53 protein level, and rescued the suppressed viability and colony formation ability in butein-exposed U-2 OS cells. Reactive Oxygen Species 25-28 tumor protein p53 Homo sapiens 78-81
33781788-6 2021 Pre-treatment with N-acetylcysteine (NAC, a ROS scavenger) demonstrated that reactive oxygen species (ROS) mediated T-17-induced p53-independent apoptosis. Reactive Oxygen Species 77-100 tumor protein p53 Homo sapiens 129-132
33781788-6 2021 Pre-treatment with N-acetylcysteine (NAC, a ROS scavenger) demonstrated that reactive oxygen species (ROS) mediated T-17-induced p53-independent apoptosis. Reactive Oxygen Species 102-105 tumor protein p53 Homo sapiens 129-132
33992677-7 2021 TF footprinting analysis of our ATAC-seq experiments identified 5 TFs or TF families with evidence for ROS-responsive changes in DNA binding: NRF2, AP-1, p53, NFY, and SP/KLF. Reactive Oxygen Species 103-106 tumor protein p53 Homo sapiens 154-157
33325610-10 2021 Taken together, our data proposed the increased ROS by butein exposure activated p53, and the activated p53 was involved in the anti-proliferative effect of butein via inducing senescence in U-2 OS cells. Reactive Oxygen Species 48-51 tumor protein p53 Homo sapiens 81-84
33713969-8 2021 Futhermore, the ferritinophagy-mediated ROS production triggered p53 activation. Reactive Oxygen Species 40-43 tumor protein p53 Homo sapiens 65-68
33181285-0 2021 Antrodia camphorata extract (ACE)-induced apoptosis is associated with BMP4 expression and p53-dependent ROS generation in human colon cancer cells. Reactive Oxygen Species 105-108 tumor protein p53 Homo sapiens 91-94
33925065-7 2021 6-Gingerol induced cellular and mitochondrial ROS that elevated DDR through ataxia-telangiectasia mutated and p53 activation. Reactive Oxygen Species 46-49 tumor protein p53 Homo sapiens 110-113
33181285-14 2021 We found that cell death is reversible via inactivation or knockdown of p53 gene and reduction of reactive oxygen species (ROS) generation in response to ACE exposure, indicating that p53 plays an important role in ROS generation induced by ACE. Reactive Oxygen Species 98-121 tumor protein p53 Homo sapiens 184-187
33181285-14 2021 We found that cell death is reversible via inactivation or knockdown of p53 gene and reduction of reactive oxygen species (ROS) generation in response to ACE exposure, indicating that p53 plays an important role in ROS generation induced by ACE. Reactive Oxygen Species 123-126 tumor protein p53 Homo sapiens 184-187
33181285-14 2021 We found that cell death is reversible via inactivation or knockdown of p53 gene and reduction of reactive oxygen species (ROS) generation in response to ACE exposure, indicating that p53 plays an important role in ROS generation induced by ACE. Reactive Oxygen Species 215-218 tumor protein p53 Homo sapiens 72-75
33181285-14 2021 We found that cell death is reversible via inactivation or knockdown of p53 gene and reduction of reactive oxygen species (ROS) generation in response to ACE exposure, indicating that p53 plays an important role in ROS generation induced by ACE. Reactive Oxygen Species 215-218 tumor protein p53 Homo sapiens 184-187
33181285-16 2021 CONCLUSION: Our findings demonstrate that ACE has potential as an anticancer agent that induces apoptosis through BMP4 and p53-dependent response to ROS in human colon cancer. Reactive Oxygen Species 149-152 tumor protein p53 Homo sapiens 123-126
33546421-5 2021 Frequent genetic alterations observed in pancreatic ductal adenocarcinoma (PDAC) affect KRAS and p53 proteins, which have a role in ROS production and control, respectively. Reactive Oxygen Species 132-135 tumor protein p53 Homo sapiens 97-100
33271245-9 2021 Probably triggered by the higher ROS levels and mitochondrial dysfunction, the gene expression of p53 and p21 increased and the gene expression of CDK4/6 decreased in response to the methoxyeugenol treatment. Reactive Oxygen Species 33-36 tumor protein p53 Homo sapiens 98-101
33670160-2 2021 Today we know that p53 plays a role in different biological processes such as proliferation, invasion, pluripotency, metabolism, cell cycle control, ROS (reactive oxygen species) production, apoptosis, inflammation and autophagy. Reactive Oxygen Species 149-152 tumor protein p53 Homo sapiens 19-22
33670160-2 2021 Today we know that p53 plays a role in different biological processes such as proliferation, invasion, pluripotency, metabolism, cell cycle control, ROS (reactive oxygen species) production, apoptosis, inflammation and autophagy. Reactive Oxygen Species 154-177 tumor protein p53 Homo sapiens 19-22
33542214-2 2021 In response to low-level ROS stress, the expression of Delta133p53, a human p53 isoform, is upregulated to promote cell survival and protect cells from senescence by enhancing the expression of antioxidant genes. Reactive Oxygen Species 25-28 tumor protein p53 Homo sapiens 63-66
33356180-11 2021 Taken together, DFS triggered p53-dependent apoptosis in HCEP cells via ROS-mediated crosstalk between the extrinsic and intrinsic pathways. Reactive Oxygen Species 72-75 tumor protein p53 Homo sapiens 30-33
33498875-6 2021 Particularly, basal-like TNBC cells characterized by inactivated BRCA1 and mutated TP53 produce high ROS levels and rely on ROS signaling for their survival and malignant progression. Reactive Oxygen Species 101-104 tumor protein p53 Homo sapiens 83-87
33446200-11 2021 Interestingly, VP treated protein lysates showed a ROS-dependent high molecular weight (HMW) band when probed for P62 and P53 protein. Reactive Oxygen Species 51-54 tumor protein p53 Homo sapiens 122-125
33137455-2 2021 To elucidate the manner in which p53 deals with glucose-deprived, reactive oxygen species (ROS)-prone conditions in this regard, two isogenic cancer subclones (HN3R-A and HN3R-B) bearing distinct p53 mutations as an in vitro model of intratumoral p53 heterogeneity were identified. Reactive Oxygen Species 66-89 tumor protein p53 Homo sapiens 33-36
33128380-6 2021 A significant increase in intracellular reactive oxygen species level was also observed, suggesting that regulation of apoptotic proteins triggered by myricetin exposure in lymphocytes from myeloma patients occurred through P53 and oxidative stress-dependent pathways. Reactive Oxygen Species 40-63 tumor protein p53 Homo sapiens 224-227
33137455-2 2021 To elucidate the manner in which p53 deals with glucose-deprived, reactive oxygen species (ROS)-prone conditions in this regard, two isogenic cancer subclones (HN3R-A and HN3R-B) bearing distinct p53 mutations as an in vitro model of intratumoral p53 heterogeneity were identified. Reactive Oxygen Species 91-94 tumor protein p53 Homo sapiens 33-36
33137455-5 2021 However, in glucose-deprived and ROS-prone conditions, HN3R-B, the subclone with the original p53 increased the utilization of glutamine by GLS2, thereby maintaining redox homeostasis and ATP. Reactive Oxygen Species 33-36 tumor protein p53 Homo sapiens 94-97
33137455-6 2021 Conversely, HN3R-A, the p53-deficient radioresistant subclone displayed an impairment in glutamine usage and high susceptibility to metabolic stresses as well as ROS-inducing agents despite the increased ROS scavenging system. Reactive Oxygen Species 162-165 tumor protein p53 Homo sapiens 24-27
33137455-6 2021 Conversely, HN3R-A, the p53-deficient radioresistant subclone displayed an impairment in glutamine usage and high susceptibility to metabolic stresses as well as ROS-inducing agents despite the increased ROS scavenging system. Reactive Oxygen Species 204-207 tumor protein p53 Homo sapiens 24-27
33137455-7 2021 Collectively, our findings suggest that p53 governs the alternative utilization of metabolic ingredients, such as glucose and glutamine, in ROS-prone conditions. Reactive Oxygen Species 140-143 tumor protein p53 Homo sapiens 40-43
33137455-8 2021 Thus, p53 status may be an important biomarker for selecting cancer treatment strategies, including metabolic drugs and ROS-inducing agents, for recurrent cancers after radiotherapy. Reactive Oxygen Species 120-123 tumor protein p53 Homo sapiens 6-9
32958825-5 2020 RESULTS: CB11 causes cell death via ROS-mediated ATM-p53-GADD45alpha signalling in human NSCLC cells, and diphenyleneiodonium (DPI), an NADPH oxidase inhibitor, decreases cell death by inhibiting CB11-mediated ATM signalling. Reactive Oxygen Species 36-39 tumor protein p53 Homo sapiens 53-56
32864863-3 2021 This study evaluates the role of p53 in curcumin mediated ROS generation and cell death. Reactive Oxygen Species 58-61 tumor protein p53 Homo sapiens 33-36
32864863-5 2021 ROS generation occurs within 1 hour of 40 microM curcumin treatment and a reduction was observed by third hour in HCT-116 insinuating p53 involvement. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 134-137
33179088-4 2021 The present study demonstrated that reactive oxygen species induced by H2O2 resulted in human granulosa COV434 cell apoptosis via the regulation of sirtuin 1 (SIRT1)-mediated p53 activity. Reactive Oxygen Species 36-59 tumor protein p53 Homo sapiens 197-200
33293849-5 2020 Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFkappaB/IkappaB, Nrf2/KEAP1, AP-1, p53, HIF-1). Reactive Oxygen Species 28-31 tumor protein p53 Homo sapiens 286-289
32151151-0 2020 ROS induced p53 activation: DNA damage, redox signaling or both? Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 12-15
31875760-8 2020 ROS-mediated DNA damage was observed as reflected by the activation of ATM/ATR, p53 and histone. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 80-83
32905825-0 2020 4-Aminobiphenyl suppresses homologous recombination repair by a reactive oxygen species-dependent p53/miR-513a-5p/p53 loop. Reactive Oxygen Species 64-87 tumor protein p53 Homo sapiens 98-101
32905825-0 2020 4-Aminobiphenyl suppresses homologous recombination repair by a reactive oxygen species-dependent p53/miR-513a-5p/p53 loop. Reactive Oxygen Species 64-87 tumor protein p53 Homo sapiens 114-117
32905825-5 2020 On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells. Reactive Oxygen Species 149-172 tumor protein p53 Homo sapiens 33-36
32905825-5 2020 On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells. Reactive Oxygen Species 149-172 tumor protein p53 Homo sapiens 189-192
32905825-5 2020 On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells. Reactive Oxygen Species 174-177 tumor protein p53 Homo sapiens 33-36
32905825-6 2020 These findings indicated that the ROS/p53/miR-513a-5p/p53 loop axis plays a relevant role in regulating HR repair which may facilitate our understanding of molecular mechanisms regarding how miR-513a-5p impacts DSB repair in 4-ABP-treated cells. Reactive Oxygen Species 34-37 tumor protein p53 Homo sapiens 38-41
32905825-6 2020 These findings indicated that the ROS/p53/miR-513a-5p/p53 loop axis plays a relevant role in regulating HR repair which may facilitate our understanding of molecular mechanisms regarding how miR-513a-5p impacts DSB repair in 4-ABP-treated cells. Reactive Oxygen Species 34-37 tumor protein p53 Homo sapiens 54-57
32093585-6 2020 Previous studies have also shown that p53 reduces intracellular ROS. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 38-41
32151151-4 2020 It is therefore not clear whether the observed activation of p53 by ROS is mediated through the DNA damage response, redox signaling or both. Reactive Oxygen Species 68-71 tumor protein p53 Homo sapiens 61-64
32818504-0 2020 Aconitase 2 sensitizes MCF-7 cells to cisplatin eliciting p53-mediated apoptosis in a ROS-dependent manner. Reactive Oxygen Species 86-89 tumor protein p53 Homo sapiens 58-61
32818504-5 2020 This response was driven by the accumulation of reactive oxygen species (ROS) following both ACO2 overexpression and CDDP exposure that permit the stabilization/activation of p53 in nuclear and mitochondrial compartments. Reactive Oxygen Species 48-71 tumor protein p53 Homo sapiens 175-178
32818504-5 2020 This response was driven by the accumulation of reactive oxygen species (ROS) following both ACO2 overexpression and CDDP exposure that permit the stabilization/activation of p53 in nuclear and mitochondrial compartments. Reactive Oxygen Species 73-76 tumor protein p53 Homo sapiens 175-178
32317087-1 2020 Protein kinase CK2 downregulation induces premature senescence in various human cell types via activation of the reactive oxygen species (ROS)-p53-p21Cip1/WAF1 pathway. Reactive Oxygen Species 113-136 tumor protein p53 Homo sapiens 143-146
32578917-0 2020 A synthetic coumarin derivative (4-flourophenylacetamide-acetyl coumarin) impedes cell cycle at G0/G1 stage, induces apoptosis, and inhibits metastasis via ROS-mediated p53 and AKT signaling pathways in A549 cells. Reactive Oxygen Species 156-159 tumor protein p53 Homo sapiens 169-172
33041795-10 2020 Furthermore, TQ-stimulated increase of reactive oxygen species (ROS) in p53-depleted cells was more pronounced than that in cells with intact p53. Reactive Oxygen Species 39-62 tumor protein p53 Homo sapiens 72-75
32878253-7 2020 These ROS-mediated responses induce caspase-dependent apoptosis via the activation of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), CCAAT/enhancer-binding protein homologous protein (chop), and phosphoprotein p53 gene expressions. Reactive Oxygen Species 6-9 tumor protein p53 Homo sapiens 207-225
32294550-11 2020 ROS might contribute to ER stress and further induce apoptosis via the JNK/p53/p21 pathway. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 75-78
32508052-11 2020 RNA-seq analysis identified p53 activation and other signatures accompanying this transdifferentiation; however, the p53 stabilizer nutlin-3 induced alphaSMA expression through reactive oxygen species generation but not through the p53 transcription/mitochondria-dependent pathway, whereas the p38 inhibitor SB203580 could partially inhibit alphaSMA expression. Reactive Oxygen Species 177-200 tumor protein p53 Homo sapiens 117-120
32508052-11 2020 RNA-seq analysis identified p53 activation and other signatures accompanying this transdifferentiation; however, the p53 stabilizer nutlin-3 induced alphaSMA expression through reactive oxygen species generation but not through the p53 transcription/mitochondria-dependent pathway, whereas the p38 inhibitor SB203580 could partially inhibit alphaSMA expression. Reactive Oxygen Species 177-200 tumor protein p53 Homo sapiens 117-120
32297368-6 2020 The biomarker p53 (K373) was able to distinguish genotoxicants from non-genotoxicants (2/4), while the induction of reactive oxygen species (ROS), potentially causing DNA damage, was associated with a positive Nrf2 (S40) response (2/2). Reactive Oxygen Species 141-144 tumor protein p53 Homo sapiens 14-17
32552932-8 2020 CONCLUSION: DHA can induce ROS production in Jurkat cells, which can cause DNA damage, activate the P53 apoptotic pathway, and promote apoptosis of cells. Reactive Oxygen Species 27-30 tumor protein p53 Homo sapiens 100-103
32942193-7 2020 Further study revealed that ROS-related mitochondrial translocation of p53 was also involved in 1f-induced mitochondrial apoptotic pathway. Reactive Oxygen Species 28-31 tumor protein p53 Homo sapiens 71-74
33041795-10 2020 Furthermore, TQ-stimulated increase of reactive oxygen species (ROS) in p53-depleted cells was more pronounced than that in cells with intact p53. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 72-75
32317087-1 2020 Protein kinase CK2 downregulation induces premature senescence in various human cell types via activation of the reactive oxygen species (ROS)-p53-p21Cip1/WAF1 pathway. Reactive Oxygen Species 138-141 tumor protein p53 Homo sapiens 143-146
32391458-10 2020 Experimental data suggest that CeO2 treatment causes DNA fragmentation through enhanced generation of ROS, which ultimately leads to cellular apoptosis through the p53-dependent mitochondrial signaling pathway. Reactive Oxygen Species 102-105 tumor protein p53 Homo sapiens 164-167
31894323-14 2020 The present results suggested that miR-335-5p expression levels in trophoblast cells could be increased by ROS in a p53-dependent manner, leading to the downregulation of Sp1 and subsequent inhibition of epithelial to mesenchymal transition and cell migration. Reactive Oxygen Species 107-110 tumor protein p53 Homo sapiens 116-119
32150881-2 2020 The ROS damage biomolecules such as DNA (including p53 gene), RNA, and lipids, and activate inflammatory, angiogenic, and extracellular matrix (ECM) remodeling proteins; which collectively facilitate carcinogenesis. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 51-54
32237321-9 2020 Further studies showed that after combined use, the number of clonogen formation in A549 cells was significantly reduced(P<0.01); ROS production was increased; the expression of apoptosis-related protein p53 was up-regulated, and the ratio of Bcl-2/Bax was decreased. Reactive Oxygen Species 130-133 tumor protein p53 Homo sapiens 204-207
32111081-0 2020 Mutant p53-Associated Molecular Mechanisms of ROS Regulation in Cancer Cells. Reactive Oxygen Species 46-49 tumor protein p53 Homo sapiens 7-10
32111081-4 2020 Several studies reported that in contrast with the wild type protein, mutant p53 isoforms fail to exert antioxidant activities and rather increase intracellular ROS, driving a pro-tumorigenic survival. Reactive Oxygen Species 161-164 tumor protein p53 Homo sapiens 77-80
32111081-5 2020 These pro-oxidant oncogenic abilities of GOF mutant p53 include signaling and metabolic rewiring, as well as the modulation of critical ROS-related transcription factors and antioxidant systems, which lead ROS unbalance linked to tumor progression. Reactive Oxygen Species 136-139 tumor protein p53 Homo sapiens 52-55
32111081-5 2020 These pro-oxidant oncogenic abilities of GOF mutant p53 include signaling and metabolic rewiring, as well as the modulation of critical ROS-related transcription factors and antioxidant systems, which lead ROS unbalance linked to tumor progression. Reactive Oxygen Species 206-209 tumor protein p53 Homo sapiens 52-55
32111081-6 2020 The studies summarized here highlight that GOF mutant p53 isoforms might constitute major targets for selective therapeutic intervention against several types of tumors and that ROS enhancement driven by mutant p53 might represent an "Achilles heel" of cancer cells, suggesting pro-oxidant drugs as a therapeutic approach for cancer patients bearing the mutant TP53 gene. Reactive Oxygen Species 178-181 tumor protein p53 Homo sapiens 211-214
32175417-11 2020 Gene regulation network suggested that GPX1 mainly involved in pathways including the glutathione metabolism, ferroptosis, TP53 regulates metabolic genes, reactive oxygen species (ROS) metabolic process, and several other signaling pathways. Reactive Oxygen Species 155-178 tumor protein p53 Homo sapiens 123-127
32175417-11 2020 Gene regulation network suggested that GPX1 mainly involved in pathways including the glutathione metabolism, ferroptosis, TP53 regulates metabolic genes, reactive oxygen species (ROS) metabolic process, and several other signaling pathways. Reactive Oxygen Species 180-183 tumor protein p53 Homo sapiens 123-127
31995555-8 2020 Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC). Reactive Oxygen Species 181-184 tumor protein p53 Homo sapiens 87-90
32515564-8 2020 CONCLUSION: In Namalva cells that do not produce EBV antigens the treatment of CA results in suppression of ROS generation and activation of the expression of genes ISG15 and P53 (TP53); in P3HR-1 cells producing EBV antigens, the opposite picture is observed - the formation of ROS and the expression of the IFN-alpha and IFN-lambda genes are activated and the activity of the ISG15 and P53 (TP53) genes is suppressed. Reactive Oxygen Species 279-282 tumor protein p53 Homo sapiens 180-184
31691131-6 2020 It facilitates p53-mediated apoptosis through the production of reactive oxygen species, nitric oxide and inflammatory cytokines in Mtb-infected M1 macrophages. Reactive Oxygen Species 64-87 tumor protein p53 Homo sapiens 15-18
31995555-9 2020 These findings indicate that the combination of CGA, TC-HT, and LIPEF may be a promising modality for cancer treatment, as it can induce p53-dependent cell cycle arrest and apoptosis through accumulation of ROS in PANC-1 cells. Reactive Oxygen Species 207-210 tumor protein p53 Homo sapiens 137-140
32076462-11 2020 p53 played a key role in inhibiting ROS generation in GC cells, thereby inhibiting apoptosis. Reactive Oxygen Species 36-39 tumor protein p53 Homo sapiens 0-3
31752383-15 2019 In conclusion, the above data suggested that ROS could induce DNA damage and activating p53/PUMA/Bax signaling, and thus, this resulted in the permeabilization of mitochondrial outer membrane and activating caspases as well as sensitizing the HCC cell to apoptosis induced by TRAIL and ASH treatment. Reactive Oxygen Species 45-48 tumor protein p53 Homo sapiens 88-91
31605953-10 2019 The overexpression of GSTM1 in the above cell lines led to a significant decrease in ROS and an increase in GSH concentration and TP53 levels, suggesting that the controversial role of GSTM1 resulted from the TP53 genotype of HCC cells. Reactive Oxygen Species 85-88 tumor protein p53 Homo sapiens 209-213
31605953-13 2019 GSTM1 also regulates tumor progression by disrupting the ROS-TP53 axis in HCC cells with different genetic backgrounds. Reactive Oxygen Species 57-60 tumor protein p53 Homo sapiens 61-65
31163195-6 2019 Moreover, SG significantly inhibited HCC cell proliferation in a p53-dependent manner by inducing cell cycle arrest and reactive oxygen species (ROS)-associated apoptosis. Reactive Oxygen Species 120-143 tumor protein p53 Homo sapiens 65-68
31339234-5 2019 In our research, it was also found that the reactivation of p53 induced by oridonin was closely related with the generation of ROS (reactive oxygen species). Reactive Oxygen Species 127-130 tumor protein p53 Homo sapiens 60-63
31339234-5 2019 In our research, it was also found that the reactivation of p53 induced by oridonin was closely related with the generation of ROS (reactive oxygen species). Reactive Oxygen Species 132-155 tumor protein p53 Homo sapiens 60-63
31462222-9 2019 ARE induced cell death in G361 cells through the reactive oxygen species (ROS)-dependent regulation of p53 and p21 in G361 cells. Reactive Oxygen Species 49-72 tumor protein p53 Homo sapiens 103-106
31462222-9 2019 ARE induced cell death in G361 cells through the reactive oxygen species (ROS)-dependent regulation of p53 and p21 in G361 cells. Reactive Oxygen Species 74-77 tumor protein p53 Homo sapiens 103-106
31462222-11 2019 CONCLUSION: The treatment of ARE preferentially induces apoptosis in melanoma cells by the ROS-dependent differential regulation of p53 level. Reactive Oxygen Species 91-94 tumor protein p53 Homo sapiens 132-135
31096598-8 2019 Our data indicates a pro-oxidative and apoptotic mode of EEP action in the presence of excess copper, wherein ROS/p53/p38 interactions play an important role in death cascades. Reactive Oxygen Species 110-113 tumor protein p53 Homo sapiens 114-117
31428569-0 2019 Lobaplatin-Induced Apoptosis Requires p53-Mediated p38MAPK Activation Through ROS Generation in Non-Small-Cell Lung Cancer. Reactive Oxygen Species 78-81 tumor protein p53 Homo sapiens 38-41
31428569-10 2019 Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells. Reactive Oxygen Species 87-110 tumor protein p53 Homo sapiens 61-64
31428569-10 2019 Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells. Reactive Oxygen Species 87-110 tumor protein p53 Homo sapiens 177-180
31428569-10 2019 Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells. Reactive Oxygen Species 181-184 tumor protein p53 Homo sapiens 61-64
31428569-10 2019 Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells. Reactive Oxygen Species 181-184 tumor protein p53 Homo sapiens 177-180
31360122-0 2019 p53 sensitizes chemoresistant non-small cell lung cancer via elevation of reactive oxygen species and suppression of EGFR/PI3K/AKT signaling. Reactive Oxygen Species 74-97 tumor protein p53 Homo sapiens 0-3
31360122-6 2019 In this study, we investigated the role of p53 in regulation of ROS production and EGFR signaling, and the chemosensitivity of NSCLC. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 43-46
31360122-10 2019 Results: We have demonstrated for the first time that activation of p53 sensitizes chemoresistant NSCLC cells to CDDP by down-regulating EGFR signaling pathway and promoting intracellular ROS production. Reactive Oxygen Species 188-191 tumor protein p53 Homo sapiens 68-71
31360122-12 2019 Our findings suggest that CDDP-induced apoptosis in chemosensitive NSCLC cells involves p53 activation, leading to suppressed EGFR signaling and ROS production. Reactive Oxygen Species 145-148 tumor protein p53 Homo sapiens 88-91
31059712-11 2019 The obtained results confirmed that the anti-proliferative mechanism and increased reactive oxygen species level of DS was associated with down-regulation of TrxR1 pathway which triggers the p53 mediated intrinsic apoptotic mode of cell death in NSCLC cells. Reactive Oxygen Species 83-106 tumor protein p53 Homo sapiens 191-194
31078603-6 2019 Furthermore, exposure to the Fe(II) complex led to excessive reactive oxygen species (ROS) accumulation by thioredoxin reductase (TrxR) inhibition and DNA double-strand breaks (DSBs), which in turn sequentially activated ATM, CHK1/2 and p53. Reactive Oxygen Species 61-84 tumor protein p53 Homo sapiens 237-240
31078603-6 2019 Furthermore, exposure to the Fe(II) complex led to excessive reactive oxygen species (ROS) accumulation by thioredoxin reductase (TrxR) inhibition and DNA double-strand breaks (DSBs), which in turn sequentially activated ATM, CHK1/2 and p53. Reactive Oxygen Species 86-89 tumor protein p53 Homo sapiens 237-240
31196889-6 2019 We explored the mechanism of this and found the reactive oxygen species (ROS) activity of ZMC1 negates the signal on p53 that is generated with chemotherapy and radiation. Reactive Oxygen Species 48-71 tumor protein p53 Homo sapiens 117-120
31196889-6 2019 We explored the mechanism of this and found the reactive oxygen species (ROS) activity of ZMC1 negates the signal on p53 that is generated with chemotherapy and radiation. Reactive Oxygen Species 73-76 tumor protein p53 Homo sapiens 117-120
30972978-0 2019 Zinc cooperates with p53 to inhibit the activity of mitochondrial aconitase through reactive oxygen species accumulation. Reactive Oxygen Species 84-107 tumor protein p53 Homo sapiens 21-24
30924710-2 2019 Recent studies, however, have indicated that Nrf2 induction stimulates the development of pre-existing tumors and confers resistance to chemotherapy by elevating drug metabolism and by efficient scavenging of ROS produced by the Warburg effect, which is regulated, in turn, by the p53 tumor suppressor. Reactive Oxygen Species 209-212 tumor protein p53 Homo sapiens 281-284
30972978-6 2019 Both zinc and p53 can lead to an increase in ROS. Reactive Oxygen Species 45-48 tumor protein p53 Homo sapiens 14-17
30813936-12 2019 CONCLUSIONS: The delay in DSB repair and lower sensitivity to daunorubicin seen in the B lymphocyte derived SUP-B15 cells could be due to loss of function of p53 that may be correlated to increased expression of SOD2 and lower ROS production. Reactive Oxygen Species 227-230 tumor protein p53 Homo sapiens 158-161
30865562-0 2019 Stretching magnitude-dependent inactivation of AKT by ROS led to enhanced p53 mitochondrial translocation and myoblast apoptosis. Reactive Oxygen Species 54-57 tumor protein p53 Homo sapiens 74-77
30865562-5 2019 Furthermore, we demonstrated that overaccumulation of reactive oxygen species (ROS) during HMS-inactivated AKT that was activated in LMS-treated cells, which accounted for the distinct p53 subcellular localizations under HMS and LMS. Reactive Oxygen Species 54-77 tumor protein p53 Homo sapiens 185-188
30865562-5 2019 Furthermore, we demonstrated that overaccumulation of reactive oxygen species (ROS) during HMS-inactivated AKT that was activated in LMS-treated cells, which accounted for the distinct p53 subcellular localizations under HMS and LMS. Reactive Oxygen Species 79-82 tumor protein p53 Homo sapiens 185-188
30865562-6 2019 Blocking ROS generation by N-acetylcysteine (NAC) or overexpressing constitutively active AKT vector (CA-AKT) inhibited HMS-incurred p53 mitochondrial translocation and promoted its nuclear targeting. Reactive Oxygen Species 9-12 tumor protein p53 Homo sapiens 133-136
31020875-8 2019 In particular, our study provides the mechanistic foundation that OMA reduces the expression and secretion of MMP-9 through LKB1-mediated PEA3 degradation via the ROS-dependent ATM-Chk2-p53 signalling axis, resulting from inhibition of IDH enzymes. Reactive Oxygen Species 163-166 tumor protein p53 Homo sapiens 186-189
31019655-0 2019 Hsp90 Inhibitor SNX-2112 Enhances TRAIL-Induced Apoptosis of Human Cervical Cancer Cells via the ROS-Mediated JNK-p53-Autophagy-DR5 Pathway. Reactive Oxygen Species 97-100 tumor protein p53 Homo sapiens 114-117
31019655-8 2019 ROS scavenger NAC rescued SNX-2112/TRAIL-induced apoptosis and suppressed SNX-2112-induced p-JNK and p53. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 101-104
30639360-5 2019 Mechanistically, our findings showed that OMA activated p53-mediated apoptosis through ROS-dependent ATM-Chk2 signaling and reduced the expression of vascular endothelial growth factor through ROS-dependent E2F1-mediated hypoxia inducible factor-1alpha degradation. Reactive Oxygen Species 87-90 tumor protein p53 Homo sapiens 56-59
30865562-8 2019 Finally, we found that Ser389 phosphorylation of p53 was a downstream event of ROS-inactivated AKT pathway, which was critical to p53 mitochondrial trafficking during HMS stimuli. Reactive Oxygen Species 79-82 tumor protein p53 Homo sapiens 49-52
30865562-8 2019 Finally, we found that Ser389 phosphorylation of p53 was a downstream event of ROS-inactivated AKT pathway, which was critical to p53 mitochondrial trafficking during HMS stimuli. Reactive Oxygen Species 79-82 tumor protein p53 Homo sapiens 130-133
30865562-10 2019 Altogether, our study uncovered that mitochondrial localization of p53, resulting from p53 Ser389 phosphorylation through ROS-inactivated AKT pathway, prompted C2C12 myoblast apoptosis during HMS stimulation. Reactive Oxygen Species 122-125 tumor protein p53 Homo sapiens 67-70
30865562-10 2019 Altogether, our study uncovered that mitochondrial localization of p53, resulting from p53 Ser389 phosphorylation through ROS-inactivated AKT pathway, prompted C2C12 myoblast apoptosis during HMS stimulation. Reactive Oxygen Species 122-125 tumor protein p53 Homo sapiens 87-90
30962574-3 2019 Instead, ALOX12 inactivation diminishes p53-mediated ferroptosis induced by reactive oxygen species stress and abrogates p53-dependent inhibition of tumour growth in xenograft models, suggesting that ALOX12 is critical for p53-mediated ferroptosis. Reactive Oxygen Species 76-99 tumor protein p53 Homo sapiens 40-43
29790387-5 2019 Results: In a set of in vivo studies, renal IR was found to cause severe impairment in renal tissues with massive ROS generation, which occurred contemporaneously with activation of NF-kappaB/p53/p53 upregulated modulator of apoptosis (PUMA)-mediated mitochondrial apoptosis pathways. Reactive Oxygen Species 114-117 tumor protein p53 Homo sapiens 192-195
29790387-5 2019 Results: In a set of in vivo studies, renal IR was found to cause severe impairment in renal tissues with massive ROS generation, which occurred contemporaneously with activation of NF-kappaB/p53/p53 upregulated modulator of apoptosis (PUMA)-mediated mitochondrial apoptosis pathways. Reactive Oxygen Species 114-117 tumor protein p53 Homo sapiens 196-199
30844644-6 2019 The effects of TRIM69 overexpression in UVB-induced cell apoptosis and ROS production was clearly weakened by p53 overexpression, thus suggesting a role for p53 in TRIM69 functions. Reactive Oxygen Species 71-74 tumor protein p53 Homo sapiens 110-113
30844644-6 2019 The effects of TRIM69 overexpression in UVB-induced cell apoptosis and ROS production was clearly weakened by p53 overexpression, thus suggesting a role for p53 in TRIM69 functions. Reactive Oxygen Species 71-74 tumor protein p53 Homo sapiens 157-160
30696035-10 2019 All these results proved that p53 was involved in apoptosis via mitochondria-mediated pathway and the process was regulated by ROS. Reactive Oxygen Species 127-130 tumor protein p53 Homo sapiens 30-33
29773887-7 2019 On the other hand, VCA-1 treatment enhanced intracellular ROS (reactive oxygen species) generation also in a p53-independent manner, and consequently promoted caspase activation. Reactive Oxygen Species 58-61 tumor protein p53 Homo sapiens 109-112
29773887-7 2019 On the other hand, VCA-1 treatment enhanced intracellular ROS (reactive oxygen species) generation also in a p53-independent manner, and consequently promoted caspase activation. Reactive Oxygen Species 63-86 tumor protein p53 Homo sapiens 109-112
30483736-3 2019 The current study identified a potential pathway by revealing that TRAIL and 6-sho or chloroquine acted together to trigger reactive oxygen species (ROS) production, to upregulate tumor-suppressor protein 53 (p53) expression and to change the mitochondrial transmembrane potential (MTP). Reactive Oxygen Species 149-152 tumor protein p53 Homo sapiens 209-212
30718466-3 2019 Our preliminary study revealed heat stress (HS)-induced apoptosis of vascular endothelial cells was associated with reactive oxygen species (ROS)-induced p53 translocation into mitochondria. Reactive Oxygen Species 116-139 tumor protein p53 Homo sapiens 154-157
30718466-3 2019 Our preliminary study revealed heat stress (HS)-induced apoptosis of vascular endothelial cells was associated with reactive oxygen species (ROS)-induced p53 translocation into mitochondria. Reactive Oxygen Species 141-144 tumor protein p53 Homo sapiens 154-157
30718466-5 2019 Based on these studies, we presumed Pin1 is a key intermediate in regulation of mitochondrial p53 translocation through a HS-induced ROS-p53 transcription-independent apoptosis pathway. Reactive Oxygen Species 133-136 tumor protein p53 Homo sapiens 94-97
30718466-5 2019 Based on these studies, we presumed Pin1 is a key intermediate in regulation of mitochondrial p53 translocation through a HS-induced ROS-p53 transcription-independent apoptosis pathway. Reactive Oxygen Species 133-136 tumor protein p53 Homo sapiens 137-140
30718466-8 2019 Furthermore, we also found ROS production was a critical mediator in HS-induced Pin1/p53 signaling and was involved in regulating mitochondrial apoptosis pathway activation. Reactive Oxygen Species 27-30 tumor protein p53 Homo sapiens 85-88
30431068-5 2019 Investigating the mechanism, it was revealed that necroptosis may be induced in HCT116 p53+/+ cells by significantly increasing reactive oxygen species (ROS) and decreasing mitochondrial membrane potential (MMP), whereas little alterations were detected in HCT116 p53-/- cells. Reactive Oxygen Species 128-151 tumor protein p53 Homo sapiens 87-90
30431068-5 2019 Investigating the mechanism, it was revealed that necroptosis may be induced in HCT116 p53+/+ cells by significantly increasing reactive oxygen species (ROS) and decreasing mitochondrial membrane potential (MMP), whereas little alterations were detected in HCT116 p53-/- cells. Reactive Oxygen Species 153-156 tumor protein p53 Homo sapiens 87-90
30431068-8 2019 Furthermore, western blot analysis and ROS measurements indicated that AMPK inhibition, using dorsomorphin dihydrochloride, accelerated necroptosis by increasing ROS generation in HCT116 p53-/- cells. Reactive Oxygen Species 162-165 tumor protein p53 Homo sapiens 187-190
30483050-7 2018 We found that treatment of 400 muM GM elicited the formation of ROS, which, in turn, led to PINK1 degradation, parkin recruitment, autophagy formation, an increase of p53 and cleaved-caspase 3 in HEI-OC1 cells and murine HCs. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 167-170
30261716-0 2019 Cis-3-O-p-hydroxycinnamoyl Ursolic Acid Induced ROS-Dependent p53-Mediated Mitochondrial Apoptosis in Oral Cancer Cells. Reactive Oxygen Species 48-51 tumor protein p53 Homo sapiens 62-65
29842822-0 2019 Biosynthesized composites of Au-Ag nanoparticles using Trapa peel extract induced ROS-mediated p53 independent apoptosis in cancer cells. Reactive Oxygen Species 82-85 tumor protein p53 Homo sapiens 95-98
29842822-9 2019 Mechanistically, Au-AgNPs derived with Trapa peel extract significantly enhance ROS which trigger p53-independent apoptosis in various cancer cells effectively. Reactive Oxygen Species 80-83 tumor protein p53 Homo sapiens 98-101
30450337-3 2018 Recent studies have found that p53 acts as a positive regulator of ferroptosis by promoting ROS production. Reactive Oxygen Species 92-95 tumor protein p53 Homo sapiens 31-34
30450337-4 2018 p53 directly regulates the metabolic versatility of cells by favoring mitochondrial respiration, leading to ROS-mediated ferroptosis. Reactive Oxygen Species 108-111 tumor protein p53 Homo sapiens 0-3
30450337-5 2018 In mild stress, p53 protects cell survival via eliminating ROS; additionally, in human colorectal cancer, p53 antagonizes ferroptosis by formation of the DPP4-p53 complex. Reactive Oxygen Species 59-62 tumor protein p53 Homo sapiens 16-19
30450337-5 2018 In mild stress, p53 protects cell survival via eliminating ROS; additionally, in human colorectal cancer, p53 antagonizes ferroptosis by formation of the DPP4-p53 complex. Reactive Oxygen Species 59-62 tumor protein p53 Homo sapiens 106-109
30450337-5 2018 In mild stress, p53 protects cell survival via eliminating ROS; additionally, in human colorectal cancer, p53 antagonizes ferroptosis by formation of the DPP4-p53 complex. Reactive Oxygen Species 59-62 tumor protein p53 Homo sapiens 106-109
30591679-8 2018 RNA sequencing analysis suggested that sFRP4-mediated apoptosis is via the Fas-p53 pathway by activating the Wnt calcium and reactive oxygen species pathways. Reactive Oxygen Species 125-148 tumor protein p53 Homo sapiens 79-82
30483050-8 2018 In contrast, co-treatment with ROS scavenger N-acetyl-L-cysteine (NAC) inhibited parkin recruitment, alleviated autophagy and p53 pathway-related damaged-cell elimination. Reactive Oxygen Species 31-34 tumor protein p53 Homo sapiens 126-129
30450337-6 2018 In short, the mechanisms of p53-mediated ROS production underlying cellular response are poorly understood. Reactive Oxygen Species 41-44 tumor protein p53 Homo sapiens 28-31
30450337-7 2018 In the context of recent research results, the indistinct roles of p53 on ROS-mediated ferroptosis are scrutinized to understand the mechanism underlying p53-mediated tumor suppression. Reactive Oxygen Species 74-77 tumor protein p53 Homo sapiens 67-70
29941676-2 2018 We have detected a primate-specific adrenal androgen-mediated tumor suppression system in which circulating DHEAS is converted to DHEA specifically in cells in which TP53 has been inactivated DHEA is an uncompetitive inhibitor of glucose-6-phosphate dehydrogenase (G6PD), an enzyme indispensable for maintaining reactive oxygen species within limits survivable by the cell. Reactive Oxygen Species 312-335 tumor protein p53 Homo sapiens 166-170
30450337-7 2018 In the context of recent research results, the indistinct roles of p53 on ROS-mediated ferroptosis are scrutinized to understand the mechanism underlying p53-mediated tumor suppression. Reactive Oxygen Species 74-77 tumor protein p53 Homo sapiens 154-157
29941676-6 2018 The triggering of these enzymes in the TP53-affected cell combines with the primate-specific G6PC promoter sequence motif that enables G6P substrate accumulation, driving uncompetitive inhibition of G6PD to irreversibility and ROS-mediated cell death. Reactive Oxygen Species 227-230 tumor protein p53 Homo sapiens 39-43
29923368-10 2018 Pharmacologic or genetic manipulation of the reactive oxygen species (ROS)/ATM/Chk2/TP53 pathway efficiently blocked L5-induced endothelial senescence. Reactive Oxygen Species 45-68 tumor protein p53 Homo sapiens 84-88
30003648-7 2018 Moreover, we observe that ROS produced by MAO-A lead to the accumulation of p53 in the cytosol where it inhibits parkin, an important regulator of mitophagy, resulting in mitochondrial dysfunction. Reactive Oxygen Species 26-29 tumor protein p53 Homo sapiens 76-79
30348672-7 2018 These events act in concert with a modest upregulation of p53 activity to limit the levels of reactive oxygen species (ROS). Reactive Oxygen Species 94-117 tumor protein p53 Homo sapiens 58-61
30348672-7 2018 These events act in concert with a modest upregulation of p53 activity to limit the levels of reactive oxygen species (ROS). Reactive Oxygen Species 119-122 tumor protein p53 Homo sapiens 58-61
30283098-2 2018 ROS and RNS can influence tumor cell malignancy via the redox-regulated transcription factor NF-kappaB, whose activation is further regulated by the mutation status of p53. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 168-171
30283098-5 2018 Nanoparticle activity was related to the decreased level of intracellular ROS and RNS, which downregulated NF-kappaB signaling depending on the p53 status of the cell line. Reactive Oxygen Species 74-77 tumor protein p53 Homo sapiens 144-147
29916532-8 2018 Resveratrol induced the ROS-p38-p53 pathway by increasing the gene expression of phosphorylated p38 mitogen-activated protein kinase, while it induced the p53 and ER stress pathway by increasing the gene expression levels of phosphorylated eukaryotic initiation factor 2alpha and C/EBP homologous protein. Reactive Oxygen Species 24-27 tumor protein p53 Homo sapiens 32-35
29916532-9 2018 The enhanced ROS-p38-p53 and ER stress pathways promoted apoptosis by downregulating B-cell lymphoma-2 (Bcl-2) expression and upregulating Bcl-2-associated X protein expression. Reactive Oxygen Species 13-16 tumor protein p53 Homo sapiens 21-24
29964297-13 2018 P53 expression followed by LPS-induced inflammation was also be restricted by suppressing ROS generation. Reactive Oxygen Species 90-93 tumor protein p53 Homo sapiens 0-3
29964297-14 2018 CONCLUSIONS: The present study shows that LPS-induced inflammation in HGFs is partially dependent on P53 modulating ROS and ROS stimulating P53, which suggests that P53 and ROS may form a feedback loop. Reactive Oxygen Species 116-119 tumor protein p53 Homo sapiens 101-104
29964297-14 2018 CONCLUSIONS: The present study shows that LPS-induced inflammation in HGFs is partially dependent on P53 modulating ROS and ROS stimulating P53, which suggests that P53 and ROS may form a feedback loop. Reactive Oxygen Species 124-127 tumor protein p53 Homo sapiens 101-104
29964297-14 2018 CONCLUSIONS: The present study shows that LPS-induced inflammation in HGFs is partially dependent on P53 modulating ROS and ROS stimulating P53, which suggests that P53 and ROS may form a feedback loop. Reactive Oxygen Species 124-127 tumor protein p53 Homo sapiens 101-104
29923368-10 2018 Pharmacologic or genetic manipulation of the reactive oxygen species (ROS)/ATM/Chk2/TP53 pathway efficiently blocked L5-induced endothelial senescence. Reactive Oxygen Species 70-73 tumor protein p53 Homo sapiens 84-88
29698619-8 2018 Moreover, inhibition of p53 increased the inhibitory effect in p53-wild hepatocarcinoma cells, as well as apoptotic cells and ROS generation. Reactive Oxygen Species 126-129 tumor protein p53 Homo sapiens 24-27
29786746-0 2018 Luteolin induces myelodysplastic syndrome-derived cell apoptosis via the p53-dependent mitochondrial signaling pathway mediated by reactive oxygen species. Reactive Oxygen Species 131-154 tumor protein p53 Homo sapiens 73-76
29786746-11 2018 The increased intracellular level of ROS appeared to induce the activation of p53 and elevate the B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 ratio, which modulates DeltaPsim and triggers the release of cytochrome c, and may increase the activities of apoptotic protease activating factor 1, caspase-3, -8 and -9 to further trigger the destruction of structural and specific proteins and thereby cell apoptosis. Reactive Oxygen Species 37-40 tumor protein p53 Homo sapiens 78-81
29786746-13 2018 These data suggested that luteolin exerts its pro-apoptotic action partly through the p53-dependent mitochondrial signaling pathway mediated by intracellular ROS, which provides a promising therapeutic candidate for patients with MDS. Reactive Oxygen Species 158-161 tumor protein p53 Homo sapiens 86-89
29668110-8 2018 Pre-incubation with ROS scavenger N-acetyl-l-cysteine preserved AR and PSA abundance, markedly reduced ISC-4-induced apoptosis and attenuated p53 Ser phosphorylation, p21Cip1, and p-H2A.X. Reactive Oxygen Species 20-23 tumor protein p53 Homo sapiens 142-145
29668110-0 2018 Phenylbutyl isoselenocyanate induces reactive oxygen species to inhibit androgen receptor and to initiate p53-mediated apoptosis in LNCaP prostate cancer cells. Reactive Oxygen Species 37-60 tumor protein p53 Homo sapiens 106-109
29843463-6 2018 ZMCs reactivate mutant p53 using a novel two-part mechanism that involves restoring the wild-type structure by reestablishing zinc binding and activating p53 through post-translational modifications induced by cellular reactive oxygen species (ROS). Reactive Oxygen Species 219-242 tumor protein p53 Homo sapiens 23-26
29928326-8 2018 The results of the present study demonstrated that miltirone induces apoptosis in cisplatin-resistant lung cancer cells through ROS-p53, AIF, PARP and MMP2/9 signaling pathways. Reactive Oxygen Species 128-131 tumor protein p53 Homo sapiens 132-135
29843463-6 2018 ZMCs reactivate mutant p53 using a novel two-part mechanism that involves restoring the wild-type structure by reestablishing zinc binding and activating p53 through post-translational modifications induced by cellular reactive oxygen species (ROS). Reactive Oxygen Species 244-247 tumor protein p53 Homo sapiens 23-26
29843463-6 2018 ZMCs reactivate mutant p53 using a novel two-part mechanism that involves restoring the wild-type structure by reestablishing zinc binding and activating p53 through post-translational modifications induced by cellular reactive oxygen species (ROS). Reactive Oxygen Species 244-247 tumor protein p53 Homo sapiens 154-157
29805774-8 2018 Conversely, induction of p53 expression may regulate differently the tumor cell metabolism, inducing senescence, autophagy and apoptosis, which are dependent on the regulation of the PI3K/AKT/mTOR pathway and/or ROS induction. Reactive Oxygen Species 212-215 tumor protein p53 Homo sapiens 25-28
29178461-2 2018 However, culminating from seminal findings in rodents more than a decade ago, several studies have demonstrated that p53 is required to maintain basal mitochondrial function [ie, respiration and reactive oxygen species (ROS) homeostasis]. Reactive Oxygen Species 195-218 tumor protein p53 Homo sapiens 117-120
29723979-6 2018 Phosphatase and tensin homologue deleted on chromosome 10/Protein kinase B, PKB (PTEN/AKT) and the tumor suppressor p53 pathway have been proven to play a pivotal role in regulating cell apoptosis by regulating the oxidative stress and/or ROS quenching. Reactive Oxygen Species 239-242 tumor protein p53 Homo sapiens 116-119
29568929-9 2018 Mechanistic studies demonstrated that KNDC1 triggered a p53-ROS positive feedback loop, which serves a crucial role in regulating senescence. Reactive Oxygen Species 60-63 tumor protein p53 Homo sapiens 56-59
29511347-0 2018 PARP-1 inhibition with or without ionizing radiation confers reactive oxygen species-mediated cytotoxicity preferentially to cancer cells with mutant TP53. Reactive Oxygen Species 61-84 tumor protein p53 Homo sapiens 150-154
29518119-10 2018 When p53 expression was inhibited with siRNA in parental HT-29 cells, ROS production and apoptosis increased to levels seen in the NAT1 knockout cells. Reactive Oxygen Species 70-73 tumor protein p53 Homo sapiens 5-8
29323455-0 2018 Selenocysteine inhibits human osteosarcoma cells growth through triggering mitochondrial dysfunction and ROS-mediated p53 phosphorylation. Reactive Oxygen Species 105-108 tumor protein p53 Homo sapiens 118-121
29323455-7 2018 Moreover, SeC triggered p53 phosphorylation by inducing reactive oxygen species (ROS) overproduction. Reactive Oxygen Species 56-79 tumor protein p53 Homo sapiens 24-27
29323455-7 2018 Moreover, SeC triggered p53 phosphorylation by inducing reactive oxygen species (ROS) overproduction. Reactive Oxygen Species 81-84 tumor protein p53 Homo sapiens 24-27
29323455-8 2018 ROS inhibition effectively blocked SeC-induced cytotoxicity and p53 phosphorylation. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 64-67
29323455-10 2018 These results indicated that SeC had the potential to inhibit human osteosarcoma cells growth in vitro and in vivo through triggering mitochondrial dysfunction and ROS-mediated p53 phosphorylation, which validated the potential application of Se-containing compounds in treatment of human osteosarcoma. Reactive Oxygen Species 164-167 tumor protein p53 Homo sapiens 177-180
29291545-8 2018 Impaired PPP disturbed redox-cycling, generated reactive oxygen species (ROS), which triggered cell cycle arrest and caused the switch to Chk2/p53/NF-kappaB pathway-mediated P-gp induction. Reactive Oxygen Species 48-71 tumor protein p53 Homo sapiens 143-146
29291545-8 2018 Impaired PPP disturbed redox-cycling, generated reactive oxygen species (ROS), which triggered cell cycle arrest and caused the switch to Chk2/p53/NF-kappaB pathway-mediated P-gp induction. Reactive Oxygen Species 73-76 tumor protein p53 Homo sapiens 143-146
29471006-5 2018 Astilbin significantly decreased reactive oxygen species (ROS) accumulation and alleviated ROS-induced activation of p53, MAPKs and AKT signaling cascades, which in turn attenuated cisplatin-induced HEK-293 cell apoptosis. Reactive Oxygen Species 91-94 tumor protein p53 Homo sapiens 117-120
29178461-2 2018 However, culminating from seminal findings in rodents more than a decade ago, several studies have demonstrated that p53 is required to maintain basal mitochondrial function [ie, respiration and reactive oxygen species (ROS) homeostasis]. Reactive Oxygen Species 220-223 tumor protein p53 Homo sapiens 117-120
29673545-0 2018 Curcumin induces apoptosis and cell cycle arrest via the activation of reactive oxygen species-independent mitochondrial apoptotic pathway in Smad4 and p53 mutated colon adenocarcinoma HT29 cells. Reactive Oxygen Species 71-94 tumor protein p53 Homo sapiens 152-155
29673545-4 2018 To test this hypothesis, the apoptosis-inducing potential and cell cycle inhibition effect of ROS induced by curcumin was investigated in Smd4 and p53 mutated HT-29 colon adenocarcinoma cells. Reactive Oxygen Species 94-97 tumor protein p53 Homo sapiens 147-150
29130578-8 2018 Notably, mitochondrially targeted p53 (mito-p53) directly reduced mitochondria DNA-encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption. Reactive Oxygen Species 142-165 tumor protein p53 Homo sapiens 34-37
29402413-0 2018 Inhibition of CREPT restrains gastric cancer growth by regulation of cycle arrest, migration and apoptosis via ROS-regulated p53 pathway. Reactive Oxygen Species 111-114 tumor protein p53 Homo sapiens 125-128
29466247-8 2018 Collectively, down-regulation of ZEB1 caused by UVA induced ROS could transcriptionally inhibit DNMT1, leading to low methylation level of senescence related proteins p53 and increase its expression, eventually result in cellar senescence. Reactive Oxygen Species 60-63 tumor protein p53 Homo sapiens 167-170
29130578-8 2018 Notably, mitochondrially targeted p53 (mito-p53) directly reduced mitochondria DNA-encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption. Reactive Oxygen Species 142-165 tumor protein p53 Homo sapiens 44-47
29130578-8 2018 Notably, mitochondrially targeted p53 (mito-p53) directly reduced mitochondria DNA-encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption. Reactive Oxygen Species 167-170 tumor protein p53 Homo sapiens 34-37
29130578-8 2018 Notably, mitochondrially targeted p53 (mito-p53) directly reduced mitochondria DNA-encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption. Reactive Oxygen Species 167-170 tumor protein p53 Homo sapiens 44-47
29225132-0 2018 Ginsenoside Rh4 induces apoptosis and autophagic cell death through activation of the ROS/JNK/p53 pathway in colorectal cancer cells. Reactive Oxygen Species 86-89 tumor protein p53 Homo sapiens 94-97
29433671-8 2018 The three phytochemicals activated the ROS-p38-p53 apoptotic pathway by increasing the level of phosphorylated p38 MAPK and p53, and they activated the ER stress-mediated apoptotic pathway by increasing the level of phosphorylated eIF2alpha and C/EBP homologous protein (CHOP). Reactive Oxygen Species 39-42 tumor protein p53 Homo sapiens 47-50
29568362-6 2018 The antitumor activity was partly due to NO-cGMP dependent pathway, contributing to reduced cell number and apoptosis, and partly to the salicylaldehyde moiety and reactive oxygen species (ROS) activated ERK1/2 signaling converging on p53 dependent caspase-3 cleavage. Reactive Oxygen Species 164-187 tumor protein p53 Homo sapiens 235-238
29568362-6 2018 The antitumor activity was partly due to NO-cGMP dependent pathway, contributing to reduced cell number and apoptosis, and partly to the salicylaldehyde moiety and reactive oxygen species (ROS) activated ERK1/2 signaling converging on p53 dependent caspase-3 cleavage. Reactive Oxygen Species 189-192 tumor protein p53 Homo sapiens 235-238
29433671-8 2018 The three phytochemicals activated the ROS-p38-p53 apoptotic pathway by increasing the level of phosphorylated p38 MAPK and p53, and they activated the ER stress-mediated apoptotic pathway by increasing the level of phosphorylated eIF2alpha and C/EBP homologous protein (CHOP). Reactive Oxygen Species 39-42 tumor protein p53 Homo sapiens 124-127
29433671-9 2018 Both the ROS-p38-p53 and ER stress-mediated pathway induced the mitochondrial apoptotic pathway by attenuating Bcl-2 expression and upregulating BAX. Reactive Oxygen Species 9-12 tumor protein p53 Homo sapiens 17-20
29233996-5 2017 However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species. Reactive Oxygen Species 202-225 tumor protein p53 Homo sapiens 18-21
29483824-5 2018 Mechanistically, dioscin may down-regulate the expression of SH2 domain-containing phosphatase-2 (SHP2) at the transcription level by increasing p53 binding to the SHP2 promoter due to reactive oxygen species (ROS). Reactive Oxygen Species 185-208 tumor protein p53 Homo sapiens 145-148
29233996-5 2017 However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species. Reactive Oxygen Species 202-225 tumor protein p53 Homo sapiens 46-49
29233996-5 2017 However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species. Reactive Oxygen Species 202-225 tumor protein p53 Homo sapiens 46-49
29233996-5 2017 However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species. Reactive Oxygen Species 202-225 tumor protein p53 Homo sapiens 46-49
29039537-10 2017 In conclusion, juglone potentiated TRAIL-induced apoptosis in melanoma cells, and these effects were partially mediated through the ROS-p38-p53 pathway. Reactive Oxygen Species 132-135 tumor protein p53 Homo sapiens 140-143
28835450-5 2017 At early precancerous and neoplastic stages, antioxidant activity decreases and ROS appear to promote cancer initiation via inducing oxidative damage and base pair substitution mutations in pro-oncogenes and tumor suppressor genes, such as RAS and TP53, respectively. Reactive Oxygen Species 80-83 tumor protein p53 Homo sapiens 248-252
28989024-3 2017 Forced inhibition of cPKC or aPKC induced the activation of senescence markers, including senescence-associated beta-galactosidase activity and reactive oxygen species (ROS)-p53-p21Cip1/WAF1 axis in HCT116 and HEK293 cells. Reactive Oxygen Species 144-167 tumor protein p53 Homo sapiens 174-177
28989024-3 2017 Forced inhibition of cPKC or aPKC induced the activation of senescence markers, including senescence-associated beta-galactosidase activity and reactive oxygen species (ROS)-p53-p21Cip1/WAF1 axis in HCT116 and HEK293 cells. Reactive Oxygen Species 169-172 tumor protein p53 Homo sapiens 174-177
28989024-7 2017 Therefore, this study suggests for the first time that downregulation of PKC induces senescence through the AKT-FoxO3a-ROS-p53-p21Cip1/WAF1 pathway in HCT116 and HEK293 cells. Reactive Oxygen Species 119-122 tumor protein p53 Homo sapiens 123-126
28981686-8 2017 Physiologically relevant nucleolar stress induction with reactive oxygen species reaffirms a p53-independent p27kip1 response pathway and leads to nascent pre-rRNA reduction. Reactive Oxygen Species 57-80 tumor protein p53 Homo sapiens 93-96
28931625-0 2017 PML is a ROS sensor activating p53 upon oxidative stress. Reactive Oxygen Species 9-12 tumor protein p53 Homo sapiens 31-34
29033244-4 2017 Here, we demonstrate that iASPP, a known p53 inhibitor, lowers ROS independently of p53. Reactive Oxygen Species 63-66 tumor protein p53 Homo sapiens 41-44
29127423-6 2017 We demonstrate that, in the cells with active p53, ectopic expression of NPRL2 induces NOX2-dependent production of reactive oxygen species and DNA damage. Reactive Oxygen Species 116-139 tumor protein p53 Homo sapiens 46-49
28888620-6 2017 In addition, p53-overexpressing cells accumulated intracellular ROS via cytochrome c release mediated by the BH3-only protein Noxa induction. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 13-16
28543759-11 2017 In conclusion, we established a connection among ROS, ATM and p73 in AGG-induced apoptosis, which might be useful in enhancing the therapeutic targeting of p53 deficient oral squamous cell carcinoma. Reactive Oxygen Species 49-52 tumor protein p53 Homo sapiens 156-159
28425621-6 2017 The f-G exposed p53-competent cells, but not p53-deficient cells, initiated G0 /G1 phase cell cycle arrest, suppressed reactive oxygen species, and entered apoptosis. Reactive Oxygen Species 119-142 tumor protein p53 Homo sapiens 16-19
28813624-11 2017 All mixed confluent cultures expressed enhanced radio-sensitization (P <= 0.047) characteristic of TP53 Mut cells, which could be inhibited by their exposure to the antioxidant N-acetyl-l-cysteine (NAC) indicating a role for intercellular signaling by reactive oxygen species (ROS). Reactive Oxygen Species 255-278 tumor protein p53 Homo sapiens 102-106
28944886-0 2017 Sulforaphane induces p53-deficient SW480 cell apoptosis via the ROS-MAPK signaling pathway. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 21-24
28813624-11 2017 All mixed confluent cultures expressed enhanced radio-sensitization (P <= 0.047) characteristic of TP53 Mut cells, which could be inhibited by their exposure to the antioxidant N-acetyl-l-cysteine (NAC) indicating a role for intercellular signaling by reactive oxygen species (ROS). Reactive Oxygen Species 280-283 tumor protein p53 Homo sapiens 102-106
29042481-6 2017 At the molecular level, TSP1 increased Nox1-dependent generation of reactive oxygen species (ROS), leading to the increased abundance of the transcription factor p53. Reactive Oxygen Species 68-91 tumor protein p53 Homo sapiens 162-165
29051574-7 2017 Furthermore, FLO also induces G0/G1 cell cycle arrest via increase of p21 levels through activating ROS/p53/p21 pathway. Reactive Oxygen Species 100-103 tumor protein p53 Homo sapiens 104-107
29042481-6 2017 At the molecular level, TSP1 increased Nox1-dependent generation of reactive oxygen species (ROS), leading to the increased abundance of the transcription factor p53. Reactive Oxygen Species 93-96 tumor protein p53 Homo sapiens 162-165
28971953-8 2017 Further analysis indicated that inhibition of the mammalian target of rapamycin allows efficient cardiomyocyte differentiation through overcoming p53-dependent apoptosis of human pluripotent stem cells during high-density monolayer culture via blunting p53 translation and mitochondrial reactive oxygen species production. Reactive Oxygen Species 287-310 tumor protein p53 Homo sapiens 146-149
28673807-8 2017 In addition, ROS induced by walsuronoid B upregulated p53 levels; conversely, p53 stimulated ROS. Reactive Oxygen Species 13-16 tumor protein p53 Homo sapiens 54-57
28673807-8 2017 In addition, ROS induced by walsuronoid B upregulated p53 levels; conversely, p53 stimulated ROS. Reactive Oxygen Species 93-96 tumor protein p53 Homo sapiens 78-81
29051813-0 2017 Differential impact of various reactive oxygen species (ROS) on HIF-1alpha/p53 direct interaction in SK-N-MC neuroblastoma cells. Reactive Oxygen Species 31-54 tumor protein p53 Homo sapiens 75-78
29051813-0 2017 Differential impact of various reactive oxygen species (ROS) on HIF-1alpha/p53 direct interaction in SK-N-MC neuroblastoma cells. Reactive Oxygen Species 56-59 tumor protein p53 Homo sapiens 75-78
29051813-2 2017 Aside from its transcriptional regulation, other mechanisms, such as post translational modifications and protein-protein interactions, the interaction between HIF-1alpha and p53 has attracted more attention mainly due to simultaneous enhancement in the protein levels of these two anti- and pro-apoptotic vital transcriptional factors within the ROS-stressed cells. Reactive Oxygen Species 347-350 tumor protein p53 Homo sapiens 175-178
29051813-5 2017 Then, the effect of different ROS on interaction between HIF-1alpha and p53 proteins was examined by co-immunoprecipitation. Reactive Oxygen Species 30-33 tumor protein p53 Homo sapiens 72-75
29051813-8 2017 It appeared that direct communication between HIF-1alpha and p53 proteins by ROS stresses, under both normoxic and hypoxic conditions, was governed by HIF-1alpha at a certain induced level. Reactive Oxygen Species 77-80 tumor protein p53 Homo sapiens 61-64
28346428-7 2017 The ROS-p53-positive feedback loop is an essential mechanism of this synergistic cytotoxicity. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 8-11
28609685-9 2017 CONCLUSIONS: Our results suggest that palmitate-induced apoptosis depends on the activation of the TLR4/ROS/p53 signaling pathway, and that TLR4 may be a potential therapeutic target for the prevention and treatment of atherosclerosis. Reactive Oxygen Species 104-107 tumor protein p53 Homo sapiens 108-111
28691365-9 2017 The mechanistic analysis revealed that Akt increased ROS levels through NOX4 induction, and increased Akt-dependent NF-kappaB binding to the NOX4 promoter is responsible for NOX4 induction upon p53 expression. Reactive Oxygen Species 53-56 tumor protein p53 Homo sapiens 194-197
28927457-5 2017 Azelaic acid leads to mitochondrial damage associated with increased release of reactive oxygen species inducing p53. Reactive Oxygen Species 80-103 tumor protein p53 Homo sapiens 113-116
27927016-0 2017 Inhibition of Cathepsin S Induces Mitochondrial ROS That Sensitizes TRAIL-Mediated Apoptosis Through p53-Mediated Downregulation of Bcl-2 and c-FLIP. Reactive Oxygen Species 48-51 tumor protein p53 Homo sapiens 101-104
27927016-8 2017 Interestingly, ZFL induced p53 expression via production of mitochondrial reactive oxygen species (ROS). Reactive Oxygen Species 74-97 tumor protein p53 Homo sapiens 27-30
27927016-8 2017 Interestingly, ZFL induced p53 expression via production of mitochondrial reactive oxygen species (ROS). Reactive Oxygen Species 99-102 tumor protein p53 Homo sapiens 27-30
27927016-11 2017 CONCLUSION: Our results indicated that inhibition of cathepsin S stimulates TRAIL-induced apoptosis through downregulation of Bcl-2 and Cbl-mediated c-FLIP by ROS-mediated p53 expression. Reactive Oxygen Species 159-162 tumor protein p53 Homo sapiens 172-175
28258023-4 2017 Additionally, excessive ROS caused by physapubescin B also induced p53-dependent apoptotic cell death. Reactive Oxygen Species 24-27 tumor protein p53 Homo sapiens 67-70
28574838-1 2017 Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration. Reactive Oxygen Species 82-105 tumor protein p53 Homo sapiens 54-57
28574838-1 2017 Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration. Reactive Oxygen Species 190-193 tumor protein p53 Homo sapiens 54-57
28574838-1 2017 Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration. Reactive Oxygen Species 190-193 tumor protein p53 Homo sapiens 150-153
28574838-1 2017 Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration. Reactive Oxygen Species 190-193 tumor protein p53 Homo sapiens 150-153
28574838-1 2017 Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration. Reactive Oxygen Species 82-105 tumor protein p53 Homo sapiens 150-153
28574838-1 2017 Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration. Reactive Oxygen Species 82-105 tumor protein p53 Homo sapiens 150-153
28574838-1 2017 Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration. Reactive Oxygen Species 107-110 tumor protein p53 Homo sapiens 54-57
28574838-1 2017 Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration. Reactive Oxygen Species 107-110 tumor protein p53 Homo sapiens 150-153
28574838-1 2017 Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration. Reactive Oxygen Species 107-110 tumor protein p53 Homo sapiens 150-153
28661480-5 2017 The reason for this may be an increase in the level of cellular ROS after knockdown of Prdx2, which may subsequently lead to an increase in the expression of phosphorylated p53 (p-p53) and p38-MAPK/p21. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 173-176
28560439-13 2017 Taken together, the present study provides the first report that ISL induces apoptosis in Caki cells via generation of ROS, which causes induction of p53 and inhibition of the STAT3 signaling pathway. Reactive Oxygen Species 119-122 tumor protein p53 Homo sapiens 150-153
28502718-0 2017 Mitochondrial ND5 mutation mediated elevated ROS regulates apoptotic pathway epigenetically in a P53 dependent manner for generating pro-cancerous phenotypes. Reactive Oxygen Species 45-48 tumor protein p53 Homo sapiens 97-100
28502718-5 2017 Cells over-expressing mtND5 variant produced both peroxide as well as super-oxide ROS; the generation of which was dependent on the functional status of P53; modulating epigenetically the expression of key apoptosis pathway genes. Reactive Oxygen Species 82-85 tumor protein p53 Homo sapiens 153-156
28502718-7 2017 We propose that somatic mutation in mtND5 resulting in down-regulated complex I enzyme activity, elevated ROS and up-regulation of a set of nuclear anti-apoptotic genes epigenetically in the P53 dysfunctional cellular background, has provided a unique understanding of the molecular mechanism of mitochondrial mutation; and the concomitant existence of somatically acquired mitochondrial and nuclear p53 mutations, in cancer progression and promotion. Reactive Oxygen Species 106-109 tumor protein p53 Homo sapiens 191-194
28661480-5 2017 The reason for this may be an increase in the level of cellular ROS after knockdown of Prdx2, which may subsequently lead to an increase in the expression of phosphorylated p53 (p-p53) and p38-MAPK/p21. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 180-183
28356713-0 2017 Artonin E induces p53-independent G1 cell cycle arrest and apoptosis through ROS-mediated mitochondrial pathway and livin suppression in MCF-7 cells. Reactive Oxygen Species 77-80 tumor protein p53 Homo sapiens 18-21
28653879-5 2017 In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. Reactive Oxygen Species 35-58 tumor protein p53 Homo sapiens 122-126
28653879-5 2017 In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. Reactive Oxygen Species 35-58 tumor protein p53 Homo sapiens 228-232
28130753-7 2017 Our data indicated that up-regulation of intracellular ROS induced by H2O2 significantly inhibited proliferation and induced apoptosis accompanying G1 cell cycle arrest and elevated expression of p53. Reactive Oxygen Species 55-58 tumor protein p53 Homo sapiens 196-199
28130753-9 2017 Our results suggested that up-regulation of intracellular ROS inhibited proliferation by promoting expression of p53 and induced G1 cycle arrest and apoptosis. Reactive Oxygen Species 58-61 tumor protein p53 Homo sapiens 113-116
28653879-5 2017 In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. Reactive Oxygen Species 35-58 tumor protein p53 Homo sapiens 228-232
28131902-6 2017 In addition, ROS induced by CQ plus SN-38 upregulated p53 levels by activating p38, conversely, p53 stimulated ROS. Reactive Oxygen Species 13-16 tumor protein p53 Homo sapiens 54-57
28131902-9 2017 Altogether, all results suggested that CQ synergistically sensitized human CRC cells with WT p53 to SN-38 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk. Reactive Oxygen Species 168-171 tumor protein p53 Homo sapiens 164-167
28150492-4 2017 This antiangiogenesis effect was derived from the particle size dependent uptake and production of intracellular reactive oxygen species (ROS) that directly interfered with p53 tumor suppressor pathway. Reactive Oxygen Species 113-136 tumor protein p53 Homo sapiens 173-176
28150492-4 2017 This antiangiogenesis effect was derived from the particle size dependent uptake and production of intracellular reactive oxygen species (ROS) that directly interfered with p53 tumor suppressor pathway. Reactive Oxygen Species 138-141 tumor protein p53 Homo sapiens 173-176
28131902-6 2017 In addition, ROS induced by CQ plus SN-38 upregulated p53 levels by activating p38, conversely, p53 stimulated ROS. Reactive Oxygen Species 111-114 tumor protein p53 Homo sapiens 96-99
28272690-15 2017 CONCLUSIONS: These results suggest that LE and GA ameliorate cisplatin-induced apoptosis through reduction of ROS-mediating p53 activation and promotion of p21 expression in HK-2 cells. Reactive Oxygen Species 110-113 tumor protein p53 Homo sapiens 124-127
28280421-1 2017 The p53-inducible gene 3 (PIG3), initially identified as a gene downstream of p53, plays an important role in the apoptotic process triggered by p53-mediated reactive oxygen species (ROS) production. Reactive Oxygen Species 158-181 tumor protein p53 Homo sapiens 4-7
28280421-1 2017 The p53-inducible gene 3 (PIG3), initially identified as a gene downstream of p53, plays an important role in the apoptotic process triggered by p53-mediated reactive oxygen species (ROS) production. Reactive Oxygen Species 158-181 tumor protein p53 Homo sapiens 78-81
28280421-1 2017 The p53-inducible gene 3 (PIG3), initially identified as a gene downstream of p53, plays an important role in the apoptotic process triggered by p53-mediated reactive oxygen species (ROS) production. Reactive Oxygen Species 183-186 tumor protein p53 Homo sapiens 4-7
28280421-1 2017 The p53-inducible gene 3 (PIG3), initially identified as a gene downstream of p53, plays an important role in the apoptotic process triggered by p53-mediated reactive oxygen species (ROS) production. Reactive Oxygen Species 183-186 tumor protein p53 Homo sapiens 78-81
28272690-0 2017 Licorice and its active compound glycyrrhizic acid ameliorates cisplatin-induced nephrotoxicity through inactivation of p53 by scavenging ROS and overexpression of p21 in human renal proximal tubular epithelial cells. Reactive Oxygen Species 138-141 tumor protein p53 Homo sapiens 120-123
28272690-2 2017 Cisplatin-induced apoptosis in renal cells is associated with reactive oxygen species (ROS)-mediated p53 activation. Reactive Oxygen Species 62-85 tumor protein p53 Homo sapiens 101-104
28272690-2 2017 Cisplatin-induced apoptosis in renal cells is associated with reactive oxygen species (ROS)-mediated p53 activation. Reactive Oxygen Species 87-90 tumor protein p53 Homo sapiens 101-104
27634759-0 2016 Posttranscriptional Upregulation of p53 by Reactive Oxygen Species in Chronic Lymphocytic Leukemia. Reactive Oxygen Species 43-66 tumor protein p53 Homo sapiens 36-39
28081741-0 2017 Depletion of NFBD1/MDC1 Induces Apoptosis in Nasopharyngeal Carcinoma Cells Through the p53-ROS-Mitochondrial Pathway. Reactive Oxygen Species 92-95 tumor protein p53 Homo sapiens 88-91
28081741-6 2017 Further analysis showed that loss of NFBD1 resulted in increased production of intracellular reactive oxygen species (ROS) depending on p53, which subsequently triggered the mitochondrial apoptotic pathway. Reactive Oxygen Species 93-116 tumor protein p53 Homo sapiens 136-139
28081741-6 2017 Further analysis showed that loss of NFBD1 resulted in increased production of intracellular reactive oxygen species (ROS) depending on p53, which subsequently triggered the mitochondrial apoptotic pathway. Reactive Oxygen Species 118-121 tumor protein p53 Homo sapiens 136-139
28749708-3 2017 Here, we investigate whether SMG-1 and p53 blunt this vicious cycle of progressive ROS production and decline in mitochondrial respiration seen during hyperoxia. Reactive Oxygen Species 83-86 tumor protein p53 Homo sapiens 39-42
28749708-9 2017 Genetic depletion of p53 in A549 cells and ablation of the p53 gene in H1299 or HCT116 cells revealed that SMG-1 influences mitochondrial ROS through activation of p53. Reactive Oxygen Species 138-141 tumor protein p53 Homo sapiens 59-62
28749708-9 2017 Genetic depletion of p53 in A549 cells and ablation of the p53 gene in H1299 or HCT116 cells revealed that SMG-1 influences mitochondrial ROS through activation of p53. Reactive Oxygen Species 138-141 tumor protein p53 Homo sapiens 59-62
28749708-10 2017 CONCLUSIONS: Our findings show that hyperoxia does not promote a vicious cycle of progressive mitochondrial ROS and dysfunction because SMG-1-p53 signaling attenuates production of mitochondrial ROS without preserving respiration. Reactive Oxygen Species 195-198 tumor protein p53 Homo sapiens 142-145
27994465-7 2016 Furthermore, Ag@PEI@PTX enhanced cytotoxic effects on HepG2 cells and triggered intracellular reactive oxygen species; the signaling pathways of AKT, p53, and MAPK were activated to advance cell apoptosis. Reactive Oxygen Species 94-117 tumor protein p53 Homo sapiens 150-153
26756900-0 2016 COX-2 inhibitor NS-398 suppresses doxorubicin-induced p53 accumulation through inhibition of ROS-mediated Jnk activation. Reactive Oxygen Species 93-96 tumor protein p53 Homo sapiens 54-57
26756900-10 2016 Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation. Reactive Oxygen Species 21-44 tumor protein p53 Homo sapiens 133-136
26756900-10 2016 Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation. Reactive Oxygen Species 46-49 tumor protein p53 Homo sapiens 133-136
26756900-12 2016 These results suggest that COX-2 activates Jnk through modulation of ROS levels, leading to accumulation of p53. Reactive Oxygen Species 69-72 tumor protein p53 Homo sapiens 108-111
27238838-9 2017 Collectively, these results suggest that Foxp3 is a downstream target of p53 that is sufficient to induce p21 expression, ROS production and p53-mediated senescence. Reactive Oxygen Species 122-125 tumor protein p53 Homo sapiens 73-76
27976481-5 2017 Accumulation of ROS and subsequent activation of NRF2, p53, AP-1 and NF-kappaB-dependent pathways, with downstream activation of antioxidant mechanisms (e.g., SOD2 and HMOX1 expression), is observed in the UV-treated cells. Reactive Oxygen Species 16-19 tumor protein p53 Homo sapiens 55-58
28149884-7 2016 So, mutant p53 has been reported to supply the cancer cells of glucose and nutrients, and, to avoid reactive oxygen species (ROS) mediated damage during oxidative stress. Reactive Oxygen Species 100-123 tumor protein p53 Homo sapiens 11-14
28149884-7 2016 So, mutant p53 has been reported to supply the cancer cells of glucose and nutrients, and, to avoid reactive oxygen species (ROS) mediated damage during oxidative stress. Reactive Oxygen Species 125-128 tumor protein p53 Homo sapiens 11-14
27701048-10 2016 Overall, we observed that CIO NPs induced cytotoxicity and apoptosis in HepG2 cells through ROS via p53 pathway. Reactive Oxygen Species 92-95 tumor protein p53 Homo sapiens 100-103
27634759-8 2016 p53 induction relied on the increase in intracellular reactive oxygen species observed after CD154 and IL4 stimulation. Reactive Oxygen Species 54-77 tumor protein p53 Homo sapiens 0-3
27698449-0 2016 Cr(VI) induces premature senescence through ROS-mediated p53 pathway in L-02 hepatocytes. Reactive Oxygen Species 44-47 tumor protein p53 Homo sapiens 57-60
27774504-1 2016 This article contains raw and processed data related to a research, "Honokiol induces autophagic cell death in malignant glioma through reactive oxygen species-mediated regulation of the p53/PI3K/Akt/mTOR signaling pathway" (C.J. Reactive Oxygen Species 136-159 tumor protein p53 Homo sapiens 187-190
27698449-6 2016 By applying antioxidant Trolox, we also confirmed that ROS mediated p53 activation. Reactive Oxygen Species 55-58 tumor protein p53 Homo sapiens 68-71
27698449-8 2016 We found p53 could inhibit pro-survival genes B-cell lymphoma-2 (Bcl-2), myeloid leukemia-1 (Mcl-1) and S phase related cell cycle proteins cyclin-dependent kinase 2 (CDK2), Cyclin E to induce premature senescence, and the functional role of ROS in Cr(VI)-induced premature senescence is depend on p53. Reactive Oxygen Species 242-245 tumor protein p53 Homo sapiens 9-12
27698449-9 2016 The results suggest that Cr(VI) has a role in premature senescence by promoting ROS-dependent p53 activation in L-02 hepatocytes. Reactive Oxygen Species 80-83 tumor protein p53 Homo sapiens 94-97
27520561-5 2016 p53-deficient cancer cells produced reactive oxygen species, which activated fibroblasts to mediate angiogenesis by secreting vascular endothelial growth factor (VEGF) both in vivo and in vitro Activated fibroblasts significantly contributed to tumor progression. Reactive Oxygen Species 36-59 tumor protein p53 Homo sapiens 0-3
27599894-8 2016 H2O2-induced ROS production increased the levels of phosphorylated-p38 mitogen activated protein kinase, c-Jun N-terminal kinase, ataxia telangiectasia mutated and p53; these increases were inhibited by pretreatment with C. setidens. Reactive Oxygen Species 13-16 tumor protein p53 Homo sapiens 164-167
27229883-8 2016 These data provide the first evidence that beta-Ecd protects SH-SY5Y cells against 6-OHDA-induced apoptosis, possibly through mitochondria protection and p53 modulation via ROS-dependent ASK1-p38(MAPK) pathways. Reactive Oxygen Species 173-176 tumor protein p53 Homo sapiens 154-157
27689798-12 2016 Collectively, our findings demonstrate, for the first time, that 1800MHz EMR induces apoptosis-related events such as ROS burst and more oxidative DNA damage, which in turn promote p53-dependent caspase-3 activation through release of cytochrome c from mitochondrion. Reactive Oxygen Species 118-121 tumor protein p53 Homo sapiens 181-184
27339904-6 2016 In addition, we investigated an increased level of intracellular ROS (reactive oxygen species), which was preceded by p53 activation. Reactive Oxygen Species 65-68 tumor protein p53 Homo sapiens 118-121
27470586-1 2016 We previously showed that protein kinase CK2 downregulation mediates senescence through the reactive oxygen species (ROS)-p53-p21(Cip1/WAF1) pathway in various human cells. Reactive Oxygen Species 92-115 tumor protein p53 Homo sapiens 122-125
27470586-1 2016 We previously showed that protein kinase CK2 downregulation mediates senescence through the reactive oxygen species (ROS)-p53-p21(Cip1/WAF1) pathway in various human cells. Reactive Oxygen Species 117-120 tumor protein p53 Homo sapiens 122-125
27339904-6 2016 In addition, we investigated an increased level of intracellular ROS (reactive oxygen species), which was preceded by p53 activation. Reactive Oxygen Species 70-93 tumor protein p53 Homo sapiens 118-121
27260513-3 2016 We detected a significant "in vitro" generation of 8-oxodG between the codons 163 and 175, corresponding to a TP53 region with high mutation prevalence, after treatment with xanthine plus xanthine oxidase, a ROS-generating system. Reactive Oxygen Species 208-211 tumor protein p53 Homo sapiens 110-114
27496966-0 2016 Nimbolide sensitizes human colon cancer cells to TRAIL through reactive oxygen species- and ERK-dependent up-regulation of death receptors, p53, and Bax. Reactive Oxygen Species 63-86 tumor protein p53 Homo sapiens 140-143
27501149-4 2016 Cell death was attributed to dysfunction of mitochondrial bioenergetics in p53-deficient cells, which was characterized by decreased mitochondrial respiration, steady-state ATP level and membrane potential, but augmented reactive oxygen species (ROS). Reactive Oxygen Species 221-244 tumor protein p53 Homo sapiens 75-78
27501149-4 2016 Cell death was attributed to dysfunction of mitochondrial bioenergetics in p53-deficient cells, which was characterized by decreased mitochondrial respiration, steady-state ATP level and membrane potential, but augmented reactive oxygen species (ROS). Reactive Oxygen Species 246-249 tumor protein p53 Homo sapiens 75-78
27462151-13 2016 Moreover, Se@PEI@siRNA exhibited enhanced cytotoxic effects on cancer cells and triggered intracellular reactive oxygen species, and the signaling pathways of p53 and AKT were activated to advance cell apoptosis. Reactive Oxygen Species 104-127 tumor protein p53 Homo sapiens 159-162
27233942-5 2016 Stronger intracellular TrxR inhibition and higher accumulation of ROS (O2( -) and H2O2) are responsible for more effective S-phase arrest and mitochondria-mediated apoptotic induction of A549 cells by PL-CL than PLvia p53-p21-cyclinA/CDK2 and ASK1-JNK/p38 signaling cascade pathways, respectively. Reactive Oxygen Species 66-69 tumor protein p53 Homo sapiens 218-221
27236003-0 2016 Honokiol induces autophagic cell death in malignant glioma through reactive oxygen species-mediated regulation of the p53/PI3K/Akt/mTOR signaling pathway. Reactive Oxygen Species 67-90 tumor protein p53 Homo sapiens 118-121
27236003-13 2016 Taken together, our data indicated that honokiol induced ROS-mediated autophagic cell death through regulating the p53/PI3K/Akt/mTOR signaling pathway. Reactive Oxygen Species 57-60 tumor protein p53 Homo sapiens 115-118
27323408-2 2016 Cellular stressors such as reactive oxygen species can promote translocation of p53 into mitochondria where it acts to protect mitochondrial genome or trigger cell death via transcription-independent manner. Reactive Oxygen Species 27-50 tumor protein p53 Homo sapiens 80-83
27270209-9 2016 Citral increases intracellular oxygen radicals and this leads to activation of p53. Reactive Oxygen Species 31-46 tumor protein p53 Homo sapiens 79-82
27399772-7 2016 It generated a distinct response in reactive oxygen species (ROS) generation and p53 levels depending on the p53 cell line status (wild type or mutant). Reactive Oxygen Species 36-59 tumor protein p53 Homo sapiens 109-112
27399772-7 2016 It generated a distinct response in reactive oxygen species (ROS) generation and p53 levels depending on the p53 cell line status (wild type or mutant). Reactive Oxygen Species 61-64 tumor protein p53 Homo sapiens 109-112
27371670-4 2016 Similarly, during oxygen stress, p53 facilitates redirection of cellular metabolism toward energy generation through nonoxidative means, the suppression of reactive oxygen species (ROS) generation, and ROS detoxification-promoting cell survival. Reactive Oxygen Species 156-179 tumor protein p53 Homo sapiens 33-36
27371670-4 2016 Similarly, during oxygen stress, p53 facilitates redirection of cellular metabolism toward energy generation through nonoxidative means, the suppression of reactive oxygen species (ROS) generation, and ROS detoxification-promoting cell survival. Reactive Oxygen Species 181-184 tumor protein p53 Homo sapiens 33-36
27371670-4 2016 Similarly, during oxygen stress, p53 facilitates redirection of cellular metabolism toward energy generation through nonoxidative means, the suppression of reactive oxygen species (ROS) generation, and ROS detoxification-promoting cell survival. Reactive Oxygen Species 202-205 tumor protein p53 Homo sapiens 33-36
26630137-8 2016 TP53 participated in ROS- and DNA damage-induced cell death differently. Reactive Oxygen Species 21-24 tumor protein p53 Homo sapiens 0-4
27148686-3 2016 Costunolide induced an ROS-dependent increase in p53 abrogated telomerase activity. Reactive Oxygen Species 23-26 tumor protein p53 Homo sapiens 49-52
26984266-11 2016 Based on these results, kaempferol-induced HUVEC apoptosis was involved in an ROS-mediated p53/ATM/death receptor signaling. Reactive Oxygen Species 78-81 tumor protein p53 Homo sapiens 91-94
26936454-7 2016 Furthermore, CA generated reactive oxygen species (ROS), and pretreatment with ROS scavenger N-acetyl cysteine (NAC) abrogated CA-induced cleavage of PARP and expression of p53. Reactive Oxygen Species 79-82 tumor protein p53 Homo sapiens 173-176
27102814-13 2016 The increased ROS production up-regulated the p53 protein level, which led to the up-regulation of Bax and down-regulation of Bcl-2. Reactive Oxygen Species 14-17 tumor protein p53 Homo sapiens 46-49
26936104-11 2016 Notably, these effects were shown to be mediated, at least in part, via inhibition of the ROS-p38-p53 pathway. Reactive Oxygen Species 90-93 tumor protein p53 Homo sapiens 98-101
26934645-7 2016 Moreover, N-acetylcysteine (reactive oxygen species scavenger) blocked the SK inhibitor-induced increase in p21 and p53 expression but had no effect on the proteasomal degradation of SK1a. Reactive Oxygen Species 28-51 tumor protein p53 Homo sapiens 116-119
26675982-1 2016 The TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene known to regulate glycolysis by acting as fructose bis-phosphatase (FBPase) and modulate reactive oxygen species. Reactive Oxygen Species 170-193 tumor protein p53 Homo sapiens 65-68
26691054-1 2016 The TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene, which functions to suppress reactive oxygen species (ROS) damage and protect cells from apoptosis. Reactive Oxygen Species 110-133 tumor protein p53 Homo sapiens 65-68
26691054-1 2016 The TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene, which functions to suppress reactive oxygen species (ROS) damage and protect cells from apoptosis. Reactive Oxygen Species 135-138 tumor protein p53 Homo sapiens 65-68
27032906-7 2016 Furthermore, NF-kappaB/p53 pathway was activated during the process of autophagy induced by TCS and the ROS generation was mediated by it in MKN-45 cells. Reactive Oxygen Species 104-107 tumor protein p53 Homo sapiens 23-26
26936104-0 2016 Paeoniflorin attenuates ultraviolet B-induced apoptosis in human keratinocytes by inhibiting the ROS-p38-p53 pathway. Reactive Oxygen Species 97-100 tumor protein p53 Homo sapiens 105-108
26936104-6 2016 The present study evaluated the protective effects of PF on UV-induced skin damage in vitro, and demonstrated that the effects were mediated via the ROS-p38-p53 pathway. Reactive Oxygen Species 149-152 tumor protein p53 Homo sapiens 157-160
26936104-9 2016 Treatment with PF markedly reduced the production of ROS, and inhibited the activation of p38 and p53 in human keratinocytes, thus suggesting that the ROS-p38-p53 pathway has a role in UV-B-induced skin damage. Reactive Oxygen Species 151-154 tumor protein p53 Homo sapiens 98-101
26794443-7 2016 In contrast, NADPH oxidase and p53 (especially acetylation-defective mutant p53) act as positive regulators of ferroptosis by promotion of ROS production and inhibition of expression of SLC7A11 (a specific light-chain subunit of the cystine/glutamate antiporter), respectively. Reactive Oxygen Species 139-142 tumor protein p53 Homo sapiens 31-34
26794443-7 2016 In contrast, NADPH oxidase and p53 (especially acetylation-defective mutant p53) act as positive regulators of ferroptosis by promotion of ROS production and inhibition of expression of SLC7A11 (a specific light-chain subunit of the cystine/glutamate antiporter), respectively. Reactive Oxygen Species 139-142 tumor protein p53 Homo sapiens 76-79
26727575-7 2016 Knockdown of p53, Mieap or BNIP3 in LS174T cells severely impaired the hypoxia-activated function, leading to the accumulation of unhealthy mitochondria and increase of mitochondrial reactive oxygen species generation. Reactive Oxygen Species 183-206 tumor protein p53 Homo sapiens 13-16
26592665-3 2016 Exposure of H460 cells to radiation induced a marked accumulation of cell death-promoting reactive oxygen species, but this effect was blocked in radiation-treated H460 PSMC5-knockdown cells through downregulation of the p53-p21 pathway. Reactive Oxygen Species 90-113 tumor protein p53 Homo sapiens 221-224
26727575-8 2016 The mitochondrial reactive oxygen species generated by unhealthy mitochondria in the p53/Mieap/BNIP3-deficient cells remarkably enhanced cancer cell migration and invasion under hypoxic condition. Reactive Oxygen Species 18-41 tumor protein p53 Homo sapiens 85-88
26264138-2 2015 P53 overproduction led to transcriptional downregulation of some yeast genes, such as the TRX1/2 thioredoxin system, which plays a key role in cell protection against various oxidative stresses induced by reactive oxygen species (ROS). Reactive Oxygen Species 205-228 tumor protein p53 Homo sapiens 0-3
26472020-11 2015 These findings suggest that ROS and p53 mutations may trigger a series of events, beginning with overexpressing miR-182 by ROS and beta-catenin, impairing the DNA damage response, promoting DNA instability, bypassing senescence and eventually leading to DNA instable tumors in FTSE cells. Reactive Oxygen Species 123-126 tumor protein p53 Homo sapiens 36-39
26535076-5 2015 H2O2-induced ROS increased the levels of phosphorylated p38 mitogen activated protein kinase (MAPK), Jun-N-terminal kinase (JNK), ataxia telangiectasia mutated (ATM), and p53, which were inhibited by lycopene pretreatment. Reactive Oxygen Species 13-16 tumor protein p53 Homo sapiens 171-174
26259609-5 2015 Mitochondrial biogenesis and cytosolic production of reactive oxygen species were also reduced after p53 inhibition; the latter change induced mitochondrial superoxide accumulation and mitochondrial damage, which triggered the activation of caspase 3. Reactive Oxygen Species 53-76 tumor protein p53 Homo sapiens 101-104
26408691-5 2015 Zinc induces apoptosis in melanoma cells by increasing ROS and this effect may be mediated by the ROS-dependent induction of p53 and FAS/FAS ligand. Reactive Oxygen Species 98-101 tumor protein p53 Homo sapiens 125-128
26363031-7 2015 When p53 and Rb were turned down, the FF-exposed secretory cells overcame apoptosis and expanded the population carrying ROS and DSB. Reactive Oxygen Species 121-124 tumor protein p53 Homo sapiens 5-8
26363031-11 2015 The study revealed ROS and mitogens in mature ovarian follicles could initiate the transformation of fimbria epithelium in the context of p53 loss and melatonin is a potent preventive agent. Reactive Oxygen Species 19-22 tumor protein p53 Homo sapiens 138-141
26459859-8 2015 All these parameters conclude that elevated unconjugated bilirubin causes thrombocytopenia by stimulating platelet apoptosis via mitochondrial ROS-induced p38 and p53 activation. Reactive Oxygen Species 143-146 tumor protein p53 Homo sapiens 163-166
26264138-2 2015 P53 overproduction led to transcriptional downregulation of some yeast genes, such as the TRX1/2 thioredoxin system, which plays a key role in cell protection against various oxidative stresses induced by reactive oxygen species (ROS). Reactive Oxygen Species 230-233 tumor protein p53 Homo sapiens 0-3
26264138-5 2015 Furthermore, measurements of ROS amounts by flow cytometry and fluorescence microscopy indicated that the TRX2 protein acted probably through its increased detoxifying activity on the P53-generated ROS. Reactive Oxygen Species 29-32 tumor protein p53 Homo sapiens 184-187
26264138-5 2015 Furthermore, measurements of ROS amounts by flow cytometry and fluorescence microscopy indicated that the TRX2 protein acted probably through its increased detoxifying activity on the P53-generated ROS. Reactive Oxygen Species 198-201 tumor protein p53 Homo sapiens 184-187
26264138-8 2015 Our data strengthen the idea that overexpression of a single gene (trx2) decreases the p53-mediated cell death by decreasing ROS accumulation. Reactive Oxygen Species 125-128 tumor protein p53 Homo sapiens 87-90
26148435-4 2015 Importantly, it has been reported that arsenic induces reactive oxygen species (ROS), a process counteracted by p53. Reactive Oxygen Species 55-78 tumor protein p53 Homo sapiens 112-115
26133772-1 2015 The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS). Reactive Oxygen Species 158-181 tumor protein p53 Homo sapiens 4-7
26133772-1 2015 The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS). Reactive Oxygen Species 158-181 tumor protein p53 Homo sapiens 66-69
26133772-1 2015 The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS). Reactive Oxygen Species 158-181 tumor protein p53 Homo sapiens 66-69
26133772-1 2015 The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS). Reactive Oxygen Species 183-186 tumor protein p53 Homo sapiens 4-7
26133772-1 2015 The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS). Reactive Oxygen Species 183-186 tumor protein p53 Homo sapiens 66-69
26133772-1 2015 The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS). Reactive Oxygen Species 183-186 tumor protein p53 Homo sapiens 66-69
26148435-4 2015 Importantly, it has been reported that arsenic induces reactive oxygen species (ROS), a process counteracted by p53. Reactive Oxygen Species 80-83 tumor protein p53 Homo sapiens 112-115
26148435-7 2015 Furthermore, for the first time, we demonstrate that arsenic activates p53-dependent transcription of ROS detoxification genes, such as SESN1, and by an indirect mechanism involving ATF3, genes that could be responsible for the S phase cell cycle arrest, such as CDC25A. Reactive Oxygen Species 102-105 tumor protein p53 Homo sapiens 71-74
26114728-6 2015 ROS production by LFBL mediated p53-dependent apoptosis and recovery was suppressed by promoting G1/S phase arrest and failure of cellular tight junctions. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 32-35
26122615-3 2015 p53 regulates various metabolic pathways, helping to balance glycolysis and oxidative phosphorylation, limiting the production of reactive oxygen species, and contributing to the ability of cells to adapt to and survive mild metabolic stresses. Reactive Oxygen Species 130-153 tumor protein p53 Homo sapiens 0-3
26051007-0 2015 Proteomic Analysis of G2/M Arrest Triggered by Natural Borneol/Curcumin in HepG2 Cells, the Importance of the Reactive Oxygen Species-p53 Pathway. Reactive Oxygen Species 110-133 tumor protein p53 Homo sapiens 134-137
26162681-7 2015 Downstream events, measured by time-series reverse-phase protein microarrays, high-content imaging, and flow cytometry, showed a dramatic increase in mitochondrially produced reactive oxygen species (ROS) and subsequent DNA damage with up-regulation of ATM, p53, and p21 proteins. Reactive Oxygen Species 175-198 tumor protein p53 Homo sapiens 258-261
26162681-7 2015 Downstream events, measured by time-series reverse-phase protein microarrays, high-content imaging, and flow cytometry, showed a dramatic increase in mitochondrially produced reactive oxygen species (ROS) and subsequent DNA damage with up-regulation of ATM, p53, and p21 proteins. Reactive Oxygen Species 200-203 tumor protein p53 Homo sapiens 258-261
26049746-4 2015 This apparently irreversible EPHOSS phenomenon results from increased mitochondrial reactive oxygen species, mediated by a p53-cyclophilin D-mitochondrial permeability transition pore axis, and involves hypoxia inducing factor-1alpha and micro-RNA 210. Reactive Oxygen Species 84-107 tumor protein p53 Homo sapiens 123-126
25947292-0 2015 PLGA-Loaded Gold-Nanoparticles Precipitated with Quercetin Downregulate HDAC-Akt Activities Controlling Proliferation and Activate p53-ROS Crosstalk to Induce Apoptosis in Hepatocarcinoma Cells. Reactive Oxygen Species 135-138 tumor protein p53 Homo sapiens 131-134
26105784-5 2015 Taken together, our results indicate that heat stress induces apoptosis through the mitochondrial pathway with ROS dependent mitochondrial p53 translocation and Ca(2+) dyshomeostasis, and the ensuing intro Bax mitochondrial translocation as the upstream events involved in triggering the apoptotic process observed upon cellular exposure to heat stress. Reactive Oxygen Species 111-114 tumor protein p53 Homo sapiens 139-142
25947292-9 2015 NQ induced apoptosis in HepG2 cells by activating p53-ROS crosstalk and induces epigenetic modifications leading to inhibited proliferation and cell cycle arrest. Reactive Oxygen Species 54-57 tumor protein p53 Homo sapiens 50-53
25839657-4 2015 Intracellular ROS levels were increased in hBM-MSCs; this was accompanied by a decrease in the expression of the antioxidant enzymes catalase and superoxide dismutase (SOD)1 and 2 and of phosphorylated forkhead box O1 (p-FOXO1) as well as an increase in the expression of p53 and p16, along with a reduction in differentiation potential. Reactive Oxygen Species 14-17 tumor protein p53 Homo sapiens 272-275
26024660-0 2015 ROS-p53-cyclophilin-D signaling mediates salinomycin-induced glioma cell necrosis. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 4-7
27314071-2 2016 We have uncovered a novel function of p53 that contributes to tumor suppression through regulation of cystine metabolism, reactive oxygen species responses, and ferroptosis. Reactive Oxygen Species 122-145 tumor protein p53 Homo sapiens 38-41
26024660-9 2015 Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 78-81
26024660-9 2015 Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 228-231
26024660-9 2015 Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death. Reactive Oxygen Species 25-28 tumor protein p53 Homo sapiens 78-81
26024660-9 2015 Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death. Reactive Oxygen Species 25-28 tumor protein p53 Homo sapiens 228-231
25839657-5 2015 When the antioxidant ascorbic acid was used to eliminate excess ROS, the levels of antioxidant enzymes (catalase, SOD1 and 2, p-FOXO1, and p53) were partly restored. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 139-142
24858040-9 2015 The increased production of ROS because of p53 loss was rescued by SLC2A9 expression. Reactive Oxygen Species 28-31 tumor protein p53 Homo sapiens 43-46
25814188-8 2015 It was also shown that OXAZ-1 potently triggered a p53-dependent mitochondria-mediated apoptosis, characterized by reactive oxygen species generation, mitochondrial membrane potential dissipation, Bax translocation to mitochondria, and cytochrome c release, and exhibited a p53-dependent synergistic effect with conventional chemotherapeutic drugs. Reactive Oxygen Species 115-138 tumor protein p53 Homo sapiens 51-54
24858040-6 2015 We identified the uric acid transporter SLC2A9 (also known as GLUT9) as a direct p53 target gene and a key downstream effector in the reduction of reactive oxygen species (ROS) through transporting uric acid as a source of antioxidant. Reactive Oxygen Species 147-170 tumor protein p53 Homo sapiens 81-84
24858040-6 2015 We identified the uric acid transporter SLC2A9 (also known as GLUT9) as a direct p53 target gene and a key downstream effector in the reduction of reactive oxygen species (ROS) through transporting uric acid as a source of antioxidant. Reactive Oxygen Species 172-175 tumor protein p53 Homo sapiens 81-84
25799988-3 2015 Notably, p53(3KR), an acetylation-defective mutant that fails to induce cell-cycle arrest, senescence and apoptosis, fully retains the ability to regulate SLC7A11 expression and induce ferroptosis upon reactive oxygen species (ROS)-induced stress. Reactive Oxygen Species 202-225 tumor protein p53 Homo sapiens 9-12
25799988-3 2015 Notably, p53(3KR), an acetylation-defective mutant that fails to induce cell-cycle arrest, senescence and apoptosis, fully retains the ability to regulate SLC7A11 expression and induce ferroptosis upon reactive oxygen species (ROS)-induced stress. Reactive Oxygen Species 227-230 tumor protein p53 Homo sapiens 9-12
24858040-7 2015 Oxidative stress induced SLC2A9 expression in a p53-dependent manner, and inhibition of SLC2A9 by small interfering RNA (siRNA) or anti-gout drugs such as probenecid significantly increased ROS levels in an uric acid-dependent manner and greatly sensitized cancer cells to chemotherapeutic drugs. Reactive Oxygen Species 190-193 tumor protein p53 Homo sapiens 48-51
25799988-6 2015 Our findings uncover a new mode of tumour suppression based on p53 regulation of cystine metabolism, ROS responses and ferroptosis. Reactive Oxygen Species 101-104 tumor protein p53 Homo sapiens 63-66
24858040-11 2015 Our findings suggest that the p53-SLC2A9 pathway is a novel antioxidant mechanism that uses uric acid to maintain ROS homeostasis and prevent accumulation of ROS-associated damage that potentially contributes to cancer development. Reactive Oxygen Species 114-117 tumor protein p53 Homo sapiens 30-33
24858040-11 2015 Our findings suggest that the p53-SLC2A9 pathway is a novel antioxidant mechanism that uses uric acid to maintain ROS homeostasis and prevent accumulation of ROS-associated damage that potentially contributes to cancer development. Reactive Oxygen Species 158-161 tumor protein p53 Homo sapiens 30-33
24469051-4 2015 Interestingly, p53 promotes miR-506 expression level, indicating that miR-506 mediates cross talk between p53, NF-kappaB p65 and ROS. Reactive Oxygen Species 129-132 tumor protein p53 Homo sapiens 15-18
25658320-7 2015 To a different extent, either the antioxidant N-acetyl-cysteine or the p53 inhibitor, Pifithrin-alpha, recover cell viability and decrease ROS formation. Reactive Oxygen Species 139-142 tumor protein p53 Homo sapiens 71-74
32262124-7 2015 Furthermore, the intracellular nanosystem triggered the overproduction of reactive oxygen species (ROS) as early as 25 min after treatment, which activated various downstream signaling pathways such as p53, AKT and MAPKs to induce the cell death. Reactive Oxygen Species 74-97 tumor protein p53 Homo sapiens 202-205
32262124-7 2015 Furthermore, the intracellular nanosystem triggered the overproduction of reactive oxygen species (ROS) as early as 25 min after treatment, which activated various downstream signaling pathways such as p53, AKT and MAPKs to induce the cell death. Reactive Oxygen Species 99-102 tumor protein p53 Homo sapiens 202-205
25766317-0 2015 Reactive oxygen species and p21Waf1/Cip1 are both essential for p53-mediated senescence of head and neck cancer cells. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 64-67
25766317-4 2015 DNA-damaging reactive oxygen species (ROS) are a by-product of ionizing radiation that lead to the activation of p53, transcription of p21(cip1/waf1) and, in the case of wild-type TP53 HNSCC cells, cause senescence. Reactive Oxygen Species 13-36 tumor protein p53 Homo sapiens 113-116
25766317-4 2015 DNA-damaging reactive oxygen species (ROS) are a by-product of ionizing radiation that lead to the activation of p53, transcription of p21(cip1/waf1) and, in the case of wild-type TP53 HNSCC cells, cause senescence. Reactive Oxygen Species 13-36 tumor protein p53 Homo sapiens 180-184
25766317-4 2015 DNA-damaging reactive oxygen species (ROS) are a by-product of ionizing radiation that lead to the activation of p53, transcription of p21(cip1/waf1) and, in the case of wild-type TP53 HNSCC cells, cause senescence. Reactive Oxygen Species 38-41 tumor protein p53 Homo sapiens 113-116
25766317-4 2015 DNA-damaging reactive oxygen species (ROS) are a by-product of ionizing radiation that lead to the activation of p53, transcription of p21(cip1/waf1) and, in the case of wild-type TP53 HNSCC cells, cause senescence. Reactive Oxygen Species 38-41 tumor protein p53 Homo sapiens 180-184
25766317-6 2015 For the first time, we show that persistent exposure to low levels of the ROS, hydrogen peroxide, leads to the long-term expression of p21 in HNSCC cells with a partially functional TP53, resulting in senescence. Reactive Oxygen Species 74-77 tumor protein p53 Homo sapiens 182-186
25766317-7 2015 We conclude that the level of ROS is crucial in initiating p53"s transcription of p21 leading to senescence. Reactive Oxygen Species 30-33 tumor protein p53 Homo sapiens 59-62
25766317-8 2015 It is p21"s ability to sustain elevated levels of ROS, in turn, that allows for a long-term oxidative stress, and ensures an active p53-p21-ROS signaling loop. Reactive Oxygen Species 50-53 tumor protein p53 Homo sapiens 132-135
25766317-8 2015 It is p21"s ability to sustain elevated levels of ROS, in turn, that allows for a long-term oxidative stress, and ensures an active p53-p21-ROS signaling loop. Reactive Oxygen Species 140-143 tumor protein p53 Homo sapiens 132-135
25575314-4 2015 Although 1, 2 and pifithrin-alpha caused serious inhibition on p53, 1 and 2 significantly cause the loss of mitochondrial membrane potential and increase of the reactive oxygen species level, cytochrome c, apaf-1 and caspase-3/9 ratio in BEL-7404 cells. Reactive Oxygen Species 161-184 tumor protein p53 Homo sapiens 63-75
24469051-4 2015 Interestingly, p53 promotes miR-506 expression level, indicating that miR-506 mediates cross talk between p53, NF-kappaB p65 and ROS. Reactive Oxygen Species 129-132 tumor protein p53 Homo sapiens 106-109
25583481-7 2015 p53 genetic inactivation in ETC-impaired neural stem cells is caused by increased reactive oxygen species and associated oxidative DNA damage. Reactive Oxygen Species 82-105 tumor protein p53 Homo sapiens 0-3
25404486-0 2015 Selective ROS-dependent p53-associated anticancer effects of the hypoxoside derivative rooperol on human teratocarcinomal cancer stem-like cells. Reactive Oxygen Species 10-13 tumor protein p53 Homo sapiens 24-27
25464270-0 2015 CUL4B impedes stress-induced cellular senescence by dampening a p53-reactive oxygen species positive feedback loop. Reactive Oxygen Species 68-91 tumor protein p53 Homo sapiens 64-67
25464270-1 2015 Tumor suppressor p53 is known to regulate the level of intracellular reactive oxygen species (ROS). Reactive Oxygen Species 69-92 tumor protein p53 Homo sapiens 17-20
25464270-1 2015 Tumor suppressor p53 is known to regulate the level of intracellular reactive oxygen species (ROS). Reactive Oxygen Species 94-97 tumor protein p53 Homo sapiens 17-20
25464270-3 2015 We here report that a p53-ROS positive feedback loop drives a senescence program in normal human fibroblasts (NHFs) and this senescence-driving loop is negatively regulated by CUL4B. Reactive Oxygen Species 26-29 tumor protein p53 Homo sapiens 22-25
25464270-5 2015 We observed that p53-dependent ROS production was significantly augmented and stress-induced senescence was greatly enhanced when CUL4B was absent or depleted. Reactive Oxygen Species 31-34 tumor protein p53 Homo sapiens 17-20
25464270-8 2015 Together, our results established a critical role of CUL4B in negatively regulating the p53-ROS positive feedback loop that drives cellular senescence. Reactive Oxygen Species 92-95 tumor protein p53 Homo sapiens 88-91
25483438-14 2015 Such a decrease generates intracellular ROS, which increases ER stress-mediated p53 expression, and subsequently causes apoptosis by increasing Bax promoter activity. Reactive Oxygen Species 40-43 tumor protein p53 Homo sapiens 80-83
25252686-4 2015 In this study, we show that virus-mediated ROS upregulation activates the protein kinase, ataxia telangiectasia mutated, which in turn phosphorylates serine 15 on p53. Reactive Oxygen Species 43-46 tumor protein p53 Homo sapiens 163-166
25483068-0 2015 ATM regulates cell fate choice upon p53 activation by modulating mitochondrial turnover and ROS levels. Reactive Oxygen Species 92-95 tumor protein p53 Homo sapiens 36-39
26218928-0 2015 Dynamic roles of p53-mediated metabolic activities in ROS-induced stress responses. Reactive Oxygen Species 54-57 tumor protein p53 Homo sapiens 17-20
26218928-5 2015 Here, we report that wild type p53 can induce both apoptosis and ferroptosis upon reactive oxygen species (ROS)-induced stress. Reactive Oxygen Species 82-105 tumor protein p53 Homo sapiens 31-34
26218928-5 2015 Here, we report that wild type p53 can induce both apoptosis and ferroptosis upon reactive oxygen species (ROS)-induced stress. Reactive Oxygen Species 107-110 tumor protein p53 Homo sapiens 31-34
26218928-7 2015 Notably, activated p53 dynamically modulates intracellular ROS, causing an initial reduction and a subsequent increase of ROS levels. Reactive Oxygen Species 59-62 tumor protein p53 Homo sapiens 19-22
26218928-7 2015 Notably, activated p53 dynamically modulates intracellular ROS, causing an initial reduction and a subsequent increase of ROS levels. Reactive Oxygen Species 122-125 tumor protein p53 Homo sapiens 19-22
25464291-7 2015 Firstly, reactive oxygen species (ROS) is generated induced by MnO@SiO2 NPs, then p53 is activated followed by an increase in the bax and a decrease in the bcl-2, ultimately leading to G2/M phase arrest, increasing the activity of caspase-3 and inducing apoptosis. Reactive Oxygen Species 9-32 tumor protein p53 Homo sapiens 82-85
25464291-7 2015 Firstly, reactive oxygen species (ROS) is generated induced by MnO@SiO2 NPs, then p53 is activated followed by an increase in the bax and a decrease in the bcl-2, ultimately leading to G2/M phase arrest, increasing the activity of caspase-3 and inducing apoptosis. Reactive Oxygen Species 34-37 tumor protein p53 Homo sapiens 82-85
25252686-6 2015 Rather p53 appears to be involved in suppressing intracellular ROS levels in astrocytes under oxidative stress. Reactive Oxygen Species 63-66 tumor protein p53 Homo sapiens 7-10
25217696-5 2014 Normal hematopoietic cells showed elevated ROS levels through increased intracellular iron levels when treated with lipocalin-2, which led to p53 pathway activation, increased apoptosis, and decreased cellular proliferation. Reactive Oxygen Species 43-46 tumor protein p53 Homo sapiens 142-145
26123305-5 2015 In heart, RGS6-dependent reactive oxygen species (ROS) production promotes doxorubicin (Dox)-induced cardiomyopathy, while in cancer cells RGS6/ROS signaling is necessary for activation of the ataxia telangiectasia mutated/p53/apoptosis pathway required for the chemotherapeutic efficacy of Dox. Reactive Oxygen Species 144-147 tumor protein p53 Homo sapiens 223-226
25333296-2 2015 In the present study, the antiproliferative effects of IS on A375 human melanoma cells were examined in vitro and a possible mechanism through the ROS-p38-p53 pathway is discussed. Reactive Oxygen Species 147-150 tumor protein p53 Homo sapiens 155-158
25333296-8 2015 Crucially, it was confirmed that these effects were mediated at least in part by activating the ROS-p38-p53 pathway. Reactive Oxygen Species 96-99 tumor protein p53 Homo sapiens 104-107
25302047-2 2014 Evidence showed that tumor suppressor p53 plays an important role in regulating the generation of cellular ROS, either by reducing oxidative stress under physiological and mildly stressed conditions, or by promoting oxidative stress under highly stressed conditions. Reactive Oxygen Species 107-110 tumor protein p53 Homo sapiens 38-41
25448679-5 2014 Finally, HEPN1 overexpression increases the expression of p53, p21, and Bax, all of which are ROS-upregulated proteins. Reactive Oxygen Species 94-97 tumor protein p53 Homo sapiens 58-61
25108166-9 2014 These results collectively suggest that ROS are involved in activation of both the defensive and pro-apoptotic pathways encompassing HIF-1alpha and p53, respectively. Reactive Oxygen Species 40-43 tumor protein p53 Homo sapiens 148-151
25429619-0 2014 ROS inhibit autophagy by downregulating ULK1 mediated by the phosphorylation of p53 in selenite-treated NB4 cells. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 80-83
25429619-6 2014 Collectively, our results show that ROS inhibited autophagy by downregulating the p70S6K/p53/ULK1 axis in selenite-treated NB4 cells. Reactive Oxygen Species 36-39 tumor protein p53 Homo sapiens 89-92
24930072-6 2014 Up-regulation of p38 MAPK activity in responding the ROS stabilize p53 and activate p21 transcription, the critical regulatory in G1/S checkpoint. Reactive Oxygen Species 53-56 tumor protein p53 Homo sapiens 67-70
25139326-4 2014 This process is characterized by an early generation of reactive oxygen species (ROS) resulting in p53 up-regulation. Reactive Oxygen Species 56-79 tumor protein p53 Homo sapiens 99-102
25139326-4 2014 This process is characterized by an early generation of reactive oxygen species (ROS) resulting in p53 up-regulation. Reactive Oxygen Species 81-84 tumor protein p53 Homo sapiens 99-102
25139326-9 2014 On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES. Reactive Oxygen Species 56-59 tumor protein p53 Homo sapiens 63-66
25139326-9 2014 On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES. Reactive Oxygen Species 56-59 tumor protein p53 Homo sapiens 111-114
25139326-9 2014 On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES. Reactive Oxygen Species 56-59 tumor protein p53 Homo sapiens 111-114
25139326-9 2014 On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES. Reactive Oxygen Species 151-154 tumor protein p53 Homo sapiens 63-66
25139326-9 2014 On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES. Reactive Oxygen Species 151-154 tumor protein p53 Homo sapiens 111-114
25139326-9 2014 On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES. Reactive Oxygen Species 151-154 tumor protein p53 Homo sapiens 111-114
25139326-9 2014 On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES. Reactive Oxygen Species 151-154 tumor protein p53 Homo sapiens 63-66
25139326-9 2014 On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES. Reactive Oxygen Species 151-154 tumor protein p53 Homo sapiens 111-114
25139326-9 2014 On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES. Reactive Oxygen Species 151-154 tumor protein p53 Homo sapiens 111-114
25139326-10 2014 In sum, p53 up-regulation by ROS triggers a positive feedback loop responsible of further increasing ROS production and reinforcing PES-driven non-necroptotic necrosis. Reactive Oxygen Species 29-32 tumor protein p53 Homo sapiens 8-11
25139326-10 2014 In sum, p53 up-regulation by ROS triggers a positive feedback loop responsible of further increasing ROS production and reinforcing PES-driven non-necroptotic necrosis. Reactive Oxygen Species 101-104 tumor protein p53 Homo sapiens 8-11
25086499-3 2014 Furthermore, while p53R2, a p53-inducible peptide involved in the synthesis of dNTPs normally works toward suppression of cancer through elimination of reactive oxygen species (ROS), inhibition of MAPK/ERK pathway and providing dNTPs for DNA repair, the overexpression of p53R2 is reported to be associated with cancer progression and resistance to therapy. Reactive Oxygen Species 177-180 tumor protein p53 Homo sapiens 19-22
25115399-2 2014 Here, we show that cytoplasmic p53 suppresses cell invasion by reducing mitochondrial reactive oxygen species (ROS) levels. Reactive Oxygen Species 86-109 tumor protein p53 Homo sapiens 31-34
25115399-2 2014 Here, we show that cytoplasmic p53 suppresses cell invasion by reducing mitochondrial reactive oxygen species (ROS) levels. Reactive Oxygen Species 111-114 tumor protein p53 Homo sapiens 31-34
25115399-3 2014 Analysis revealed that this function is mediated by Bcl-2 family proteins: Cytoplasmic p53 binds Bcl-w, liberating Bax, which then binds ND5, a subunit of respiratory complex-I, thereby suppressing complex-I activity and thus ROS production. Reactive Oxygen Species 226-229 tumor protein p53 Homo sapiens 87-90
25115399-7 2014 This study demonstrates a link between p53 and Bcl-2 proteins as regulators of ROS production and cellular invasiveness, and reveals complex-I, especially ND5, as their functional target. Reactive Oxygen Species 79-82 tumor protein p53 Homo sapiens 39-42
25086499-3 2014 Furthermore, while p53R2, a p53-inducible peptide involved in the synthesis of dNTPs normally works toward suppression of cancer through elimination of reactive oxygen species (ROS), inhibition of MAPK/ERK pathway and providing dNTPs for DNA repair, the overexpression of p53R2 is reported to be associated with cancer progression and resistance to therapy. Reactive Oxygen Species 152-175 tumor protein p53 Homo sapiens 19-22
24839208-2 2014 Reactive oxygen species (ROS) and reactive nitrogen species generations have been proposed to be an important mechanism of DOX-induced cardiotoxicity and cardiomyocyte apoptosis, which may be mediated by p53 protein. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 204-207
24839208-2 2014 Reactive oxygen species (ROS) and reactive nitrogen species generations have been proposed to be an important mechanism of DOX-induced cardiotoxicity and cardiomyocyte apoptosis, which may be mediated by p53 protein. Reactive Oxygen Species 25-28 tumor protein p53 Homo sapiens 204-207
25064843-0 2014 Phospholipase D2 downregulation induces cellular senescence through a reactive oxygen species-p53-p21Cip1/WAF1 pathway. Reactive Oxygen Species 70-93 tumor protein p53 Homo sapiens 94-97
25064843-7 2014 Taken together, these results show that PLD2 downregulation causes senescence through the p53-p21(Cip1/WAF1) pathway by stimulating ROS production, which is induced by CK2 inhibition. Reactive Oxygen Species 132-135 tumor protein p53 Homo sapiens 90-93
24859470-0 2014 As a novel p53 direct target, bidirectional gene HspB2/alphaB-crystallin regulates the ROS level and Warburg effect. Reactive Oxygen Species 87-90 tumor protein p53 Homo sapiens 11-14
24946211-8 2014 Our data found that in prostate cancer cells, berberine induced reactive oxygen species (ROS) production, which dictated P53 translocation to mitochondria, where it physically interacted with Cyp-D to open mitochondrial permeability transition pore (mPTP). Reactive Oxygen Species 89-92 tumor protein p53 Homo sapiens 121-124
24918814-7 2014 RESULTS: Ionising radiation induced a dramatic reactive oxygen species (ROS)-mediated inhibition of GI, leading to AP-modified Hsp27 protein accumulation that, in a mechanism involving p53 and NF-kappaB, triggered an apoptotic mitochondrial pathway. Reactive Oxygen Species 47-70 tumor protein p53 Homo sapiens 185-188
24918814-7 2014 RESULTS: Ionising radiation induced a dramatic reactive oxygen species (ROS)-mediated inhibition of GI, leading to AP-modified Hsp27 protein accumulation that, in a mechanism involving p53 and NF-kappaB, triggered an apoptotic mitochondrial pathway. Reactive Oxygen Species 72-75 tumor protein p53 Homo sapiens 185-188
24859470-9 2014 The ROS level and the Warburg effect are affected after the depletion of p53, HspB2 and alphaB-crystallin respectively. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 73-76
24859470-11 2014 These findings provide novel insights into the role of p53 as a regulator of bidirectional gene pair HspB2/alphaB-crystallin-mediated ROS and the Warburg effect. Reactive Oxygen Species 134-137 tumor protein p53 Homo sapiens 55-58
24841907-7 2014 These results demonstrated for the first time that ISO simultaneously induced apoptosis and autophagy by ROS-related p53, PI3K/Akt, JNK, and p38 signaling pathways. Reactive Oxygen Species 105-108 tumor protein p53 Homo sapiens 117-120
24932684-7 2014 Finally, increased p53 activation was found to be independent of aberrantly activated AMP-activated protein kinase (AMPK) that occurs in response to MIF/D-DT-deficiency but is dependent on reactive oxygen species (ROS) that mediate aberrant AMPK activation in these cells. Reactive Oxygen Species 189-212 tumor protein p53 Homo sapiens 19-22
24932684-7 2014 Finally, increased p53 activation was found to be independent of aberrantly activated AMP-activated protein kinase (AMPK) that occurs in response to MIF/D-DT-deficiency but is dependent on reactive oxygen species (ROS) that mediate aberrant AMPK activation in these cells. Reactive Oxygen Species 214-217 tumor protein p53 Homo sapiens 19-22
24841907-0 2014 Isoorientin induces apoptosis and autophagy simultaneously by reactive oxygen species (ROS)-related p53, PI3K/Akt, JNK, and p38 signaling pathways in HepG2 cancer cells. Reactive Oxygen Species 62-85 tumor protein p53 Homo sapiens 100-103
24841907-0 2014 Isoorientin induces apoptosis and autophagy simultaneously by reactive oxygen species (ROS)-related p53, PI3K/Akt, JNK, and p38 signaling pathways in HepG2 cancer cells. Reactive Oxygen Species 87-90 tumor protein p53 Homo sapiens 100-103
24829158-4 2014 CDDP induced apoptosis within cells through the generation of reactive oxygen species (ROS), regulated the ROS-mediated expression of Bax, Bcl-2, and p53, and induced the degradation of the poly (ADP-ribosyl) polymerase (PARP). Reactive Oxygen Species 107-110 tumor protein p53 Homo sapiens 150-153
24875531-8 2014 Our data suggest that RP loss promotes the aberrant activation of both S6 kinase and p53 by increasing intracellular ROS levels. Reactive Oxygen Species 117-120 tumor protein p53 Homo sapiens 85-88
24714748-10 2014 RESULTS: We found that WT-p53 is a potent suppressor of TGF-beta-induced Nox4, ROS production, and cell migration in p53-null lung epithelial (H1299) cells. Reactive Oxygen Species 79-82 tumor protein p53 Homo sapiens 26-29
24831807-0 2014 Interactions between exosomes from breast cancer cells and primary mammary epithelial cells leads to generation of reactive oxygen species which induce DNA damage response, stabilization of p53 and autophagy in epithelial cells. Reactive Oxygen Species 115-138 tumor protein p53 Homo sapiens 190-193
24759730-0 2014 Non-thermal atmospheric pressure plasma preferentially induces apoptosis in p53-mutated cancer cells by activating ROS stress-response pathways. Reactive Oxygen Species 115-118 tumor protein p53 Homo sapiens 76-79
24462821-7 2014 Furthermore, combining p53 inhibition and nutrient deprivation or 5-FU treatment resulted in a marked increase in reactive oxygen species generation and mitochondrial damage. Reactive Oxygen Species 114-137 tumor protein p53 Homo sapiens 23-26
24727577-12 2014 These findings show that CPF induced hNPCs death in part through NF-kappaB activation via ROS generation, enabling the interaction of p53 with Bcl-2 and Bax and subsequent release of cytochrome c. Reactive Oxygen Species 90-93 tumor protein p53 Homo sapiens 134-137
24381013-6 2014 p53 affects many aspects of cellular metabolism including catabolism, anabolism and reactive oxygen species levels. Reactive Oxygen Species 84-107 tumor protein p53 Homo sapiens 0-3
24535669-0 2014 Quercetin regulates the sestrin 2-AMPK-p38 MAPK signaling pathway and induces apoptosis by increasing the generation of intracellular ROS in a p53-independent manner. Reactive Oxygen Species 134-137 tumor protein p53 Homo sapiens 143-146
24413150-0 2014 ROS-dependent activation of JNK converts p53 into an efficient inhibitor of oncogenes leading to robust apoptosis. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 41-44
24413150-4 2014 Here, we report that concurrent pharmacological activation of p53 and inhibition of thioredoxin reductase followed by generation of reactive oxygen species (ROS), result in the synthetic lethality in cancer cells. Reactive Oxygen Species 132-155 tumor protein p53 Homo sapiens 62-65
24413150-4 2014 Here, we report that concurrent pharmacological activation of p53 and inhibition of thioredoxin reductase followed by generation of reactive oxygen species (ROS), result in the synthetic lethality in cancer cells. Reactive Oxygen Species 157-160 tumor protein p53 Homo sapiens 62-65
24413150-5 2014 ROS promote the activation of c-Jun N-terminal kinase (JNK) and DNA damage response, which establishes a positive feedback loop with p53. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 133-136
24413150-10 2014 Further, our results may enable new pharmacological strategy to exploit abnormally high ROS level, often linked with higher aggressiveness in cancer, to selectively kill cancer cells upon pharmacological reactivation of p53. Reactive Oxygen Species 88-91 tumor protein p53 Homo sapiens 220-223
24063548-5 2014 The reduction of PTEN in the nucleus, in turn, decreased p53 acetylation and transcription, reduced the expression of the p53 target gene glutathione peroxidase-1 (GPX1), resulting in reactive oxygen species (ROS) accumulation and endothelial damage. Reactive Oxygen Species 209-212 tumor protein p53 Homo sapiens 122-125
24959493-3 2014 In chronic hypoxia, there is a liberation of Reactive Oxygen Species (ROS) due to tissue injury as a result of ischemia and induction of hypoxia inducible factor - 1HIF-1 and p53 which in turn activates pro-apoptotic factors leading to alteration in the regulation of pro-apoptotic gene Blc-2 to be involved in causing the DNA damage. Reactive Oxygen Species 45-68 tumor protein p53 Homo sapiens 175-178
24959493-3 2014 In chronic hypoxia, there is a liberation of Reactive Oxygen Species (ROS) due to tissue injury as a result of ischemia and induction of hypoxia inducible factor - 1HIF-1 and p53 which in turn activates pro-apoptotic factors leading to alteration in the regulation of pro-apoptotic gene Blc-2 to be involved in causing the DNA damage. Reactive Oxygen Species 70-73 tumor protein p53 Homo sapiens 175-178
24667842-4 2014 Here, we aimed to determine the effect of SFN on ROS levels and to identify key biomarkers leading to ROS unbalance and apoptosis in the p53-null MG-63 osteosarcoma cell line. Reactive Oxygen Species 102-105 tumor protein p53 Homo sapiens 137-140
24063548-5 2014 The reduction of PTEN in the nucleus, in turn, decreased p53 acetylation and transcription, reduced the expression of the p53 target gene glutathione peroxidase-1 (GPX1), resulting in reactive oxygen species (ROS) accumulation and endothelial damage. Reactive Oxygen Species 184-207 tumor protein p53 Homo sapiens 122-125
24052409-0 2014 Mahanine synergistically enhances cytotoxicity of 5-fluorouracil through ROS-mediated activation of PTEN and p53/p73 in colon carcinoma. Reactive Oxygen Species 73-76 tumor protein p53 Homo sapiens 109-112
24356923-4 2014 The resultant p53 suppresses cell growth and induces a shorter cellular lifespan, and also compromises mitochondrial biogenesis leading to the overproduction of reactive oxygen species (ROS) causing multiple aging phenotypes. Reactive Oxygen Species 161-184 tumor protein p53 Homo sapiens 14-17
24356923-4 2014 The resultant p53 suppresses cell growth and induces a shorter cellular lifespan, and also compromises mitochondrial biogenesis leading to the overproduction of reactive oxygen species (ROS) causing multiple aging phenotypes. Reactive Oxygen Species 186-189 tumor protein p53 Homo sapiens 14-17
24052409-3 2014 We demonstrated that mahanine-induced apoptosis involved reactive oxygen species (ROS)-mediated nuclear accumulation of PTEN and its interaction with p53/p73. Reactive Oxygen Species 57-80 tumor protein p53 Homo sapiens 150-153
24052409-3 2014 We demonstrated that mahanine-induced apoptosis involved reactive oxygen species (ROS)-mediated nuclear accumulation of PTEN and its interaction with p53/p73. Reactive Oxygen Species 82-85 tumor protein p53 Homo sapiens 150-153
24361399-14 2014 SIGNIFICANCE: These results demonstrate that tamoxifen promotes senescence through a ROS-p53-p21(Cip1/WAF1) dependent pathway by inhibiting CK2 activity in breast cancer and colon cancer cells. Reactive Oxygen Species 85-88 tumor protein p53 Homo sapiens 89-92
24418562-0 2014 Reactive oxygen species activate NFkappaB (p65) and p53 and induce apoptosis in RVFV infected liver cells. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 52-55
24418562-5 2014 Increased ROS levels correlated with activation of NFkappaB (p65) and p53 responses, which in conjunction with infection, was also reflected as macromolecular rearrangements observed using size fractionation of protein lysates. Reactive Oxygen Species 10-13 tumor protein p53 Homo sapiens 70-73
23872073-6 2013 Reactive oxygen species (ROS)-dependent mechanisms initiated by TGF-beta1 were critical for EGFR(Y845) and p53(Ser15) phosphorylation and target gene expression. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 107-110
25013761-9 2014 Our results also demonstrated that p53 was activated followed by generation of reactive oxygen species (ROS) and activation of c-Jun N-terminal kinase (JNK). Reactive Oxygen Species 79-102 tumor protein p53 Homo sapiens 35-38
25013761-9 2014 Our results also demonstrated that p53 was activated followed by generation of reactive oxygen species (ROS) and activation of c-Jun N-terminal kinase (JNK). Reactive Oxygen Species 104-107 tumor protein p53 Homo sapiens 35-38
25140197-1 2014 While p53-dependent apoptosis is triggered by combination of methyltransferase inhibitor decitabine (DAC) and histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in leukemic cell line CML-T1, reactive oxygen species (ROS) generation as well as survivin and Bcl-2 deregulation participated in DAC + SAHA-induced apoptosis in p53-deficient HL-60 cell line. Reactive Oxygen Species 209-232 tumor protein p53 Homo sapiens 6-9
25140197-1 2014 While p53-dependent apoptosis is triggered by combination of methyltransferase inhibitor decitabine (DAC) and histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in leukemic cell line CML-T1, reactive oxygen species (ROS) generation as well as survivin and Bcl-2 deregulation participated in DAC + SAHA-induced apoptosis in p53-deficient HL-60 cell line. Reactive Oxygen Species 234-237 tumor protein p53 Homo sapiens 6-9
24359630-14 2013 Collectively, these data reveal a role for p53 in cellular metabolic reprogramming under acidosis, in order to permit increased bioenergetic capacity and ROS neutralization. Reactive Oxygen Species 154-157 tumor protein p53 Homo sapiens 43-46
24967384-6 2014 Our further studies demonstrated that ERR alpha suppressed ROS induction of tumor suppressor P53 and its target genes NOXA and XAF1 which are mediators of P53-dependent apoptosis. Reactive Oxygen Species 59-62 tumor protein p53 Homo sapiens 93-96
24967384-6 2014 Our further studies demonstrated that ERR alpha suppressed ROS induction of tumor suppressor P53 and its target genes NOXA and XAF1 which are mediators of P53-dependent apoptosis. Reactive Oxygen Species 59-62 tumor protein p53 Homo sapiens 155-158
24967384-7 2014 In conclusion, this study demonstrated that ERR alpha plays an important role in the development of MTX resistance through blocking MTX-induced ROS production and attenuating the activation of p53 mediated apoptosis signaling pathway, and points to ERR alpha as a novel target for improving osteosarcoma therapy. Reactive Oxygen Species 144-147 tumor protein p53 Homo sapiens 193-196
24376853-10 2013 Moreover, the p53 was phosphorylated, translocated into nucleus, and bound to Rp following ROS stimulation. Reactive Oxygen Species 91-94 tumor protein p53 Homo sapiens 14-17
24376853-11 2013 The results suggest ROS play an important role in initiation of EBV reactivation by MNNG through a p53-dependent mechanism. Reactive Oxygen Species 20-23 tumor protein p53 Homo sapiens 99-102
32261335-7 2013 Furthermore, Se@Trolox effectively blocked the cisplatin-induced reactive oxygen species (ROS) accumulation, activation of AKT and MAPK signaling and DNA damage-mediated p53 phosphorylation in HK-2 cells. Reactive Oxygen Species 65-88 tumor protein p53 Homo sapiens 170-173
32261335-7 2013 Furthermore, Se@Trolox effectively blocked the cisplatin-induced reactive oxygen species (ROS) accumulation, activation of AKT and MAPK signaling and DNA damage-mediated p53 phosphorylation in HK-2 cells. Reactive Oxygen Species 90-93 tumor protein p53 Homo sapiens 170-173
24090840-4 2013 At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53. Reactive Oxygen Species 32-35 tumor protein p53 Homo sapiens 37-40
24090840-4 2013 At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53. Reactive Oxygen Species 236-239 tumor protein p53 Homo sapiens 37-40
24090840-6 2013 p53 deficient cells cancer cells such as DLD-1 and SW480 are more susceptible to ZnO induced cell death compared to p53 proficient cells such as colon epithelial cells NCM460 and HCT116 cells in a ROS dependent manner. Reactive Oxygen Species 197-200 tumor protein p53 Homo sapiens 0-3
24090840-6 2013 p53 deficient cells cancer cells such as DLD-1 and SW480 are more susceptible to ZnO induced cell death compared to p53 proficient cells such as colon epithelial cells NCM460 and HCT116 cells in a ROS dependent manner. Reactive Oxygen Species 197-200 tumor protein p53 Homo sapiens 116-119
23786650-0 2013 Alpha particle-induced bystander effect is mediated by ROS via a p53-dependent SCO2 pathway in hepatoma cells. Reactive Oxygen Species 55-58 tumor protein p53 Homo sapiens 65-68
23703322-0 2013 p53 regulates a non-apoptotic death induced by ROS. Reactive Oxygen Species 47-50 tumor protein p53 Homo sapiens 0-3
23703322-1 2013 DNA damage induced by reactive oxygen species and several chemotherapeutic agents promotes both p53 and poly (ADP-ribose) polymerase (PARP) activation. Reactive Oxygen Species 22-45 tumor protein p53 Homo sapiens 96-99
23872073-6 2013 Reactive oxygen species (ROS)-dependent mechanisms initiated by TGF-beta1 were critical for EGFR(Y845) and p53(Ser15) phosphorylation and target gene expression. Reactive Oxygen Species 25-28 tumor protein p53 Homo sapiens 107-110
23807740-0 2013 Condurango-glycoside-A fraction of Gonolobus condurango induces DNA damage associated senescence and apoptosis via ROS-dependent p53 signalling pathway in HeLa cells. Reactive Oxygen Species 115-118 tumor protein p53 Homo sapiens 129-132
23768371-5 2013 Coumestrol promoted senescence through the p53-p21(Cip1/WAF1) pathway by inducing reactive oxygen species (ROS) production in MCF-7 and HCT116 cells. Reactive Oxygen Species 82-105 tumor protein p53 Homo sapiens 43-46
23768371-5 2013 Coumestrol promoted senescence through the p53-p21(Cip1/WAF1) pathway by inducing reactive oxygen species (ROS) production in MCF-7 and HCT116 cells. Reactive Oxygen Species 107-110 tumor protein p53 Homo sapiens 43-46
23807740-9 2013 Expression profiles of certain relevant genes and proteins like p53, Akt, Bcl-2, Bax, cytochrome c and caspase 3 also provided evidence of ROS mediated p53 up-regulation and further boost in Bax expression and followed by cytochrome c release and activation of caspase 3. Reactive Oxygen Species 139-142 tumor protein p53 Homo sapiens 64-67
23807740-9 2013 Expression profiles of certain relevant genes and proteins like p53, Akt, Bcl-2, Bax, cytochrome c and caspase 3 also provided evidence of ROS mediated p53 up-regulation and further boost in Bax expression and followed by cytochrome c release and activation of caspase 3. Reactive Oxygen Species 139-142 tumor protein p53 Homo sapiens 152-155
24005866-4 2013 Accumulation of reactive oxygen species (ROS) was observed in the progression of cell cycle arrest, which was associated with the increased expression of cell cycle regulating factors, p53 and p21. Reactive Oxygen Species 16-39 tumor protein p53 Homo sapiens 185-188
24005866-4 2013 Accumulation of reactive oxygen species (ROS) was observed in the progression of cell cycle arrest, which was associated with the increased expression of cell cycle regulating factors, p53 and p21. Reactive Oxygen Species 41-44 tumor protein p53 Homo sapiens 185-188
23966169-9 2013 Taking into account that deregulations of mitochondrial respiration and reactive oxygen species production are tightly linked to cancer development, we suggest that mitochondrial p53 may be an important regulator of normal mitochondrial and cellular physiology, potentially exerting tumor suppression activity inside mitochondria. Reactive Oxygen Species 72-95 tumor protein p53 Homo sapiens 179-182
23376438-7 2013 Use of an inhibitor specific to c-Jun N-terminal kinase (JNK), p38 kinase or p53, but not pan-caspase or caspase-8, decreased the toxin-induced generation of reactive oxygen species (ROS) and also attenuated the alpha-ZOL- or beta-ZOL-induced decrease of cell viability. Reactive Oxygen Species 158-181 tumor protein p53 Homo sapiens 77-80
23680455-3 2013 In normal conditions, ROS have an important role in signal transduction and gene transcription, nevertheless, ROS may act as a trigger for carcinogenesis via persistent DNA injuries as well as mutations in p53 such as conditions observed in skin, hepatocellular, and colon cancers. Reactive Oxygen Species 22-25 tumor protein p53 Homo sapiens 206-209
23817040-2 2013 TIGAR (TP53-induced glycolysis and apoptosis regulator), which is a p53-inducible gene, functions in the suppression of ROS (reactive oxygen species) and protects U2OS cells from undergoing cell death. Reactive Oxygen Species 120-123 tumor protein p53 Homo sapiens 68-71
23817040-2 2013 TIGAR (TP53-induced glycolysis and apoptosis regulator), which is a p53-inducible gene, functions in the suppression of ROS (reactive oxygen species) and protects U2OS cells from undergoing cell death. Reactive Oxygen Species 125-148 tumor protein p53 Homo sapiens 68-71
23684722-0 2013 Physalin A induces apoptosis via p53-Noxa-mediated ROS generation, and autophagy plays a protective role against apoptosis through p38-NF-kappaB survival pathway in A375-S2 cells. Reactive Oxygen Species 51-54 tumor protein p53 Homo sapiens 33-36
23376438-10 2013 Collectively, these results suggest that the activation of p53, JNK or p38 kinase by ZEN metabolites is the main upstream signal required for the mitochondrial alteration of Bcl-2/Bax signaling pathways and intracellular ROS generation, while MMP loss and nuclear translocation of AIF are the critical downstream events for ZEN metabolite-mediated apoptosis in macrophages. Reactive Oxygen Species 221-224 tumor protein p53 Homo sapiens 59-62
23684722-12 2013 CONCLUSIONS: Physalin A induced apoptotic cell death via p53-Noxa-mediated ROS generation, and autophagy played a protective role against apoptosis through up-regulating the p38-NF-kappaB survival pathway in A375-S2 cells. Reactive Oxygen Species 75-78 tumor protein p53 Homo sapiens 57-60
23844043-11 2013 Our study demonstrates that UVB irradiation results in ROS accumulation and ERK activation, which causes the nuclear p53 accumulation and TM promoter binding to inhibit TM expression. Reactive Oxygen Species 55-58 tumor protein p53 Homo sapiens 117-120
23376438-7 2013 Use of an inhibitor specific to c-Jun N-terminal kinase (JNK), p38 kinase or p53, but not pan-caspase or caspase-8, decreased the toxin-induced generation of reactive oxygen species (ROS) and also attenuated the alpha-ZOL- or beta-ZOL-induced decrease of cell viability. Reactive Oxygen Species 183-186 tumor protein p53 Homo sapiens 77-80
23492768-7 2013 We will also introduce several pivotal ROS-sensitive molecules, such as hypoxia-inducible factors, p38 mitogen-activated protein kinase (p38) and p53, involved in the redox-regulated stem cell self-renewal. Reactive Oxygen Species 39-42 tumor protein p53 Homo sapiens 146-149
23863680-6 2013 And the ROS related signaling factors of p-p38MAPK, p38 MAPK, P53 were measured by Western blot. Reactive Oxygen Species 8-11 tumor protein p53 Homo sapiens 62-65
23863680-15 2013 And ROS stimulates the signaling pathways of p-p38MAPK and P53. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 59-62
23187459-5 2013 However, the upregulation of the p53-mediated protein p53 upregulated modulator of apoptosis (PUMA) by nutlin-3 is likely to be ROS independent because antioxidants failed to block PUMA upregulation. Reactive Oxygen Species 128-131 tumor protein p53 Homo sapiens 33-36
23187459-5 2013 However, the upregulation of the p53-mediated protein p53 upregulated modulator of apoptosis (PUMA) by nutlin-3 is likely to be ROS independent because antioxidants failed to block PUMA upregulation. Reactive Oxygen Species 128-131 tumor protein p53 Homo sapiens 54-57
23274516-4 2013 The changes of p53 status were dependent on DNA damage which was caused by compound C induced reactive oxygen species (ROS) generation and associated with activated ataxia-telangiectasia mutated (ATM) protein. Reactive Oxygen Species 94-117 tumor protein p53 Homo sapiens 15-18
23314357-8 2013 Of note, nutlin-3 caused the accumulation of mitochondrial reactive oxygen species (ROS) and this correlated with the mitochondrial translocation of p53. Reactive Oxygen Species 59-82 tumor protein p53 Homo sapiens 149-152
23314357-8 2013 Of note, nutlin-3 caused the accumulation of mitochondrial reactive oxygen species (ROS) and this correlated with the mitochondrial translocation of p53. Reactive Oxygen Species 84-87 tumor protein p53 Homo sapiens 149-152
23274516-4 2013 The changes of p53 status were dependent on DNA damage which was caused by compound C induced reactive oxygen species (ROS) generation and associated with activated ataxia-telangiectasia mutated (ATM) protein. Reactive Oxygen Species 119-122 tumor protein p53 Homo sapiens 15-18
23124852-5 2013 After scavenging ROS with N-acetylcysteine, Wnt/beta-catenin signaling-induced MSC aging was significantly attenuated and the DNA damage and the expression of p16(INK4A), p53, and p21 were reduced in MSCs. Reactive Oxygen Species 17-20 tumor protein p53 Homo sapiens 171-174
23469783-8 2013 CONCLUSION: Iron overload can inhibit the proliferation of MSCs and induce their apoptosis through the generation of ROS, which is probably due to the stimulation of p38MAPK- p53 signaling pathway. Reactive Oxygen Species 117-120 tumor protein p53 Homo sapiens 175-178
23841076-0 2013 The omega-3 polyunsaturated fatty acid DHA induces simultaneous apoptosis and autophagy via mitochondrial ROS-mediated Akt-mTOR signaling in prostate cancer cells expressing mutant p53. Reactive Oxygen Species 106-109 tumor protein p53 Homo sapiens 181-184
22918438-1 2013 The tumor suppressor p53 is an important regulator of intracellular reactive oxygen species (ROS) levels, although downstream mediators of p53 remain to be elucidated. Reactive Oxygen Species 68-91 tumor protein p53 Homo sapiens 21-24
23063463-5 2013 Recent findings suggest a novel role for p53 in TGF-beta1-induced PAI-1 transcription that involves ROS generation and p53/SMAD interactions. Reactive Oxygen Species 100-103 tumor protein p53 Homo sapiens 41-44
22918438-1 2013 The tumor suppressor p53 is an important regulator of intracellular reactive oxygen species (ROS) levels, although downstream mediators of p53 remain to be elucidated. Reactive Oxygen Species 93-96 tumor protein p53 Homo sapiens 21-24
22918438-2 2013 Here, we show that p53 and its downstream targets, p53-inducible ribonucleotide reductase (p53R2) and p53-inducible gene 3 (PIG3), physically and functionally interact with catalase for efficient regulation of intracellular ROS, depending on stress intensity. Reactive Oxygen Species 224-227 tumor protein p53 Homo sapiens 19-22
22918438-2 2013 Here, we show that p53 and its downstream targets, p53-inducible ribonucleotide reductase (p53R2) and p53-inducible gene 3 (PIG3), physically and functionally interact with catalase for efficient regulation of intracellular ROS, depending on stress intensity. Reactive Oxygen Species 224-227 tumor protein p53 Homo sapiens 51-54
22918438-3 2013 Under physiological conditions, the antioxidant functions of p53 are mediated by p53R2, which maintains increased catalase activity and thereby protects against endogenous ROS. Reactive Oxygen Species 172-175 tumor protein p53 Homo sapiens 61-64
22918438-5 2013 These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively. Reactive Oxygen Species 71-74 tumor protein p53 Homo sapiens 58-61
22918438-5 2013 These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively. Reactive Oxygen Species 71-74 tumor protein p53 Homo sapiens 107-110
22918438-5 2013 These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively. Reactive Oxygen Species 71-74 tumor protein p53 Homo sapiens 107-110
22918438-5 2013 These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively. Reactive Oxygen Species 198-201 tumor protein p53 Homo sapiens 58-61
22918438-5 2013 These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively. Reactive Oxygen Species 198-201 tumor protein p53 Homo sapiens 107-110
22918438-5 2013 These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively. Reactive Oxygen Species 198-201 tumor protein p53 Homo sapiens 107-110
23841076-5 2013 Similarly, pretreatment with the antioxidant N-acetyl-cysteine (NAC) markedly inhibited both the autophagy and the apoptosis triggered by DHA, indicating that mitochondrial ROS mediate the cytotoxicity of DHA in mutant p53 cells. Reactive Oxygen Species 173-176 tumor protein p53 Homo sapiens 219-222
23841076-7 2013 Collectively, these findings present a novel mechanism of ROS-regulated apoptosis and autophagy that involves Akt-mTOR signaling in prostate cancer cells with mutant p53 exposed to DHA. Reactive Oxygen Species 58-61 tumor protein p53 Homo sapiens 166-169
23216904-6 2013 This suggests that Nox-generated ROS transduce senescence signals by activating the p53 and p16Ink4a pathway. Reactive Oxygen Species 33-36 tumor protein p53 Homo sapiens 84-87
22201594-3 2013 In addition, as the byproducts of metabolism, reactive oxygen species (ROS) generated in the mitochondria can serve as signaling molecules to regulate p53 function. Reactive Oxygen Species 46-69 tumor protein p53 Homo sapiens 151-154
22201594-3 2013 In addition, as the byproducts of metabolism, reactive oxygen species (ROS) generated in the mitochondria can serve as signaling molecules to regulate p53 function. Reactive Oxygen Species 71-74 tumor protein p53 Homo sapiens 151-154
23533526-5 2013 The elevated ROS triggered the activation of ataxia-telangiectasia mutation (ATM), which further enhanced the ATF3 upregulation and subsequently enhanced p53 function by phosphorylation at Serine 15 and Serine 392. Reactive Oxygen Species 13-16 tumor protein p53 Homo sapiens 154-157
23137536-9 2012 Therefore, the present results show that miR-186, miR-216b, miR-337-3p, and miR-760 cooperatively promote cellular senescence through the p53-p21(Cip1/WAF1) pathway by CKII downregulation-mediated ROS production in HCT116 cells. Reactive Oxygen Species 197-200 tumor protein p53 Homo sapiens 138-141
23665932-12 2013 Taken together, the findings of the present study suggest that MSC partially induces p53-mediated apoptosis through ROS generation in human lung epithelial cells and this may have broader implications for our understanding of pulmonary diseases. Reactive Oxygen Species 116-119 tumor protein p53 Homo sapiens 85-88
23116945-2 2013 Chronic inflammatory processes share a common mechanism in which increased production of reactive oxygen species activates p53 and NF-kappaB signaling, leading to up-regulation of pro-inflammatory cytokine expression and impairment of glucose metabolism. Reactive Oxygen Species 89-112 tumor protein p53 Homo sapiens 123-126
22178897-6 2012 The first is that of ROS producer linked to p53 induced apoptosis. Reactive Oxygen Species 21-24 tumor protein p53 Homo sapiens 44-47
22559194-3 2012 Under low levels of reactive oxygen species (ROS), "normal" amounts of p53 upregulates expression of antioxidant genes, protecting macromolecules from ROS-induced damage. Reactive Oxygen Species 20-43 tumor protein p53 Homo sapiens 71-74
22559194-3 2012 Under low levels of reactive oxygen species (ROS), "normal" amounts of p53 upregulates expression of antioxidant genes, protecting macromolecules from ROS-induced damage. Reactive Oxygen Species 45-48 tumor protein p53 Homo sapiens 71-74
22559194-3 2012 Under low levels of reactive oxygen species (ROS), "normal" amounts of p53 upregulates expression of antioxidant genes, protecting macromolecules from ROS-induced damage. Reactive Oxygen Species 151-154 tumor protein p53 Homo sapiens 71-74
22559194-4 2012 However, at high levels or extended exposure of ROS, p53 expression is enhanced, activating pro-oxidant genes and resulting in p53-dependent apoptosis. Reactive Oxygen Species 48-51 tumor protein p53 Homo sapiens 53-56
22559194-4 2012 However, at high levels or extended exposure of ROS, p53 expression is enhanced, activating pro-oxidant genes and resulting in p53-dependent apoptosis. Reactive Oxygen Species 48-51 tumor protein p53 Homo sapiens 127-130
23185017-1 2012 The p53-inducible protein TIGAR (Tp53-induced Glycolysis and Apoptosis Regulator) functions as a fructose-2,6-bisphosphatase (Fru-2,6-BPase), and through promotion of the pentose phosphate pathway, increases NADPH production to help limit reactive oxygen species (ROS). Reactive Oxygen Species 239-262 tumor protein p53 Homo sapiens 4-7
23185017-1 2012 The p53-inducible protein TIGAR (Tp53-induced Glycolysis and Apoptosis Regulator) functions as a fructose-2,6-bisphosphatase (Fru-2,6-BPase), and through promotion of the pentose phosphate pathway, increases NADPH production to help limit reactive oxygen species (ROS). Reactive Oxygen Species 264-267 tumor protein p53 Homo sapiens 4-7
23257465-5 2012 The roles of p53-p21 and p16-Rb pathways can induce hematopoietic dysfunction and lead to ROS-induced HSC senescence. Reactive Oxygen Species 90-93 tumor protein p53 Homo sapiens 13-16
22886373-0 2012 Hexavalent chromium induces energy metabolism disturbance and p53-dependent cell cycle arrest via reactive oxygen species in L-02 hepatocytes. Reactive Oxygen Species 98-121 tumor protein p53 Homo sapiens 62-65
22886373-8 2012 ROS-mediated p53 activation was found to involve in Cr(VI)-induced cell cycle arrest, and p53 inhibitor Pifithrin-alpha (PFT-alpha) rescued Cr(VI)-induced reduction of check point proteins Mrc1 and BubR1, thus inhibiting cell cycle arrest. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 13-16
23177934-6 2012 PYGL depletion and the consequent glycogen accumulation led to increased reactive oxygen species (ROS) levels that contributed to a p53-dependent induction of senescence and markedly impaired tumorigenesis in vivo. Reactive Oxygen Species 73-96 tumor protein p53 Homo sapiens 132-135
23177934-6 2012 PYGL depletion and the consequent glycogen accumulation led to increased reactive oxygen species (ROS) levels that contributed to a p53-dependent induction of senescence and markedly impaired tumorigenesis in vivo. Reactive Oxygen Species 98-101 tumor protein p53 Homo sapiens 132-135
22886373-9 2012 In summary, the present study provides experimental evidence that Cr(VI) leads to energy metabolism disturbance and p53-dependent cell cycle arrest via ROS in L-02 hepatocytes. Reactive Oxygen Species 152-155 tumor protein p53 Homo sapiens 116-119
22750558-9 2012 p53 knock-down abrogated H(2)O(2)-induced premature senescence of vector control- and IkappaBalphaSR-expressing HDFs functionally linking canonical NF-kappaB-dependent control of p53 levels to ROS-induced HDF senescence. Reactive Oxygen Species 193-196 tumor protein p53 Homo sapiens 0-3
22899716-5 2012 Herein, we examine the effect of p53(R273H), a commonly occurring mutated p53 form, on the expression of phase 2 ROS-detoxifying enzymes and on the ability of cells to readopt a reducing environment after exposure to oxidative stress. Reactive Oxygen Species 113-116 tumor protein p53 Homo sapiens 33-36
22899716-5 2012 Herein, we examine the effect of p53(R273H), a commonly occurring mutated p53 form, on the expression of phase 2 ROS-detoxifying enzymes and on the ability of cells to readopt a reducing environment after exposure to oxidative stress. Reactive Oxygen Species 113-116 tumor protein p53 Homo sapiens 74-77
22899716-8 2012 This effect of mutant p53 is manifested by decreased expression of phase 2 detoxifying enzymes NQO1 and HO-1 and high ROS levels. Reactive Oxygen Species 118-121 tumor protein p53 Homo sapiens 22-25
22951418-8 2012 Lowered p53 and increased NF-kappaB are associated with elevated reactive oxygen species. Reactive Oxygen Species 65-88 tumor protein p53 Homo sapiens 8-11
23031740-2 2012 Loss of p53 results in increased expression of CD44, a cancer stem cell (CSC) marker, which is involved in the scavenging of reactive oxygen species (ROS). Reactive Oxygen Species 125-148 tumor protein p53 Homo sapiens 8-11
22892142-6 2012 p53-dependent enhancement of ascorbate cytotoxicity is caused by increased reactive oxygen species generation via a differentially regulated p53 transcriptional network. Reactive Oxygen Species 75-98 tumor protein p53 Homo sapiens 0-3
22892142-6 2012 p53-dependent enhancement of ascorbate cytotoxicity is caused by increased reactive oxygen species generation via a differentially regulated p53 transcriptional network. Reactive Oxygen Species 75-98 tumor protein p53 Homo sapiens 141-144
23031740-2 2012 Loss of p53 results in increased expression of CD44, a cancer stem cell (CSC) marker, which is involved in the scavenging of reactive oxygen species (ROS). Reactive Oxygen Species 150-153 tumor protein p53 Homo sapiens 8-11
22796259-4 2012 The present results show that MED induces DNA damage through the production of reactive oxygen species (ROS), which resulted in the phosphorylation of H2AX and the activation of the Ataxia telangiectasia mutated kinase (ATM) and p53 signaling pathways. Reactive Oxygen Species 79-102 tumor protein p53 Homo sapiens 229-232
22796259-4 2012 The present results show that MED induces DNA damage through the production of reactive oxygen species (ROS), which resulted in the phosphorylation of H2AX and the activation of the Ataxia telangiectasia mutated kinase (ATM) and p53 signaling pathways. Reactive Oxygen Species 104-107 tumor protein p53 Homo sapiens 229-232
22446899-12 2012 ROS production was partially dependent on the upregulation of p53 upon shikonin treatment. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 62-65
22641095-7 2012 In primary cultured hepatocytes, transforming growth factor (TGF)-beta treatment increased p53 and p66Shc signaling, leading to exaggerated reactive oxygen species (ROS) accumulation and apoptosis. Reactive Oxygen Species 140-163 tumor protein p53 Homo sapiens 91-94
22641095-7 2012 In primary cultured hepatocytes, transforming growth factor (TGF)-beta treatment increased p53 and p66Shc signaling, leading to exaggerated reactive oxygen species (ROS) accumulation and apoptosis. Reactive Oxygen Species 165-168 tumor protein p53 Homo sapiens 91-94
22641095-8 2012 Deficient p53 signaling inhibited TGF-beta-induced p66Shc signaling, ROS accumulation, and hepatocyte apoptosis. Reactive Oxygen Species 69-72 tumor protein p53 Homo sapiens 10-13
22641095-12 2012 CONCLUSIONS: p53 in hepatocytes regulates steatohepatitis progression by controlling p66Shc signaling, ROS levels, and apoptosis, all of which may be regulated by TGF-beta. Reactive Oxygen Species 103-106 tumor protein p53 Homo sapiens 13-16
23705067-5 2012 FoxOs, sirtuins and the p53/p66shc signaling cascade alter osteoblast number and bone formation via ROS-dependent and -independent mechanisms. Reactive Oxygen Species 100-103 tumor protein p53 Homo sapiens 24-27
22796327-3 2012 PRODH expression is inducible by p53, leading to increased proline oxidation, reactive oxygen species formation, and induction of apoptosis. Reactive Oxygen Species 78-101 tumor protein p53 Homo sapiens 33-36
22607092-10 2012 JNK and p53 have been shown to mediate the depletion of GSH [ 2 , 3 ], and we previously demonstrated the existence of a ROS-JNK-p53 cycle in silibinin-treated HeLa cells [ 4 ]. Reactive Oxygen Species 121-124 tumor protein p53 Homo sapiens 129-132
22576012-0 2012 Autophagy is induced through the ROS-TP53-DRAM1 pathway in response to mitochondrial protein synthesis inhibition. Reactive Oxygen Species 33-36 tumor protein p53 Homo sapiens 37-41
22576012-6 2012 The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 84-88
22576012-6 2012 The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 139-143
22576012-6 2012 The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 139-143
22576012-6 2012 The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 139-143
22576012-6 2012 The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 139-143
22576012-8 2012 Altogether, these data indicate that autophagy is induced through the ROS-TP53-DRAM1 pathway in response to mitochondrial protein synthesis inhibition. Reactive Oxygen Species 70-73 tumor protein p53 Homo sapiens 74-78
22434045-6 2012 Knock-down of Fer also increased the level of Reactive-Oxygen Species (ROS) in CC cells, and subjection of Fer depleted cells to ROS neutralizing scavengers significantly decreased the induced phosphorylation and activation of ATM and p53. Reactive Oxygen Species 129-132 tumor protein p53 Homo sapiens 235-238
22434045-7 2012 Notably, over-expression of Fer opposed the Doxorubicin driven activation of ATM and p53, which can be mediated by ROS. Reactive Oxygen Species 115-118 tumor protein p53 Homo sapiens 85-88
22117613-2 2012 Redox-sensitive proteins, such as the tumor suppressor protein p53, are susceptible to ROS-dependent modifications, which could impact their activities and/or biological functions. Reactive Oxygen Species 87-90 tumor protein p53 Homo sapiens 63-66
22570471-0 2012 Inhibition of nicotinamide phosphoribosyltransferase (NAMPT) activity by small molecule GMX1778 regulates reactive oxygen species (ROS)-mediated cytotoxicity in a p53- and nicotinic acid phosphoribosyltransferase1 (NAPRT1)-dependent manner. Reactive Oxygen Species 106-129 tumor protein p53 Homo sapiens 163-166
22570471-0 2012 Inhibition of nicotinamide phosphoribosyltransferase (NAMPT) activity by small molecule GMX1778 regulates reactive oxygen species (ROS)-mediated cytotoxicity in a p53- and nicotinic acid phosphoribosyltransferase1 (NAPRT1)-dependent manner. Reactive Oxygen Species 131-134 tumor protein p53 Homo sapiens 163-166
22304673-4 2012 The six reviews in this Forum showcase the up-to-date knowledge on how ROS modulate or interact with the p53 protein, epithelial-mesenchymal transition, tumor stromal cells, angiogenesis, and cancer stem cells, which are essential factors in cancer development and metastasis. Reactive Oxygen Species 71-74 tumor protein p53 Homo sapiens 105-108
22570471-10 2012 GMX1778-mediated ROS induction is p53-dependent, suggesting that the status of both p53 and NAPRT1 might affect tumor apoptosis, as determined by annexin-V staining. Reactive Oxygen Species 17-20 tumor protein p53 Homo sapiens 34-37
22570471-10 2012 GMX1778-mediated ROS induction is p53-dependent, suggesting that the status of both p53 and NAPRT1 might affect tumor apoptosis, as determined by annexin-V staining. Reactive Oxygen Species 17-20 tumor protein p53 Homo sapiens 84-87
22117613-6 2012 FUTURE DIRECTIONS: In this review, we describe how ROS production regulates p53 activity and how p53 can, in turn, influence cellular ROS production. Reactive Oxygen Species 134-137 tumor protein p53 Homo sapiens 97-100
22117613-5 2012 CRITICAL ISSUES: Recent studies present evidence that ROS function upstream of p53 in some model systems, while in others ROS production could be a downstream effect of p53 activation. Reactive Oxygen Species 54-57 tumor protein p53 Homo sapiens 79-82
22117613-5 2012 CRITICAL ISSUES: Recent studies present evidence that ROS function upstream of p53 in some model systems, while in others ROS production could be a downstream effect of p53 activation. Reactive Oxygen Species 54-57 tumor protein p53 Homo sapiens 169-172
22117613-5 2012 CRITICAL ISSUES: Recent studies present evidence that ROS function upstream of p53 in some model systems, while in others ROS production could be a downstream effect of p53 activation. Reactive Oxygen Species 122-125 tumor protein p53 Homo sapiens 169-172
22117613-6 2012 FUTURE DIRECTIONS: In this review, we describe how ROS production regulates p53 activity and how p53 can, in turn, influence cellular ROS production. Reactive Oxygen Species 51-54 tumor protein p53 Homo sapiens 76-79
22614867-9 2012 In conclusion, ROS-mediated oxidative stress, the activation of p53, Bax, caspase-3 and oxidative DNA damage are involved in the mechanistic pathways of nano-TiO(2)-induced apoptosis in HEK-293 cells. Reactive Oxygen Species 15-18 tumor protein p53 Homo sapiens 64-67
22074401-8 2012 Ca(2+) signalling, p53, p300 and ROS were serially knocked down to study Ca(2+) -p53-ROS ineractions in GaQ(3) -induced apoptosis. Reactive Oxygen Species 86-89 tumor protein p53 Homo sapiens 82-85
22509835-0 2012 Quercetin enhancement of arsenic-induced apoptosis via stimulating ROS-dependent p53 protein ubiquitination in human HaCaT keratinocytes. Reactive Oxygen Species 67-70 tumor protein p53 Homo sapiens 81-84
22074401-10 2012 p53 induced higher intracellular Ca(2+) release and ROS followed by activation of p53 downstream genes including those for the micro RNA mir34a. Reactive Oxygen Species 53-56 tumor protein p53 Homo sapiens 0-3
22074401-11 2012 In p53(-/-) and p53 mutant cells, GaQ(3) -induced Ca(2+) -signalling generated ROS. Reactive Oxygen Species 80-83 tumor protein p53 Homo sapiens 17-20
22509835-8 2012 QUE plus As(+3) stimulation of apoptosis in human HaCaT keratinocytes via activating ROS-dependent p53 protein ubiquitination may offer a rationale for the use of QUE to improve the clinical efficacy of arsenics in treating psoriasis. Reactive Oxygen Species 85-88 tumor protein p53 Homo sapiens 99-102
22521640-0 2012 WITHDRAWN: Hexavalent chromium induces premature senescence through reactive oxygen species-mediated p53 pathway in L-02 hepatocytes. Reactive Oxygen Species 68-91 tumor protein p53 Homo sapiens 101-104
22537194-8 2012 We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line. Reactive Oxygen Species 47-70 tumor protein p53 Homo sapiens 188-191
22537194-8 2012 We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line. Reactive Oxygen Species 72-75 tumor protein p53 Homo sapiens 188-191
22537194-8 2012 We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line. Reactive Oxygen Species 180-183 tumor protein p53 Homo sapiens 81-84
22537194-8 2012 We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line. Reactive Oxygen Species 180-183 tumor protein p53 Homo sapiens 188-191
21766316-0 2012 Effects of SiO2 nanoparticles on HFL-I activating ROS-mediated apoptosis via p53 pathway. Reactive Oxygen Species 50-53 tumor protein p53 Homo sapiens 77-80
22513874-6 2012 ROS accumulation in turn triggers p53-dependent cell cycle arrest and apoptosis. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 34-37
22283740-0 2012 P53 activation plays a crucial role in silibinin induced ROS generation via PUMA and JNK. Reactive Oxygen Species 57-60 tumor protein p53 Homo sapiens 0-3
22298641-10 2012 The results suggest that curcumin induction of ROS activates MAPKs, at least partially by inhibiting PP2A and PP5, thereby leading to p53-independent apoptosis in tumor cells. Reactive Oxygen Species 47-50 tumor protein p53 Homo sapiens 134-137
22283740-6 2012 The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 90-93
22283740-6 2012 The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS. Reactive Oxygen Species 4-7 tumor protein p53 Homo sapiens 122-125
22283740-6 2012 The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS. Reactive Oxygen Species 148-151 tumor protein p53 Homo sapiens 122-125
22093905-5 2012 Interestingly, human p53 induces cell death in recombinant strains Mut(s) with characteristic markers of apoptosis such as DNA fragmentation, exposure of phosphatidylserine, and reactive oxygen species generation. Reactive Oxygen Species 179-202 tumor protein p53 Homo sapiens 21-24
22283740-6 2012 The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS. Reactive Oxygen Species 148-151 tumor protein p53 Homo sapiens 122-125
22283740-10 2012 Activation of p53 was suppressed by SP600125 and expression of p-JNK was inhibited by PFT-alpha, therefore silibinin might activate a ROS-JNK-p53 cycle to induce cell death. Reactive Oxygen Species 134-137 tumor protein p53 Homo sapiens 14-17
22283740-10 2012 Activation of p53 was suppressed by SP600125 and expression of p-JNK was inhibited by PFT-alpha, therefore silibinin might activate a ROS-JNK-p53 cycle to induce cell death. Reactive Oxygen Species 134-137 tumor protein p53 Homo sapiens 142-145
22283740-13 2012 These results showed that p53 could interfere with mitochondrial functions such as MMP via PUMA pathways, thus resulting in ROS generation. Reactive Oxygen Species 124-127 tumor protein p53 Homo sapiens 26-29
22283740-17 2012 p53 activation plays a crucial role in silibinin induced ROS generation. Reactive Oxygen Species 57-60 tumor protein p53 Homo sapiens 0-3
22593641-10 2012 Upregulation of proline dehydrogenase by the tumor suppressor, p53, leads to enhanced mitochondrial reactive oxygen species that induce the intrinsic apoptotic pathway. Reactive Oxygen Species 100-123 tumor protein p53 Homo sapiens 63-66
22112863-8 2012 Our results demonstrate that depsipeptide plays an anti-neoplastic role by generating ROS to elicit p53/p21 pathway activation. Reactive Oxygen Species 86-89 tumor protein p53 Homo sapiens 100-103
22393286-9 2012 CONCLUSION: Overall, our data demonstrated that ZnO NPs selectively induce apoptosis in cancer cells, which is likely to be mediated by reactive oxygen species via p53 pathway, through which most of the anticancer drugs trigger apoptosis. Reactive Oxygen Species 136-159 tumor protein p53 Homo sapiens 164-167
22117045-4 2012 The MUC1-C inhibitor-induced increases in ROS were also associated with down-regulation of the p53-inducible regulator of glycolysis and apoptosis (TIGAR). Reactive Oxygen Species 42-45 tumor protein p53 Homo sapiens 95-98
22090360-9 2012 Expression of disruptive TP53 mutations significantly decreased radiation-induced senescence, as measured by SA-beta-gal staining, p21 expression, and release of ROS. Reactive Oxygen Species 162-165 tumor protein p53 Homo sapiens 25-29
22019631-2 2012 In this review the tumor suppressor genes p53, FoxO, retinoblastoma (RB), p21, p16, and breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) and their roles in oxidative stress are summarized with a focus on the links and interplay between their pathways and reactive oxygen species (ROS). Reactive Oxygen Species 267-290 tumor protein p53 Homo sapiens 42-45
22019631-2 2012 In this review the tumor suppressor genes p53, FoxO, retinoblastoma (RB), p21, p16, and breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) and their roles in oxidative stress are summarized with a focus on the links and interplay between their pathways and reactive oxygen species (ROS). Reactive Oxygen Species 292-295 tumor protein p53 Homo sapiens 42-45
22019631-4 2012 On the other hand, recent studies have revealed a pro-oxidant role for p53 by which cellular ROS are increased by enhanced transcription of proapoptotic genes. Reactive Oxygen Species 93-96 tumor protein p53 Homo sapiens 71-74
21951851-4 2011 In this review, we summarize mitochondrial function and ROS generation, and also highlight ROS-modulated core autophagic pathways involved in ATG4-ATG8/LC3, Beclin-1, p53, PTEN, PI3K-Akt-mTOR and MAPK signaling in cancer. Reactive Oxygen Species 91-94 tumor protein p53 Homo sapiens 167-170
21859827-0 2011 Regulator of G protein signaling 6 mediates doxorubicin-induced ATM and p53 activation by a reactive oxygen species-dependent mechanism. Reactive Oxygen Species 92-115 tumor protein p53 Homo sapiens 72-75
21859827-6 2011 RGS6 mediated activation of ATM and p53 by DXR via a reactive oxygen species (ROS)-dependent and DNA damage-independent mechanism. Reactive Oxygen Species 53-76 tumor protein p53 Homo sapiens 36-39
21859827-6 2011 RGS6 mediated activation of ATM and p53 by DXR via a reactive oxygen species (ROS)-dependent and DNA damage-independent mechanism. Reactive Oxygen Species 78-81 tumor protein p53 Homo sapiens 36-39
23216635-0 2012 Reactive oxygen species mediate Cr(VI)-induced S phase arrest through p53 in human colon cancer cells. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 70-73
22160723-7 2011 These cells exhibited a high yield of ROS-induced DNA single- and double-strand breaks and activation of the ATR-Chk1-ATM-Chk2-p53 pathway that led to Fas and caspase-8, -3, and -7 activation, whereas macrophages and DCs derived from them were protected. Reactive Oxygen Species 38-41 tumor protein p53 Homo sapiens 127-130
22155925-7 2011 The proliferation defects induced by silencing LB1 are accompanied by a p53-dependent reduction in mitochondrial reactive oxygen species (ROS), which can be rescued by growth under hypoxic conditions. Reactive Oxygen Species 113-136 tumor protein p53 Homo sapiens 72-75
22155925-7 2011 The proliferation defects induced by silencing LB1 are accompanied by a p53-dependent reduction in mitochondrial reactive oxygen species (ROS), which can be rescued by growth under hypoxic conditions. Reactive Oxygen Species 138-141 tumor protein p53 Homo sapiens 72-75
21983037-6 2011 In this report, we examined the role of oncogenes, DNA damage, and reactive oxygen species, signals that stabilize wild-type p53, on the stabilization of mutant p53 in vivo and the consequences of this expression on tumor formation and survival. Reactive Oxygen Species 67-90 tumor protein p53 Homo sapiens 161-164
21196432-4 2011 Two pathways are proposed for exploiting tyrosinase expression: (a) a p53-dependent pathway leading to apoptosis or arrest and (b) a reactive oxygen species-mediated induction of endoplasmic reticulum stress in p53 mutant tumors. Reactive Oxygen Species 133-156 tumor protein p53 Homo sapiens 211-214
20548326-9 2011 Ibuprofen induced ROS, which resulted in cellular alterations that promoted a p53-dependent G(1) blockade. Reactive Oxygen Species 18-21 tumor protein p53 Homo sapiens 78-81
21779512-7 2011 Furthermore, they discuss the potential mechanisms by which p53 regulates aging and longevity, including the p53 regulation of insulin/TOR signaling, stem/progenitor cells, and reactive oxygen species. Reactive Oxygen Species 177-200 tumor protein p53 Homo sapiens 60-63
21864926-2 2011 The decrease in intracellular ROS levels in response to TIGAR may also play a role in the ability of p53 to protect from the accumulation of genomic lesions. Reactive Oxygen Species 30-33 tumor protein p53 Homo sapiens 101-104
21687937-0 2011 The cell death response to the ROS inducer, cobalt chloride, in neuroblastoma cell lines according to p53 status. Reactive Oxygen Species 31-34 tumor protein p53 Homo sapiens 102-105
20712406-4 2011 p53 orchestrates mitochondrial redox signaling by the coordinated control of at least two key effectors: the superoxide scavenger MnSOD, and the ROS generator p66shc. Reactive Oxygen Species 145-148 tumor protein p53 Homo sapiens 0-3
20712410-5 2011 Among the many antioxidant genes activated by p53, Sestrins (Sesns) are critical for suppression of reactive oxygen species (ROS) and protection from oxidative stress, transformation, and genomic instability. Reactive Oxygen Species 100-123 tumor protein p53 Homo sapiens 46-49
20712410-5 2011 Among the many antioxidant genes activated by p53, Sestrins (Sesns) are critical for suppression of reactive oxygen species (ROS) and protection from oxidative stress, transformation, and genomic instability. Reactive Oxygen Species 125-128 tumor protein p53 Homo sapiens 46-49
20919943-0 2011 Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production. Reactive Oxygen Species 95-118 tumor protein p53 Homo sapiens 15-18
20919943-5 2011 Here, it has been considered p53 broad potential contribution through its ability to regulate selected key cancer signaling pathways, where ROS participate as inductors or effectors of the final biological outcome. Reactive Oxygen Species 140-143 tumor protein p53 Homo sapiens 29-32
20919943-7 2011 In addition, we have considered potential mechanisms by which p53 could collaborate with signal transduction pathways such as transforming growth factor-beta (TGF-beta) and stress-activated protein kinases (SAPK) that produce ROS, to stop or eliminate uncontrolled proliferating cells. Reactive Oxygen Species 226-229 tumor protein p53 Homo sapiens 62-65
21194382-5 2011 We propose that interactions between p53 and its isoforms Delta40p53 or Delta133p53 play critical roles in intracellular signaling by reactive oxygen species. Reactive Oxygen Species 134-157 tumor protein p53 Homo sapiens 37-40
21696969-0 2011 18beta-Glycyrrhetinic acid derivatives induced mitochondrial-mediated apoptosis through reactive oxygen species-mediated p53 activation in NTUB1 cells. Reactive Oxygen Species 88-111 tumor protein p53 Homo sapiens 121-124
21696969-9 2011 These results suggested that 25 induced a mitochondrial-mediated apoptosis in NTUB1 cells through activation of p53, which are mainly mediated ROS generated by 25. Reactive Oxygen Species 143-146 tumor protein p53 Homo sapiens 112-115
21489989-0 2011 Serine/threonine kinase 17A is a novel p53 target gene and modulator of cisplatin toxicity and reactive oxygen species in testicular cancer cells. Reactive Oxygen Species 95-118 tumor protein p53 Homo sapiens 39-42
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 tumor protein p53 Homo sapiens 118-121
21047991-10 2011 This phenomenon is associated with p53 activation caused by increasing reactive oxygen species (ROS) levels because of the downregulation of superoxide dismutase expression in si-c-Jun-transfected cells. Reactive Oxygen Species 71-94 tumor protein p53 Homo sapiens 35-38
21047991-10 2011 This phenomenon is associated with p53 activation caused by increasing reactive oxygen species (ROS) levels because of the downregulation of superoxide dismutase expression in si-c-Jun-transfected cells. Reactive Oxygen Species 96-99 tumor protein p53 Homo sapiens 35-38
20601193-0 2010 Manganese superoxide dismutase vs. p53: regulation of mitochondrial ROS. Reactive Oxygen Species 68-71 tumor protein p53 Homo sapiens 35-38
21264228-10 2011 These results suggest that (1) mitochondrial ROS and NIX are essential factors for MALM, (2) MIV is a novel mechanism for lysosomal degradation of mitochondria, and (3) the p53-Mieap pathway plays a pivotal role in MQC by repairing or eliminating unhealthy mitochondria via MALM or MIV generation, respectively. Reactive Oxygen Species 45-48 tumor protein p53 Homo sapiens 173-176
21078664-0 2011 Nimbolide sensitizes human colon cancer cells to TRAIL through reactive oxygen species- and ERK-dependent up-regulation of death receptors, p53, and Bax. Reactive Oxygen Species 63-86 tumor protein p53 Homo sapiens 140-143
21212516-12 2011 These results suggest that silibinin might induce p53-mediated autophagic cell death by activating ROS-p38 and JNK pathways, as well as inhibiting MEK/ERK and PI3K/Akt pathways. Reactive Oxygen Species 99-102 tumor protein p53 Homo sapiens 50-53
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 tumor protein p53 Homo sapiens 178-181
21673964-6 2011 Mechanistic studies (both in vitro and in vivo) revealed that FBA-TPQ might exert its activity through Reactive Oxygen Species (ROS)-associated activation of the death receptor, p53-MDM2, and PI3K-Akt pathways in OVCAR-3 cells, which is in accordance with in vitro microarray (Human genome microarrays, Agilent) data analysis (GEO accession number: GSE25317). Reactive Oxygen Species 128-131 tumor protein p53 Homo sapiens 178-181
21473121-3 2011 Assumption about the leading part of a p53-dependent way in realization apoptosis human lymphocytes in the conditions of influence of UV-light and reactive oxygen species is put forward. Reactive Oxygen Species 147-170 tumor protein p53 Homo sapiens 39-42
20727582-8 2010 Moreover, inhibition of ROS attenuated silica nanoparticles-induced apoptosis and inflammation and the activation of JNK, c-Jun, p53 and NF-kappaB. Reactive Oxygen Species 24-27 tumor protein p53 Homo sapiens 129-132
21418001-4 2010 Under relatively favorable conditions, p53 helps to maintain intracellular homeostasis by balancing anabolic and catabolic processes and by timely elimination of reactive oxygen species. Reactive Oxygen Species 162-185 tumor protein p53 Homo sapiens 39-42
20380827-4 2010 Specifically, we focus on the role of asbestos in augmenting AEC apoptosis by the mitochondria- and p53-regulated death pathways that result from the production of iron-derived reactive oxygen species (ROS) and DNA damage. Reactive Oxygen Species 202-205 tumor protein p53 Homo sapiens 100-103
20601193-3 2010 p53 affect mitochondrial ROS production, in part, by regulating the expression of the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD). Reactive Oxygen Species 25-28 tumor protein p53 Homo sapiens 0-3
20601193-4 2010 Recent evidence suggests mitochondrial regulation of p53 activity through mechanisms that affect ROS production, and a breakdown of communication amongst mitochondria, p53, and the nucleus can have broad implications in disease development. Reactive Oxygen Species 97-100 tumor protein p53 Homo sapiens 53-56
20643100-2 2010 Previous data indicated that the cytosolic serine peptidase tripeptidyl-peptidase II (TPPII) translocates into the nucleus of most tumor cell lines in response to gamma-irradiation and ROS production; an event that promoted p53 expression as well as caspase-activation. Reactive Oxygen Species 185-188 tumor protein p53 Homo sapiens 224-227
20976134-2 2010 In addition to its transcriptional activation, a fraction of p53 translocates to mitochondria at the very early stage of apoptosis, which eventually contributes to the loss of mitochondrial membrane potential, generation of reactive oxygen species (ROS), cytochrome c release, and caspase activation. Reactive Oxygen Species 224-247 tumor protein p53 Homo sapiens 61-64
20976134-2 2010 In addition to its transcriptional activation, a fraction of p53 translocates to mitochondria at the very early stage of apoptosis, which eventually contributes to the loss of mitochondrial membrane potential, generation of reactive oxygen species (ROS), cytochrome c release, and caspase activation. Reactive Oxygen Species 249-252 tumor protein p53 Homo sapiens 61-64
20649542-7 2010 Manganese superoxide dismutase (MnSOD), a p53-regulated gene that is a vital antioxidant enzyme localized in the matrix of mitochondria, scavenges reactive oxygen species. Reactive Oxygen Species 147-170 tumor protein p53 Homo sapiens 42-45
20682800-8 2010 Apoptosis induced by CP-31398 occurred with translocation of p53 to mitochondria, leading to altered mitochondrial membrane potential, cytochrome c release, and reactive oxygen species release. Reactive Oxygen Species 161-184 tumor protein p53 Homo sapiens 61-64
20706634-13 2010 Reduced formation of reactive oxygen species in HIF-1alpha-competent cells was identified as the molecular mechanism of HIF-1alpha-mediated inhibition of p53. Reactive Oxygen Species 21-44 tumor protein p53 Homo sapiens 154-157
20682800-0 2010 Targeting wild-type and mutant p53 with small molecule CP-31398 blocks the growth of rhabdomyosarcoma by inducing reactive oxygen species-dependent apoptosis. Reactive Oxygen Species 114-137 tumor protein p53 Homo sapiens 31-34
20649542-8 2010 Recent studies suggest that mitochondria can regulate p53 activity and that assaults on the cell that affect mitochondrial ROS production and mitochondrial function can influence p53 activity. Reactive Oxygen Species 123-126 tumor protein p53 Homo sapiens 179-182
20353787-0 2010 ROS leads to MnSOD upregulation through ERK2 translocation and p53 activation in selenite-induced apoptosis of NB4 cells. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 63-66
20446899-2 2010 This study suggested that G2/M cell cycle arrest was triggered by ROS/NO productions with regulations of p53, p21, cell division cycle 25C (Cdc25C), Cdc2 and cyclin B1, which were able to be prevented by protein tyrosine kinase (PTK) activity inhibitor genistein or JNK inhibitor SP600125. Reactive Oxygen Species 66-69 tumor protein p53 Homo sapiens 105-108
20525364-3 2010 In the two decades since its original discovery, p53 has found a singularly prominent place in our understanding of human gastric cancer and H. pylori cause accumulation of reactive oxygen species in the mucosa compartment. Reactive Oxygen Species 173-196 tumor protein p53 Homo sapiens 49-52
20356045-9 2010 Taken together, these data suggested that in addition to the mitochondrial- and Fas receptor-mediated apoptotic pathways involved, ROS-dependent and p53-regulated DR5 expression was also demonstrated to play a pivotal role in the synergistic enhancement of TRAIL-induced apoptosis instigated by 6-DG in Hep G2 cells. Reactive Oxygen Species 131-134 tumor protein p53 Homo sapiens 149-152
20544694-5 2010 Critical proteins in pathways for DNA damage detection/repair signaling, like p53 and ataxia telangiectasia mutated, and DNA repair itself, like oxoguanine glycosylase 1 and Cockayne syndrome B, can often, but not always, protect the embryo from ROS-initiating teratogens. Reactive Oxygen Species 246-249 tumor protein p53 Homo sapiens 78-81
20483782-6 2010 We also demonstrate that IFN-gamma treatment, which is used to induce IgG2a switching, increases intracellular ROS levels, and activates p53 in switching B cells, and show that p53 inhibits IgG2a class switching through its antioxidant-regulating function. Reactive Oxygen Species 111-114 tumor protein p53 Homo sapiens 177-180
20060462-10 2010 In conclusion, ROS-mediated oxidative stress, the activation of p53 and up-regulation of Bax/Bcl-2 ratio are involved in mechanistic pathways of 21 nm SiO(2) induced apoptosis in L-02 cells. Reactive Oxygen Species 15-18 tumor protein p53 Homo sapiens 64-67
20378837-7 2010 Consistent with these functions of GLS2, the activation of p53 increases the levels of glutamate and alpha-ketoglutarate, mitochondrial respiration rate, and GSH levels and decreases reactive oxygen species (ROS) levels in cells. Reactive Oxygen Species 183-206 tumor protein p53 Homo sapiens 59-62
20378837-7 2010 Consistent with these functions of GLS2, the activation of p53 increases the levels of glutamate and alpha-ketoglutarate, mitochondrial respiration rate, and GSH levels and decreases reactive oxygen species (ROS) levels in cells. Reactive Oxygen Species 208-211 tumor protein p53 Homo sapiens 59-62
20351271-0 2010 Phosphate-activated glutaminase (GLS2), a p53-inducible regulator of glutamine metabolism and reactive oxygen species. Reactive Oxygen Species 94-117 tumor protein p53 Homo sapiens 42-45
20351271-4 2010 Further, siRNA down-regulation of either GLS2 or p53 compromises the GSH-dependent antioxidant system and increases intracellular ROS levels. Reactive Oxygen Species 130-133 tumor protein p53 Homo sapiens 49-52
20351271-5 2010 High ROS levels following GLS2 knockdown also coincide with stimulation of p53-induced cell death. Reactive Oxygen Species 5-8 tumor protein p53 Homo sapiens 75-78
20351271-6 2010 We propose that GLS2 control of intracellular ROS levels and the apoptotic response facilitates the ability of p53 to protect cells from accumulation of genomic damage and allows cells to survive after mild and repairable genotoxic stress. Reactive Oxygen Species 46-49 tumor protein p53 Homo sapiens 111-114
20351271-9 2010 Thus, our results provide evidence for a unique metabolic role for p53, linking glutamine metabolism, energy, and ROS homeostasis, which may contribute to p53 tumor suppressor function. Reactive Oxygen Species 114-117 tumor protein p53 Homo sapiens 67-70
20351271-9 2010 Thus, our results provide evidence for a unique metabolic role for p53, linking glutamine metabolism, energy, and ROS homeostasis, which may contribute to p53 tumor suppressor function. Reactive Oxygen Species 114-117 tumor protein p53 Homo sapiens 155-158
20447055-9 2010 It was further demonstrated that XCT-790-induced ROS modulated p53 and Rb signalling pathways and suppressed cell replication. Reactive Oxygen Species 49-52 tumor protein p53 Homo sapiens 63-66
20393586-5 2010 In terms of transcriptional regulation, ROS affect the phosphorylation, activation, oxidation, and DNA binding of transcription factors such as AP-1, NF-kappaB, p53, and HIF-1alpha, leading to changes in target gene expression. Reactive Oxygen Species 40-43 tumor protein p53 Homo sapiens 161-164
19883646-0 2010 Theaflavins retard human breast cancer cell migration by inhibiting NF-kappaB via p53-ROS cross-talk. Reactive Oxygen Species 86-89 tumor protein p53 Homo sapiens 82-85
19855432-5 2010 ROS generation was attributed to the suppression of B-cell lymphoma-2 (Bcl-2) phosphorylation, and resulted in DNA damage and p53 activation. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 126-129
19883646-2 2010 Our data suggest that p53-dependent reactive oxygen species (ROS) induce p53-phosphorylation via p38MAPK in a feedback loop to inhibit IkappaBalpha-phosphorylation and NF-kappaB/p65 nuclear translocation, thereby down-regulating the metastatic proteins metalloproteinase (MMP)-2 and MMP-9. Reactive Oxygen Species 36-59 tumor protein p53 Homo sapiens 22-25
19883646-2 2010 Our data suggest that p53-dependent reactive oxygen species (ROS) induce p53-phosphorylation via p38MAPK in a feedback loop to inhibit IkappaBalpha-phosphorylation and NF-kappaB/p65 nuclear translocation, thereby down-regulating the metastatic proteins metalloproteinase (MMP)-2 and MMP-9. Reactive Oxygen Species 36-59 tumor protein p53 Homo sapiens 73-76
19883646-2 2010 Our data suggest that p53-dependent reactive oxygen species (ROS) induce p53-phosphorylation via p38MAPK in a feedback loop to inhibit IkappaBalpha-phosphorylation and NF-kappaB/p65 nuclear translocation, thereby down-regulating the metastatic proteins metalloproteinase (MMP)-2 and MMP-9. Reactive Oxygen Species 61-64 tumor protein p53 Homo sapiens 22-25
19883646-2 2010 Our data suggest that p53-dependent reactive oxygen species (ROS) induce p53-phosphorylation via p38MAPK in a feedback loop to inhibit IkappaBalpha-phosphorylation and NF-kappaB/p65 nuclear translocation, thereby down-regulating the metastatic proteins metalloproteinase (MMP)-2 and MMP-9. Reactive Oxygen Species 61-64 tumor protein p53 Homo sapiens 73-76
19883646-5 2010 These results indicate that inhibition of NF-kappaB via p53-ROS crosstalk is a pre-requisite for theaflavins to accomplish the anti-migratory effect in breast cancer cells. Reactive Oxygen Species 60-63 tumor protein p53 Homo sapiens 56-59
20557688-9 2010 In conclusion, the release of ROS by PU- or PTFE-treated THP-1 cells may induce iNOS expression and cause apoptosis in HUVECs via the p53, Bax and Bcl-2 proteins. Reactive Oxygen Species 30-33 tumor protein p53 Homo sapiens 134-137
19906512-0 2009 Telomeric DNA induces p53-dependent reactive oxygen species and protects against oxidative damage. Reactive Oxygen Species 36-59 tumor protein p53 Homo sapiens 22-25
20023923-2 2009 Azide, a singlet oxygen quencher, greatly reduced the p53 photocrosslinking, consistent with the idea that singlet oxygen is the reactive oxygen species involved in p53 photocrosslinking. Reactive Oxygen Species 129-152 tumor protein p53 Homo sapiens 54-57
20023923-2 2009 Azide, a singlet oxygen quencher, greatly reduced the p53 photocrosslinking, consistent with the idea that singlet oxygen is the reactive oxygen species involved in p53 photocrosslinking. Reactive Oxygen Species 129-152 tumor protein p53 Homo sapiens 165-168
19906512-7 2009 Further, T-oligo increases cellular ROS levels via a p53-dependent pathway, and these increases are abrogated by the NAD(P)H oxidase inhibitor diphenyliodonium chloride. Reactive Oxygen Species 36-39 tumor protein p53 Homo sapiens 53-56
19706526-7 2009 Moreover, HIF2alpha inhibition promotes p53-mediated responses by disrupting cellular redox homeostasis, thereby permitting reactive oxygen species (ROS) accumulation and DNA damage. Reactive Oxygen Species 124-147 tumor protein p53 Homo sapiens 40-43
19544329-3 2009 It caused oxidative stress by early generation of nitric oxide and reactive oxygen species that robustly up regulated time-dependent expression of p53/p21/PUMA while conversely abrogating phosphatidylinositol-3-kinase (PI3K)/Akt pathways in parallel. Reactive Oxygen Species 67-90 tumor protein p53 Homo sapiens 147-150
19917243-2 2009 (2009) have identified the enzyme guanidinoacetate methyltransferase (GAMT) that regulates creatine metabolism as a p53 target involved in apoptosis, reactive oxygen species (ROS), and fatty acid metabolism. Reactive Oxygen Species 150-173 tumor protein p53 Homo sapiens 116-119
19917243-2 2009 (2009) have identified the enzyme guanidinoacetate methyltransferase (GAMT) that regulates creatine metabolism as a p53 target involved in apoptosis, reactive oxygen species (ROS), and fatty acid metabolism. Reactive Oxygen Species 175-178 tumor protein p53 Homo sapiens 116-119
19713938-1 2009 The p53-inducible TIGAR protein functions as a fructose-2,6-bisphosphatase, promoting the pentose phosphate pathway and helping to lower intracellular reactive oxygen species (ROS). Reactive Oxygen Species 151-174 tumor protein p53 Homo sapiens 4-7
19713938-1 2009 The p53-inducible TIGAR protein functions as a fructose-2,6-bisphosphatase, promoting the pentose phosphate pathway and helping to lower intracellular reactive oxygen species (ROS). Reactive Oxygen Species 176-179 tumor protein p53 Homo sapiens 4-7
19744477-2 2009 Here, we demonstrate that emodin induces apoptosis in human lung adenocarcinoma A549 cells by activating a reactive oxygen species-elicited ATM-p53-Bax signaling pathway. Reactive Oxygen Species 107-130 tumor protein p53 Homo sapiens 144-147
19744477-9 2009 Taken together, our results demonstrate that emodin-induced reactive oxygen species generation activates an ATM-p53-Bax-dependent signaling pathway, which consequently leads to mitochondria-dependent apoptotic cell death in human lung adenocarcinoma A549 cells. Reactive Oxygen Species 60-83 tumor protein p53 Homo sapiens 112-115
19716362-3 2009 The tumor suppressor p53 is induced upon iron depletion, and controls reactive oxygen species level. Reactive Oxygen Species 70-93 tumor protein p53 Homo sapiens 21-24
19838062-5 2009 Interestingly, a novel approximately 130 kDa form of TrxR1, presumably representing a stable covalently linked dimer, and an increased generation of reactive oxygen species (ROS) were induced by RITA in cancer cells in a p53-dependent manner. Reactive Oxygen Species 149-172 tumor protein p53 Homo sapiens 221-224
19838062-5 2009 Interestingly, a novel approximately 130 kDa form of TrxR1, presumably representing a stable covalently linked dimer, and an increased generation of reactive oxygen species (ROS) were induced by RITA in cancer cells in a p53-dependent manner. Reactive Oxygen Species 174-177 tumor protein p53 Homo sapiens 221-224
19706526-7 2009 Moreover, HIF2alpha inhibition promotes p53-mediated responses by disrupting cellular redox homeostasis, thereby permitting reactive oxygen species (ROS) accumulation and DNA damage. Reactive Oxygen Species 149-152 tumor protein p53 Homo sapiens 40-43
19438509-0 2009 Reactive oxygen species up-regulate p53 and Puma; a possible mechanism for apoptosis during combined treatment with TRAIL and wogonin. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 36-39
19438509-5 2009 KEY RESULTS: During combined treatment with wogonin and TRAIL, cytotoxicity, poly(ADP-ribose) polymerase cleavage and caspase activation were associated with up-regulation of p53 through DNA damage and reactive oxygen species (ROS) generation. Reactive Oxygen Species 202-225 tumor protein p53 Homo sapiens 175-178
19438509-5 2009 KEY RESULTS: During combined treatment with wogonin and TRAIL, cytotoxicity, poly(ADP-ribose) polymerase cleavage and caspase activation were associated with up-regulation of p53 through DNA damage and reactive oxygen species (ROS) generation. Reactive Oxygen Species 227-230 tumor protein p53 Homo sapiens 175-178
19158844-2 2009 UVA irradiation of human melanocytes caused generation of reactive oxygen species, which altered the intracellular redox balance and was accompanied by translocation of p53 to mitochondria. Reactive Oxygen Species 58-81 tumor protein p53 Homo sapiens 169-172
19528227-5 2009 The increase in mitochondrial mass and ROS in response to oncogenic ras depended on intact p53 and Rb tumor suppression pathways. Reactive Oxygen Species 39-42 tumor protein p53 Homo sapiens 91-94
19432898-7 2009 This observation implies that there is a feedback signaling loop involving p21/ROS/p53 in apoptotic responses. Reactive Oxygen Species 79-82 tumor protein p53 Homo sapiens 83-86
19413947-0 2009 Loss of p53 causes mitochondrial DNA depletion and altered mitochondrial reactive oxygen species homeostasis. Reactive Oxygen Species 73-96 tumor protein p53 Homo sapiens 8-11
19369702-4 2009 Although hypoxia has been shown to induce reactive oxygen species (ROS) generation in the mitochondria resulting in enhanced p53 expression, our data demonstrate that hypoxia-induced p53 expression and phosphorylation are independent of ROS. Reactive Oxygen Species 67-70 tumor protein p53 Homo sapiens 125-128
19398950-7 2009 In addition, we show that p53-inducible genes involved in reducing reactive oxygen species are upregulated by Artemis depletion. Reactive Oxygen Species 67-90 tumor protein p53 Homo sapiens 26-29
19413947-2 2009 Here we demonstrate a new conserved role for p53 in mtDNA copy number maintenance and mitochondrial reactive oxygen species (ROS) homeostasis. Reactive Oxygen Species 100-123 tumor protein p53 Homo sapiens 45-48
19413947-2 2009 Here we demonstrate a new conserved role for p53 in mtDNA copy number maintenance and mitochondrial reactive oxygen species (ROS) homeostasis. Reactive Oxygen Species 125-128 tumor protein p53 Homo sapiens 45-48
19413947-6 2009 Finally, p53-depleted cells exhibit significant disruption of cellular ROS homeostasis, characterized by reduced mitochondrial and cellular superoxide levels and increased cellular hydrogen peroxide. Reactive Oxygen Species 71-74 tumor protein p53 Homo sapiens 9-12
18992840-0 2009 The p53-p66shc-Manganese Superoxide Dismutase (MnSOD) network: a mitochondrial intrigue to generate reactive oxygen species. Reactive Oxygen Species 100-123 tumor protein p53 Homo sapiens 4-7
18992840-3 2009 The present short review summarizes recent discoveries on mitochondrial reactive oxygen species regulation by p53, a tumor suppressor protein and p66shc, a protein implicated in the life-span determination. Reactive Oxygen Species 72-95 tumor protein p53 Homo sapiens 110-113
19265193-2 2009 Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824. Reactive Oxygen Species 148-171 tumor protein p53 Homo sapiens 25-28
19243304-6 2009 In light of these new findings, the following review focuses on p53/mitochondria connections, in particular how reactive oxygen species generated at mitochondria regulate p53 activity. Reactive Oxygen Species 112-135 tumor protein p53 Homo sapiens 64-67
19475715-4 2009 Our results have revealed that reactive oxygen species (ROS) and p21 are involved in cell cycle arrest in a p53 independent manner but late hour apoptotic response was accompanied by the p53 up-regulation, loss of mitochondrial transmembrane potential (MTP), down-regulation of Bcl-xl, activation of caspase-3 and release of cytochrome c (Cyt c). Reactive Oxygen Species 31-54 tumor protein p53 Homo sapiens 108-111
19475715-4 2009 Our results have revealed that reactive oxygen species (ROS) and p21 are involved in cell cycle arrest in a p53 independent manner but late hour apoptotic response was accompanied by the p53 up-regulation, loss of mitochondrial transmembrane potential (MTP), down-regulation of Bcl-xl, activation of caspase-3 and release of cytochrome c (Cyt c). Reactive Oxygen Species 56-59 tumor protein p53 Homo sapiens 108-111
19475715-8 2009 Taken together, we have demonstrated that cadmium promotes ROS generation, which potently initiates the cell cycle arrest at early hours and finally induces p53-dependent apoptosis at later part of the event. Reactive Oxygen Species 59-62 tumor protein p53 Homo sapiens 157-160
19091459-0 2009 p53 hot-spot mutants increase tumor vascularization via ROS-mediated activation of the HIF1/VEGF-A pathway. Reactive Oxygen Species 56-59 tumor protein p53 Homo sapiens 0-3
19091459-5 2009 Effect of ROS on angiogenesis in tumors expressing hot-spot p53 mutants was correlated with their ability to increase a content of HIF1 transcriptional factor responsible for up-regulation of VEGF-A mRNAs. Reactive Oxygen Species 10-13 tumor protein p53 Homo sapiens 60-63
19197340-7 2009 We show that PLA2R regulates senescence in a reactive oxygen species-DNA damage-p53-dependent manner. Reactive Oxygen Species 45-68 tumor protein p53 Homo sapiens 80-83
20126301-6 2009 In particular, we discuss p53-mediated mechanisms that prevent damage caused by reactive oxygen species and the effects of lipotoxicity. Reactive Oxygen Species 80-103 tumor protein p53 Homo sapiens 26-29
19264704-0 2009 Induction of cellular senescence by secretory phospholipase A2 in human dermal fibroblasts through an ROS-mediated p53 pathway. Reactive Oxygen Species 102-105 tumor protein p53 Homo sapiens 115-118
19264704-7 2009 These results suggest that sPLA(2) has a role in cellular senescence in HDFs during inflammatory response by promoting ROS-dependent p53 activation and might therefore contribute to inflammatory disorders associated with aging. Reactive Oxygen Species 119-122 tumor protein p53 Homo sapiens 133-136
18951928-0 2009 Intracellular zinc increase inhibits p53(-/-) pancreatic adenocarcinoma cell growth by ROS/AIF-mediated apoptosis. Reactive Oxygen Species 87-90 tumor protein p53 Homo sapiens 37-40
19243304-6 2009 In light of these new findings, the following review focuses on p53/mitochondria connections, in particular how reactive oxygen species generated at mitochondria regulate p53 activity. Reactive Oxygen Species 112-135 tumor protein p53 Homo sapiens 171-174
18719315-0 2008 Reactive oxygen species mediate oridonin-induced HepG2 apoptosis through p53, MAPK, and mitochondrial signaling pathways. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 73-76
19144918-0 2009 The p53-cathepsin axis cooperates with ROS to activate programmed necrotic death upon DNA damage. Reactive Oxygen Species 39-42 tumor protein p53 Homo sapiens 4-7
19144918-7 2009 p53 induces cathepsin Q that cooperates with reactive oxygen species (ROS) to execute necrosis. Reactive Oxygen Species 45-68 tumor protein p53 Homo sapiens 0-3
19144918-7 2009 p53 induces cathepsin Q that cooperates with reactive oxygen species (ROS) to execute necrosis. Reactive Oxygen Species 70-73 tumor protein p53 Homo sapiens 0-3
19202565-6 2009 Scavenging of DADS-induced ROS by N-acetyl cysteine or reduced glutathione inhibited cell cycle arrest, apoptosis and p53 activation by DADS. Reactive Oxygen Species 27-30 tumor protein p53 Homo sapiens 118-121
19202565-7 2009 These results suggest that ROS trigger the DADS-induced cell cycle arrest and apoptosis and that ROS are involved in stress-induced signaling upstream of p53 activation. Reactive Oxygen Species 27-30 tumor protein p53 Homo sapiens 154-157
19202565-7 2009 These results suggest that ROS trigger the DADS-induced cell cycle arrest and apoptosis and that ROS are involved in stress-induced signaling upstream of p53 activation. Reactive Oxygen Species 97-100 tumor protein p53 Homo sapiens 154-157
19202565-9 2009 Moreover, DADS-induced apoptosis was also prevented by treatment with oligomycin, which is known to prevent p53-dependent apoptosis by reducing ROS levels in mitochondria. Reactive Oxygen Species 144-147 tumor protein p53 Homo sapiens 108-111
19202565-10 2009 These results suggest that mitochondrial ROS may serve as second messengers in DADS-induced apoptosis, which requires activation of p53. Reactive Oxygen Species 41-44 tumor protein p53 Homo sapiens 132-135
19026164-7 2008 The downregulation of p53 in the cells overexpressing nm23-H1 resulted in a higher cellular ROS level and lower cell viability. Reactive Oxygen Species 92-95 tumor protein p53 Homo sapiens 22-25
19054132-7 2008 Accordingly, we demonstrated that reactive oxygen species (ROS) are highly produced in p53 yeast induced cell death as shown by dihydrorhodamine 123 staining. Reactive Oxygen Species 34-57 tumor protein p53 Homo sapiens 87-90
19054132-7 2008 Accordingly, we demonstrated that reactive oxygen species (ROS) are highly produced in p53 yeast induced cell death as shown by dihydrorhodamine 123 staining. Reactive Oxygen Species 59-62 tumor protein p53 Homo sapiens 87-90
19054132-8 2008 These results suggest that the generation of ROS is a key event in p53 yeast induced cell death. Reactive Oxygen Species 45-48 tumor protein p53 Homo sapiens 67-70
18949386-10 2008 Therefore, it is suggested that vitamin C inhibits p53-induced senescence by preventing ROS generation, which in turn leads to the activation of p38 MAPKinase. Reactive Oxygen Species 88-91 tumor protein p53 Homo sapiens 51-54
18676676-0 2008 Reactive oxygen species mediate p53 activation and apoptosis induced by sodium nitroprusside in SH-SY5Y cells. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 32-35
18676676-8 2008 The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages. Reactive Oxygen Species 121-124 tumor protein p53 Homo sapiens 19-22
18676676-8 2008 The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages. Reactive Oxygen Species 121-124 tumor protein p53 Homo sapiens 165-168
18676676-8 2008 The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages. Reactive Oxygen Species 205-208 tumor protein p53 Homo sapiens 19-22
18676676-8 2008 The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages. Reactive Oxygen Species 205-208 tumor protein p53 Homo sapiens 165-168
18676676-8 2008 The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages. Reactive Oxygen Species 205-208 tumor protein p53 Homo sapiens 19-22
18676676-8 2008 The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages. Reactive Oxygen Species 205-208 tumor protein p53 Homo sapiens 165-168
19141477-9 2008 An shRNA-directed reduction in p53 protein by about 50% also results in extended cellular life span, reduced respiration and ROS, and increased glycolysis. Reactive Oxygen Species 125-128 tumor protein p53 Homo sapiens 31-34
18606492-10 2008 These results suggest that the ROS-ASK1-p38/JNK-p53 and Bax pathway plays a critical role in HBI"s anti-cancer effects. Reactive Oxygen Species 31-34 tumor protein p53 Homo sapiens 48-51
18949386-0 2008 Vitamin C inhibits p53-induced replicative senescence through suppression of ROS production and p38 MAPK activity. Reactive Oxygen Species 77-80 tumor protein p53 Homo sapiens 19-22
18949386-1 2008 We previously reported that tumor cells expressing p53 increase intracellular levels of reactive oxygen species (ROS). Reactive Oxygen Species 88-111 tumor protein p53 Homo sapiens 51-54
18949386-1 2008 We previously reported that tumor cells expressing p53 increase intracellular levels of reactive oxygen species (ROS). Reactive Oxygen Species 113-116 tumor protein p53 Homo sapiens 51-54
18949386-7 2008 We found that vitamin C inhibited this p53-induced ROS generation. Reactive Oxygen Species 51-54 tumor protein p53 Homo sapiens 39-42
18959823-6 2008 Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway. Reactive Oxygen Species 42-65 tumor protein p53 Homo sapiens 14-17
18959823-6 2008 Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway. Reactive Oxygen Species 42-65 tumor protein p53 Homo sapiens 148-151
18959823-6 2008 Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway. Reactive Oxygen Species 67-70 tumor protein p53 Homo sapiens 14-17
18959823-6 2008 Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway. Reactive Oxygen Species 67-70 tumor protein p53 Homo sapiens 148-151
18959823-6 2008 Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway. Reactive Oxygen Species 182-185 tumor protein p53 Homo sapiens 14-17
18959823-6 2008 Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway. Reactive Oxygen Species 182-185 tumor protein p53 Homo sapiens 148-151
18424439-6 2008 We identify ROS-independent modulations of ATM and p16(INK4a) and ROS-mediated activation of p53/p21(CIP1/WAF1/Sdi1) tumor suppressor pathways as major contributors to Foxo3-null hematopoietic stem cells defects. Reactive Oxygen Species 12-15 tumor protein p53 Homo sapiens 93-96
18424439-6 2008 We identify ROS-independent modulations of ATM and p16(INK4a) and ROS-mediated activation of p53/p21(CIP1/WAF1/Sdi1) tumor suppressor pathways as major contributors to Foxo3-null hematopoietic stem cells defects. Reactive Oxygen Species 66-69 tumor protein p53 Homo sapiens 93-96
18661100-6 2008 Moreover, generation of reactive oxygen species and subsequent induction of DNA strand breaks were found to be upstream mediators of p53 activation induced by SeC. Reactive Oxygen Species 24-47 tumor protein p53 Homo sapiens 133-136
18719315-2 2008 p53, a specific inhibitor of pifithrin alpha (PFT alpha), markedly inhibited ROS generation and apoptosis, showing that p53 was responsible for the cytotoxity of oridonin through mediation by ROS. Reactive Oxygen Species 77-80 tumor protein p53 Homo sapiens 0-3
18719315-2 2008 p53, a specific inhibitor of pifithrin alpha (PFT alpha), markedly inhibited ROS generation and apoptosis, showing that p53 was responsible for the cytotoxity of oridonin through mediation by ROS. Reactive Oxygen Species 77-80 tumor protein p53 Homo sapiens 120-123
18719315-2 2008 p53, a specific inhibitor of pifithrin alpha (PFT alpha), markedly inhibited ROS generation and apoptosis, showing that p53 was responsible for the cytotoxity of oridonin through mediation by ROS. Reactive Oxygen Species 192-195 tumor protein p53 Homo sapiens 0-3
18719315-2 2008 p53, a specific inhibitor of pifithrin alpha (PFT alpha), markedly inhibited ROS generation and apoptosis, showing that p53 was responsible for the cytotoxity of oridonin through mediation by ROS. Reactive Oxygen Species 192-195 tumor protein p53 Homo sapiens 120-123
18719315-3 2008 Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well. Reactive Oxygen Species 14-17 tumor protein p53 Homo sapiens 85-88
18719315-3 2008 Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well. Reactive Oxygen Species 14-17 tumor protein p53 Homo sapiens 260-263
18719315-3 2008 Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well. Reactive Oxygen Species 14-17 tumor protein p53 Homo sapiens 260-263
18719315-3 2008 Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well. Reactive Oxygen Species 131-134 tumor protein p53 Homo sapiens 85-88
18719315-3 2008 Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well. Reactive Oxygen Species 131-134 tumor protein p53 Homo sapiens 260-263
18719315-3 2008 Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well. Reactive Oxygen Species 131-134 tumor protein p53 Homo sapiens 260-263
18523266-0 2008 Proteasome inhibitors enhance TRAIL-induced apoptosis through the intronic regulation of DR5: involvement of NF-kappa B and reactive oxygen species-mediated p53 activation. Reactive Oxygen Species 124-147 tumor protein p53 Homo sapiens 157-160
18645026-6 2008 Andro is capable of activating p53 via increased p53 phosphorylation and protein stabilization, a process mediated by enhanced reactive oxygen species production and subsequent c-Jun NH(2)-terminal kinase activation. Reactive Oxygen Species 127-150 tumor protein p53 Homo sapiens 31-34
18661375-5 2008 RESULTS: In radio-resistant subclones generated from wt p53-transfected SAOS-2 cells DNA deletions were remarkably reduced and the accumulation of "common" deletion at mtDNA (that may let the persistence of oxidative damage by precluding detoxification from reactive oxygen species [ROS]) completely abrogated. Reactive Oxygen Species 258-281 tumor protein p53 Homo sapiens 56-59
18661375-5 2008 RESULTS: In radio-resistant subclones generated from wt p53-transfected SAOS-2 cells DNA deletions were remarkably reduced and the accumulation of "common" deletion at mtDNA (that may let the persistence of oxidative damage by precluding detoxification from reactive oxygen species [ROS]) completely abrogated. Reactive Oxygen Species 283-286 tumor protein p53 Homo sapiens 56-59
18523266-10 2008 Intracellular reactive oxygen species (ROS) generation after MG132 treatment contributed to p53, but not p65 nuclear translocation and DNA-binding activity. Reactive Oxygen Species 14-37 tumor protein p53 Homo sapiens 92-95
18523266-10 2008 Intracellular reactive oxygen species (ROS) generation after MG132 treatment contributed to p53, but not p65 nuclear translocation and DNA-binding activity. Reactive Oxygen Species 39-42 tumor protein p53 Homo sapiens 92-95
18523266-13 2008 These findings reveal that proteasome inhibitor-mediated NF-kappaB and ROS-dependent p53 activation are contributed to intronic regulation of DR5 transcription, and resulted in the subsequent enhancement of TRAIL-induced apoptosis in human lung cancer cells. Reactive Oxygen Species 71-74 tumor protein p53 Homo sapiens 85-88
17910628-6 2007 Bortezomib/PXD101 treatment markedly triggered reactive oxygen species (ROS) generation that was accompanied by p53, H2A.X and p38-mitogen-activated protein kinase phosphorylation. Reactive Oxygen Species 72-75 tumor protein p53 Homo sapiens 112-115
18287100-6 2008 In LoVo and RKO cells, which respond to adriamycin with a p53-mediated induction of POX and generation of reactive oxygen species, we found that adriamycin also induced OH-POX gene expression and markedly increased OH-POX catalytic activity, and this increase in activity was not observed in the cell lines HT29 and HCT15, which do not have a functional p53. Reactive Oxygen Species 106-129 tumor protein p53 Homo sapiens 58-61
18275858-5 2008 Recent studies have revealed that each cellular concentration and distribution of p53 has a distinct cellular function and that ROS act as both an upstream signal that triggers p53 activation and a downstream factor that mediates apoptosis. Reactive Oxygen Species 128-131 tumor protein p53 Homo sapiens 82-85
18275858-5 2008 Recent studies have revealed that each cellular concentration and distribution of p53 has a distinct cellular function and that ROS act as both an upstream signal that triggers p53 activation and a downstream factor that mediates apoptosis. Reactive Oxygen Species 128-131 tumor protein p53 Homo sapiens 177-180
18275858-6 2008 Here, we examine the newly discovered role of p53 in regulating cellular ROS generation and how ROS modulate selective transactivation of p53 target genes. Reactive Oxygen Species 73-76 tumor protein p53 Homo sapiens 46-49
18275858-6 2008 Here, we examine the newly discovered role of p53 in regulating cellular ROS generation and how ROS modulate selective transactivation of p53 target genes. Reactive Oxygen Species 96-99 tumor protein p53 Homo sapiens 138-141
18193822-5 2008 ROS and RNS escape results in the activation of cytosolic stress pathways, DNA damage, and the upregulation of JNK, p38, and p53. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 125-128
17510393-9 2007 The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent. Reactive Oxygen Species 41-44 tumor protein p53 Homo sapiens 64-67
17644309-9 2007 These findings collectively support a novel mechanism in which the PKCdelta-->IKKalpha signaling pathway contributes to ROS-induced activation of the p53 tumor suppressor. Reactive Oxygen Species 123-126 tumor protein p53 Homo sapiens 153-156
17626009-7 2007 Molecular mediators on the way from increased ROS levels to the observed growth arrest include p38 MAPK, p53, and p21. Reactive Oxygen Species 46-49 tumor protein p53 Homo sapiens 105-108
17505786-0 2007 Apoptosis by cisplatin requires p53 mediated p38alpha MAPK activation through ROS generation. Reactive Oxygen Species 78-81 tumor protein p53 Homo sapiens 32-35
17505786-3 2007 Using the HCT116 colon carcinoma derived cell line we have established that the apoptotic activity of cisplatin requires the onset of a p53-mediated p38alpha MAPK pathway through generation of reactive oxygen species (ROS). Reactive Oxygen Species 193-216 tumor protein p53 Homo sapiens 136-139
17505786-3 2007 Using the HCT116 colon carcinoma derived cell line we have established that the apoptotic activity of cisplatin requires the onset of a p53-mediated p38alpha MAPK pathway through generation of reactive oxygen species (ROS). Reactive Oxygen Species 218-221 tumor protein p53 Homo sapiens 136-139
17505786-6 2007 In addition, we have identified p38alpha as the isoform necessary for cisplatin-induced apoptosis, upon activation by p53-mediated ROS production. Reactive Oxygen Species 131-134 tumor protein p53 Homo sapiens 118-121
17505786-8 2007 We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation. Reactive Oxygen Species 25-28 tumor protein p53 Homo sapiens 21-24
17505786-8 2007 We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation. Reactive Oxygen Species 25-28 tumor protein p53 Homo sapiens 141-144
17505786-8 2007 We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation. Reactive Oxygen Species 25-28 tumor protein p53 Homo sapiens 141-144
17510393-9 2007 The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent. Reactive Oxygen Species 41-44 tumor protein p53 Homo sapiens 85-88
17510393-9 2007 The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent. Reactive Oxygen Species 41-44 tumor protein p53 Homo sapiens 85-88
17510393-9 2007 The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent. Reactive Oxygen Species 41-44 tumor protein p53 Homo sapiens 85-88
17510393-9 2007 The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent. Reactive Oxygen Species 192-195 tumor protein p53 Homo sapiens 64-67
17510393-9 2007 The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent. Reactive Oxygen Species 192-195 tumor protein p53 Homo sapiens 85-88
17510393-9 2007 The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent. Reactive Oxygen Species 192-195 tumor protein p53 Homo sapiens 85-88
17510393-9 2007 The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent. Reactive Oxygen Species 192-195 tumor protein p53 Homo sapiens 85-88
17510393-10 2007 The reversion to normal ROS levels in the Ras-expressing p53-positive cells correlated with up-regulation of p53-responsive genes, including reactivation of SESN1 gene. Reactive Oxygen Species 24-27 tumor protein p53 Homo sapiens 57-60
17510393-10 2007 The reversion to normal ROS levels in the Ras-expressing p53-positive cells correlated with up-regulation of p53-responsive genes, including reactivation of SESN1 gene. Reactive Oxygen Species 24-27 tumor protein p53 Homo sapiens 109-112
17136320-6 2007 Most importantly, sulindac-derived ROS activated p38 mitogen-activated protein kinase and p53. Reactive Oxygen Species 35-38 tumor protein p53 Homo sapiens 90-93
17289842-8 2007 OxLDL activated p53 through production of mitochondria-derived reactive oxygen species. Reactive Oxygen Species 63-86 tumor protein p53 Homo sapiens 16-19
17230520-9 2007 Furthermore a p53-dominant negative mutant attenuated selenite-induced ROS, leading to a proportionate protection against apoptosis. Reactive Oxygen Species 71-74 tumor protein p53 Homo sapiens 14-17
17381838-10 2007 CONCLUSION: These observations support a role for p53-mediated transcriptional program in mammalian aging and suggest that mechanisms other than reactive oxygen species are involved in the age-related transcriptional activation of p53 targets. Reactive Oxygen Species 145-168 tumor protein p53 Homo sapiens 231-234
16652144-2 2006 Moreover, p53 activation itself contributes to ROS accumulation. Reactive Oxygen Species 47-50 tumor protein p53 Homo sapiens 10-13
17077087-8 2006 Considering that p53-induced apoptosis requires an accumulation of reactive oxygen species, this negative control on the Nrf2 transactivation appears to be aimed to prevent the generation of a strong anti-oxidant intracellular environment that could hinder the induction of apoptosis. Reactive Oxygen Species 67-90 tumor protein p53 Homo sapiens 17-20
17145881-11 2006 Our results suggest that this MAPK-dependent ROS/p53 feedback loop is a point of vulnerability of melanoma cells that can be exploited for rational drug design. Reactive Oxygen Species 45-48 tumor protein p53 Homo sapiens 49-52
16872707-2 2006 It plays a crucial role in p53-dependent cellular response to DNA damage and oxidative stress by providing deoxyribonucleotides (dNTPs) to the DNA repair machinery and by scavenging reactive oxygen species (ROS). Reactive Oxygen Species 182-205 tumor protein p53 Homo sapiens 27-30
16872707-2 2006 It plays a crucial role in p53-dependent cellular response to DNA damage and oxidative stress by providing deoxyribonucleotides (dNTPs) to the DNA repair machinery and by scavenging reactive oxygen species (ROS). Reactive Oxygen Species 207-210 tumor protein p53 Homo sapiens 27-30
16946128-8 2006 A549-rho degrees cells that are incapable of mitochondrial reactive oxygen species production were protected against PM-induced DeltaPsi m, p53 expression, and apoptosis. Reactive Oxygen Species 59-82 tumor protein p53 Homo sapiens 140-143
16652144-3 2006 Here we show that treatment of p53-null cancer cells with sublethal concentrations of ROS triggered an arrest with some morphological similarities to cellular senescence. Reactive Oxygen Species 86-89 tumor protein p53 Homo sapiens 31-34
16763167-3 2006 We report that in a model of insulin-dependent diabetes mellitus, the generation of reactive oxygen species (ROS) leads to telomeric shortening, expression of the senescent associated proteins p53 and p16INK4a, and apoptosis of CPCs, impairing the growth reserve of the heart. Reactive Oxygen Species 84-107 tumor protein p53 Homo sapiens 193-196
16839880-6 2006 The decrease of intracellular ROS levels in response to TIGAR may also play a role in the ability of p53 to protect from the accumulation of genomic damage. Reactive Oxygen Species 30-33 tumor protein p53 Homo sapiens 101-104
16763167-3 2006 We report that in a model of insulin-dependent diabetes mellitus, the generation of reactive oxygen species (ROS) leads to telomeric shortening, expression of the senescent associated proteins p53 and p16INK4a, and apoptosis of CPCs, impairing the growth reserve of the heart. Reactive Oxygen Species 109-112 tumor protein p53 Homo sapiens 193-196
16385586-2 2006 Since genomic instability and phenotypic change are observed in presenescent cells without specific exposure to mutagens, we hypothesized that reactive oxygen species (ROS) produced during normal cell metabolism coupled with deficient p53 dependent DNA damage repair pathways make a significant contribution to immortalization related parameters. Reactive Oxygen Species 143-166 tumor protein p53 Homo sapiens 235-238
16385586-2 2006 Since genomic instability and phenotypic change are observed in presenescent cells without specific exposure to mutagens, we hypothesized that reactive oxygen species (ROS) produced during normal cell metabolism coupled with deficient p53 dependent DNA damage repair pathways make a significant contribution to immortalization related parameters. Reactive Oxygen Species 168-171 tumor protein p53 Homo sapiens 235-238
16580789-0 2006 p53 protein or BID protein select the route to either apoptosis (programmed cell death) or to cell cycle arrest opposing carcinogenesis after DNA damage by ROS. Reactive Oxygen Species 156-159 tumor protein p53 Homo sapiens 0-3
16303758-2 2006 We and others have shown that POX is a p53-induced gene that can mediate apoptosis through generation of reactive oxygen species (ROS). Reactive Oxygen Species 105-128 tumor protein p53 Homo sapiens 39-42
16303758-2 2006 We and others have shown that POX is a p53-induced gene that can mediate apoptosis through generation of reactive oxygen species (ROS). Reactive Oxygen Species 130-133 tumor protein p53 Homo sapiens 39-42
16580789-3 2006 Moreover, oxidative stress by reactive oxygen species (ROS) such as the hydroxyl radical (*OH) produced by ionizing radiation (carcinogenic) triggers p53 activation in response to the damage of DNA (followed by initiation of DNA-repair mechanisms). Reactive Oxygen Species 30-53 tumor protein p53 Homo sapiens 150-153
16580789-3 2006 Moreover, oxidative stress by reactive oxygen species (ROS) such as the hydroxyl radical (*OH) produced by ionizing radiation (carcinogenic) triggers p53 activation in response to the damage of DNA (followed by initiation of DNA-repair mechanisms). Reactive Oxygen Species 55-58 tumor protein p53 Homo sapiens 150-153
15711927-3 2005 Transactivation of p53 in MCF7 cells also led to increase in expression of Bax, proapototic Bcl-2 family member, triggering mitochondrial pore opening, and PIG3 (p53-induced gene 3 product), and also generation of intracellular reactive oxygen species (ROS). Reactive Oxygen Species 228-251 tumor protein p53 Homo sapiens 19-22
16163384-3 2005 Here, we report that the tumor suppressor molecule p53 has a novel role in maintaining mitochondrial genetic stability through its ability to translocate to mitochondria and interact with mtDNA polymerase gamma (pol gamma) in response to mtDNA damage induced by exogenous and endogenous insults including ROS. Reactive Oxygen Species 305-308 tumor protein p53 Homo sapiens 51-54
16163384-6 2005 This study provides a mechanistic explanation for the accelerating genetic instability and increased ROS stress in cancer cells associated with loss of p53. Reactive Oxygen Species 101-104 tumor protein p53 Homo sapiens 152-155
15914462-1 2005 Proline oxidase is a p53-induced redox gene that can generate reactive oxygen species (ROS) and mediate apoptosis in tumor cells. Reactive Oxygen Species 62-85 tumor protein p53 Homo sapiens 21-24
15914462-1 2005 Proline oxidase is a p53-induced redox gene that can generate reactive oxygen species (ROS) and mediate apoptosis in tumor cells. Reactive Oxygen Species 87-90 tumor protein p53 Homo sapiens 21-24
15914462-4 2005 Both proline oxidase- and p53-induced activation of NFAT were sensitive to the calcineurin inhibitors cyclosporin A and FK-506, to scavengers of ROS, and to inhibitors of calcium mobilization. Reactive Oxygen Species 145-148 tumor protein p53 Homo sapiens 26-29
15705792-0 2005 Stress-induced activation of the p53 tumor suppressor in leukemia cells and normal lymphocytes requires mitochondrial activity and reactive oxygen species. Reactive Oxygen Species 131-154 tumor protein p53 Homo sapiens 33-36
15705792-6 2005 Reactive oxygen species (ROS) localized to mitochondria decreased in the presence of oligomycin, and stress-induced p53 activation showed strong ROS sensitivity both in leukemic and normal cells. Reactive Oxygen Species 145-148 tumor protein p53 Homo sapiens 116-119
15867370-1 2005 The tumor suppressor gene p53 is activated by reactive oxygen species-generating agents. Reactive Oxygen Species 46-69 tumor protein p53 Homo sapiens 26-29
15685549-9 2005 Infliximab induced accumulation of reactive oxygen species and up-regulation of Bax, Bak, and p21(WAF1/CIP1) proteins, suggesting the involvement of p53 activation. Reactive Oxygen Species 35-58 tumor protein p53 Homo sapiens 149-152
15616590-0 2005 5-Lipoxygenase regulates senescence-like growth arrest by promoting ROS-dependent p53 activation. Reactive Oxygen Species 68-71 tumor protein p53 Homo sapiens 82-85
15711927-9 2005 Copper treatment did not result in accumulation of ROS in these cell lines with an inactive p53 even after exposure to 50 microM of copper for 6 h, indicating a key role for p53 in the ROS generation. Reactive Oxygen Species 185-188 tumor protein p53 Homo sapiens 174-177
15711927-3 2005 Transactivation of p53 in MCF7 cells also led to increase in expression of Bax, proapototic Bcl-2 family member, triggering mitochondrial pore opening, and PIG3 (p53-induced gene 3 product), and also generation of intracellular reactive oxygen species (ROS). Reactive Oxygen Species 253-256 tumor protein p53 Homo sapiens 19-22
15342409-7 2004 HCT116 p53+/+ cells exhibit a more rapid removal of 8-oxoG from DNA than p53-/- cells exposed to the same levels of reactive oxygen species (ROS) stress. Reactive Oxygen Species 116-139 tumor protein p53 Homo sapiens 7-10
15711927-10 2005 Pretreatment of MCF7 cells with p53 inhibitor, pifithrin-alpha, resulted in decrease of copper and zinc induced ROS production to the control level, suppression of both Bax expression and AIF release. Reactive Oxygen Species 112-115 tumor protein p53 Homo sapiens 32-35
15711927-11 2005 Therefore, the activation of p53 seems to play a crucial role in copper and zinc induced generation of ROS in epithelial breast cancer cells, and expression of downstream targets of p53, such as PIG3 and Bax, responsible for increased generation of the intracellular ROS, as well as disruption of mitochondrial integrity. Reactive Oxygen Species 103-106 tumor protein p53 Homo sapiens 29-32
15711927-11 2005 Therefore, the activation of p53 seems to play a crucial role in copper and zinc induced generation of ROS in epithelial breast cancer cells, and expression of downstream targets of p53, such as PIG3 and Bax, responsible for increased generation of the intracellular ROS, as well as disruption of mitochondrial integrity. Reactive Oxygen Species 267-270 tumor protein p53 Homo sapiens 29-32
15711927-11 2005 Therefore, the activation of p53 seems to play a crucial role in copper and zinc induced generation of ROS in epithelial breast cancer cells, and expression of downstream targets of p53, such as PIG3 and Bax, responsible for increased generation of the intracellular ROS, as well as disruption of mitochondrial integrity. Reactive Oxygen Species 267-270 tumor protein p53 Homo sapiens 182-185
15131591-6 2004 Two separate signaling cascades, p53-mediated ROS-dependent and -independent pathways, both of which are initiated by caspase-8 activation, thus contribute to ceramide formation in TNF-alpha-induced apoptosis of human glioma cells. Reactive Oxygen Species 46-49 tumor protein p53 Homo sapiens 33-36
15534883-3 2004 p53 is a tumor suppressor gene, and X-ray cross-complementing group 1 (XRCC1) is involved in the base-excision repair of ROS-induced DNA damage. Reactive Oxygen Species 121-124 tumor protein p53 Homo sapiens 0-3
15342409-0 2004 Role of p53 in sensing oxidative DNA damage in response to reactive oxygen species-generating agents. Reactive Oxygen Species 59-82 tumor protein p53 Homo sapiens 8-11
15342409-7 2004 HCT116 p53+/+ cells exhibit a more rapid removal of 8-oxoG from DNA than p53-/- cells exposed to the same levels of reactive oxygen species (ROS) stress. Reactive Oxygen Species 141-144 tumor protein p53 Homo sapiens 7-10
15342409-8 2004 Together, these results suggest that p53 participates in sensing oxidative DNA damage and modulates BER function in response to persistent ROS stress. Reactive Oxygen Species 139-142 tumor protein p53 Homo sapiens 37-40
14764594-11 2004 Therefore, Bcl-x(L) and E1B-19K inhibit p53-induced senescence by preventing ROS generation, which in turn leads to the activation of p38 kinase. Reactive Oxygen Species 77-80 tumor protein p53 Homo sapiens 40-43
15059885-1 2004 p53-mediated apoptosis may involve the induction of redox-controlling genes, resulting in the production of reactive oxygen species. Reactive Oxygen Species 108-131 tumor protein p53 Homo sapiens 0-3
14764594-0 2004 Bcl-xL and E1B-19K proteins inhibit p53-induced irreversible growth arrest and senescence by preventing reactive oxygen species-dependent p38 activation. Reactive Oxygen Species 104-127 tumor protein p53 Homo sapiens 36-39
14764594-4 2004 First, we found that that ROS are increased during p53-induced senescence. Reactive Oxygen Species 26-29 tumor protein p53 Homo sapiens 51-54
14764594-5 2004 Moreover, Bcl-x(L) and E1B-19K inhibit this p53-induced ROS generation. Reactive Oxygen Species 56-59 tumor protein p53 Homo sapiens 44-47
14764594-6 2004 Second, antioxidants prevent the induction of senescence and ROS by p53, but not the persistence of the senescence phenotype. Reactive Oxygen Species 61-64 tumor protein p53 Homo sapiens 68-71
15059885-10 2004 We observed both the release of cytochrome C and Ca(2+) from the mitochondria into the cytoplasm and an increased frequency of apoptotic cells after p53 induction in the TR9-7 cells that coincided with an increased expression of MnSOD and GPx, and the level of reactive oxygen species. Reactive Oxygen Species 261-284 tumor protein p53 Homo sapiens 149-152
12370809-10 2002 Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis. Reactive Oxygen Species 110-133 tumor protein p53 Homo sapiens 50-53
14871840-0 2004 Induction of apoptosis in leukemic cells by homovanillic acid derivative, capsaicin, through oxidative stress: implication of phosphorylation of p53 at Ser-15 residue by reactive oxygen species. Reactive Oxygen Species 170-193 tumor protein p53 Homo sapiens 145-148
14986171-9 2004 These results suggest that p53 might play a protective role against cell damage induced by generation of intracellular ROS, through transcriptional activation of ALDH4. Reactive Oxygen Species 119-122 tumor protein p53 Homo sapiens 27-30
12962703-8 2003 The results suggest that higher levels of intracellular ROS, generated by HA+H(2)O(2) act as a molecular switch in activating a rapidly acting p53-independent mitochondrial apoptotic pathway. Reactive Oxygen Species 56-59 tumor protein p53 Homo sapiens 143-146
14598320-7 2003 Conversely, DNA damage-induced reactive oxygen species generation was inhibited significantly by gene disruption of p53, Apaf-1, or caspase-9, and combined deficiency of Bax and Bak, but not by caspase-3 or caspase-6 deficiency. Reactive Oxygen Species 31-54 tumor protein p53 Homo sapiens 116-119
12675680-4 2003 p53 interacts with mitochondria either directly or through activation of the genes for pro-apoptotic proteins such as Bax or NOXA or genes that encode redox enzymes responsible for the production of reactive oxygen species (ROS). Reactive Oxygen Species 199-222 tumor protein p53 Homo sapiens 0-3
12675680-4 2003 p53 interacts with mitochondria either directly or through activation of the genes for pro-apoptotic proteins such as Bax or NOXA or genes that encode redox enzymes responsible for the production of reactive oxygen species (ROS). Reactive Oxygen Species 224-227 tumor protein p53 Homo sapiens 0-3
14713953-6 2004 FOXO3a influences p53 activity by regulating the level of reactive oxygen species. Reactive Oxygen Species 58-81 tumor protein p53 Homo sapiens 18-21
12899928-0 2003 Reactive oxygen species mediate doxorubicin induced p53-independent apoptosis. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 52-55
12663048-4 2003 Here, we demonstrated that p53 accumulation by WR1065 in MCF-7 cells did not result from the formation of DNA-damage as measured by DNA fragmentation and Comet assay, nor from oxidative stress as detected by measurement of glutathione levels, lipid peroxidation and reactive oxygen species production. Reactive Oxygen Species 266-289 tumor protein p53 Homo sapiens 27-30
14622914-3 2003 We also analyzed the involvement of Ca2+, mitochondria and reactive oxygen species in p53 activation. Reactive Oxygen Species 59-82 tumor protein p53 Homo sapiens 86-89
14622914-9 2003 Reactive oxygen species also participated in veratridine-induced neurotoxicity and p53 activation. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 83-86
12370809-10 2002 Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis. Reactive Oxygen Species 110-133 tumor protein p53 Homo sapiens 150-153
12370809-10 2002 Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis. Reactive Oxygen Species 135-138 tumor protein p53 Homo sapiens 50-53
12370809-10 2002 Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis. Reactive Oxygen Species 135-138 tumor protein p53 Homo sapiens 150-153
12370809-10 2002 Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis. Reactive Oxygen Species 252-255 tumor protein p53 Homo sapiens 50-53
12370809-10 2002 Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis. Reactive Oxygen Species 252-255 tumor protein p53 Homo sapiens 150-153
11447225-0 2001 Reactive oxygen species-induced phosphorylation of p53 on serine 20 is mediated in part by polo-like kinase-3. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 51-54
12359750-4 2002 Reactive oxygen species apparently derived from a flavin-containing oxidase enzyme [presumably an NAD(P)H-oxidase] appeared to be major contributors to the bystander-induced up-regulation of p53 and p21(Waf1) as well as micronucleus formation, as evidenced by the inhibition of these effects with diphenyliodonium. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 191-194
12105992-8 2002 ROS levels in cells with abrogated TP53 function were decreased in magnitude and duration. Reactive Oxygen Species 0-3 tumor protein p53 Homo sapiens 35-39
11980715-3 2002 Here we show that p21 increased intracellular levels of ROS both in normal fibroblasts and in p53-negative cancer cells. Reactive Oxygen Species 56-59 tumor protein p53 Homo sapiens 94-97
11590433-6 2001 These data, coupled with the effects of pharmacologic inhibitors of reactive oxygen species, indicate that FR contributes to p53-mediated apoptosis through the generation of oxidative stress in mitochondria. Reactive Oxygen Species 68-91 tumor protein p53 Homo sapiens 125-128
12067251-0 2002 Reactive oxygen species generated by PAH o-quinones cause change-in-function mutations in p53. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 90-93
12067251-5 2002 We employed a yeast reporter system to determine whether PAH o-quinones or the ROS they generate cause change-in-function mutations in p53. Reactive Oxygen Species 79-82 tumor protein p53 Homo sapiens 135-138
12067251-10 2002 p53 mutagenesis by BP-7,8-dione was attenuated by ROS scavengers and completely abrogated by a combination of superoxide dismutase and catalase, indicating that both superoxide anion and hydroxyl radicals were the responsible mutagens. Reactive Oxygen Species 50-53 tumor protein p53 Homo sapiens 0-3
12067251-14 2002 Together these data suggest that PAH o-quinones generate an endogenous mutagen (ROS) which leads to p53 inactivation. Reactive Oxygen Species 80-83 tumor protein p53 Homo sapiens 100-103
11822871-5 2002 Moreover, expression of functional p53 protein using a temperature-sensitive human p53val(138) induced ceramide generation by activation of neutral SMase but not acid SMase through ROS formation. Reactive Oxygen Species 181-184 tumor protein p53 Homo sapiens 35-38
11809417-3 2002 The role of p53 in ROS induced cell death has not been consistent and has been shown to be cell type dependent. Reactive Oxygen Species 19-22 tumor protein p53 Homo sapiens 12-15
11287297-11 2001 In conclusion, our current study strongly suggests that CuQ induces gene mutation, global DNA damage, and P53 expression through a ROS-dependent mechanism. Reactive Oxygen Species 131-134 tumor protein p53 Homo sapiens 106-109
11493433-4 2001 These pathways are themselves influenced by a number of lipid products (diacylglycerol, sphingosine-1 phosphate, and glucosyl ceramide), reactive oxygen species, oncogenes (such as the tumor suppressor gene p53), protein kinases (protein kinase C and phosphoinositide-3 kinase), and external stimuli (hematopoietic growth factors and the extracellular matrix). Reactive Oxygen Species 137-160 tumor protein p53 Homo sapiens 207-210
11313880-0 2001 p53 regulates ceramide formation by neutral sphingomyelinase through reactive oxygen species in human glioma cells. Reactive Oxygen Species 69-92 tumor protein p53 Homo sapiens 0-3
11368358-9 2001 Therefore, wt p53 leukemic cells respond to HHT-specific cellular stress by induction of ROS-independent apoptotic pathway characterized by translocation of Bax, mitochondrial cytochrome c release and activation of caspases. Reactive Oxygen Species 89-92 tumor protein p53 Homo sapiens 14-17
11291926-0 2001 Caspase-3 activation downstream from reactive oxygen species in heat-induced apoptosis of pancreatic carcinoma cells carrying a mutant p53 gene. Reactive Oxygen Species 37-60 tumor protein p53 Homo sapiens 135-138
11291926-7 2001 These results suggest a possible pathway by which reactive oxygen species lead to caspase-3 activation to cause heat-induced death of pancreatic carcinoma cells carrying mutant p53. Reactive Oxygen Species 50-73 tumor protein p53 Homo sapiens 177-180
11313880-3 2001 p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase. Reactive Oxygen Species 48-71 tumor protein p53 Homo sapiens 0-3
11313880-3 2001 p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase. Reactive Oxygen Species 73-76 tumor protein p53 Homo sapiens 0-3
11280728-0 2001 Proline oxidase, encoded by p53-induced gene-6, catalyzes the generation of proline-dependent reactive oxygen species. Reactive Oxygen Species 94-117 tumor protein p53 Homo sapiens 28-31
10951577-4 2000 The present study tested the hypothesis that reactive oxygen species (ROS) released from mitochondria regulate the cytosolic redox state and are required for the stabilization of p53 protein levels in response to hypoxia. Reactive Oxygen Species 45-68 tumor protein p53 Homo sapiens 179-182
10969820-3 2000 Reactive oxygen species are known to be powerful inducers of p53 activity; moreover, they play a role in the execution of p53-dependent apoptosis. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 61-64
10969820-3 2000 Reactive oxygen species are known to be powerful inducers of p53 activity; moreover, they play a role in the execution of p53-dependent apoptosis. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 122-125
11280728-9 2001 We hypothesize that proline oxidation supports the generation of ROS by donating reducing potential to an electron transport chain altered either by p53-dependent mechanisms or by overexpression of POX. Reactive Oxygen Species 65-68 tumor protein p53 Homo sapiens 149-152
10942736-1 2000 The present study investigates whether reactive oxygen species (ROS) are involved in p53 activation, and if they are, which species is responsible for the activation. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 85-88
10951577-4 2000 The present study tested the hypothesis that reactive oxygen species (ROS) released from mitochondria regulate the cytosolic redox state and are required for the stabilization of p53 protein levels in response to hypoxia. Reactive Oxygen Species 70-73 tumor protein p53 Homo sapiens 179-182
10951577-8 2000 Rotenone, an inhibitor of mitochondrial complex I, and 4,4"-diisothiocyanato-stilbene-2,2"-disulfonate, a mitochondrial anion channel inhibitor, also abolished the increase in ROS signal and p53 levels during hypoxia. Reactive Oxygen Species 176-179 tumor protein p53 Homo sapiens 191-194
10951577-12 2000 These results indicate that mitochondria regulate p53 protein levels during hypoxia through a redox-dependent mechanism involving ROS. Reactive Oxygen Species 130-133 tumor protein p53 Homo sapiens 50-53
10657969-0 2000 Transition mutation in codon 248 of the p53 tumor suppressor gene induced by reactive oxygen species and a nitric oxide-releasing compound. Reactive Oxygen Species 77-100 tumor protein p53 Homo sapiens 40-43
10828488-9 2000 However, high concentrations of exogenous ROS can also stimulate smooth muscle cell apoptosis as shown for other cell types probably via activation of p53. Reactive Oxygen Species 42-45 tumor protein p53 Homo sapiens 151-154
10728689-6 2000 Like the increased intracellular ROS bystander effect, this "decreased TP53/CDKN1A response" can be mimicked in otherwise untreated cells by the addition of low concentrations of TGF-beta1. Reactive Oxygen Species 33-36 tumor protein p53 Homo sapiens 71-75
10679306-6 2000 We show that overexpression of Prx-V prevented the p53-dependent generation of reactive oxygen species. Reactive Oxygen Species 79-102 tumor protein p53 Homo sapiens 51-54
10863531-2 2000 In vivo and in vitro DNA base modification patterns inflicted by reactive oxygen species (ROS) in the human P53 and PGK1 gene were nearly identical in vitro and in vivo. Reactive Oxygen Species 65-88 tumor protein p53 Homo sapiens 108-111
10863531-2 2000 In vivo and in vitro DNA base modification patterns inflicted by reactive oxygen species (ROS) in the human P53 and PGK1 gene were nearly identical in vitro and in vivo. Reactive Oxygen Species 90-93 tumor protein p53 Homo sapiens 108-111
10545114-0 1999 p53 regulates mitochondrial membrane potential through reactive oxygen species and induces cytochrome c-independent apoptosis blocked by Bcl-2. Reactive Oxygen Species 55-78 tumor protein p53 Homo sapiens 0-3
10574974-6 1999 p53 is activated by Cr(VI), mostly by ROS-mediated free radical reactions. Reactive Oxygen Species 38-41 tumor protein p53 Homo sapiens 0-3
10545114-8 1999 p53 induced ROS generation, which then caused a transient increase of Deltapsi followed by a decrease. Reactive Oxygen Species 12-15 tumor protein p53 Homo sapiens 0-3
10545114-12 1999 Thus, the ROS-mediated disruption of Deltapsi constitutes a pivotal step in the apoptotic pathway of p53, and this pathway does not involve cytochrome c release. Reactive Oxygen Species 10-13 tumor protein p53 Homo sapiens 101-104
14646487-6 1998 One model indicates that p53 induces redox-related genes that generate reactive oxygen species and promote the oxidative degradation of mitochondrial components. Reactive Oxygen Species 71-94 tumor protein p53 Homo sapiens 25-28
10098455-2 1998 By developing an oxidative-induced DNA damage mapping version of the Ligation-mediated polymerase chain reaction (LMPCR) technique, we investigated the il vivo and in vitro frequencies of DNA base modifications caused by ROS in the human p53 and PGK1 gene. Reactive Oxygen Species 221-224 tumor protein p53 Homo sapiens 238-241
10098455-13 1998 CEE provided a 24-fold increase in the signal strength attributable to strand breaks plus modified bases created by ROS in the human p53 and PGK1 genes, detected by LMPCR. Reactive Oxygen Species 116-119 tumor protein p53 Homo sapiens 133-136
10441517-6 1999 Our results suggest a possible connection between p53-dependent apoptosis and the production of reactive oxygen species. Reactive Oxygen Species 96-119 tumor protein p53 Homo sapiens 50-53
9305847-7 1997 These observations stimulated additional biochemical and pharmacological experiments suggesting that p53 results in apoptosis through a three-step process: (1) the transcriptional induction of redox-related genes; (2) the formation of reactive oxygen species; and (3) the oxidative degradation of mitochondrial components, culminating in cell death. Reactive Oxygen Species 235-258 tumor protein p53 Homo sapiens 101-104
9548807-9 1998 Inhibition of ROS production by the antioxidant enzyme catalase reduced AZQ- and DZQ-mediated p53 induction by about 45%. Reactive Oxygen Species 14-17 tumor protein p53 Homo sapiens 94-97
9548807-11 1998 The nonalkylator oxygen-radical-generating agent menadione (MD) caused p53 induction only when MCF-7 cells were allowed to recover in drug-free media. Reactive Oxygen Species 17-31 tumor protein p53 Homo sapiens 71-74
9074626-0 1997 The induction of apoptosis in proliferating human fibroblasts by oxygen radicals is associated with a p53- and p21WAF1CIP1 induction. Reactive Oxygen Species 65-80 tumor protein p53 Homo sapiens 102-105
33782397-6 2021 TP53I3 is transcriptionally activated by p53 and believed to play a role in DNA damage response and reactive oxygen species-induced apoptosis. Reactive Oxygen Species 100-123 tumor protein p53 Homo sapiens 41-44
8876226-0 1996 Reactive oxygen species are downstream mediators of p53-dependent apoptosis. Reactive Oxygen Species 0-23 tumor protein p53 Homo sapiens 52-55
8876226-3 1996 We sought to determine whether a central modulator of apoptosis, p53, regulates the levels of intracellular ROS and whether a rise in ROS levels is required for the induction of p53-dependent apoptosis. Reactive Oxygen Species 108-111 tumor protein p53 Homo sapiens 65-68
8876226-3 1996 We sought to determine whether a central modulator of apoptosis, p53, regulates the levels of intracellular ROS and whether a rise in ROS levels is required for the induction of p53-dependent apoptosis. Reactive Oxygen Species 134-137 tumor protein p53 Homo sapiens 178-181
8876226-5 1996 Cells sensitive to p53-mediated apoptosis produced ROS concomitantly with p53 overexpression, whereas cells resistant to p53 failed to produce ROS. Reactive Oxygen Species 51-54 tumor protein p53 Homo sapiens 19-22
8876226-7 1996 These results suggest that p53 acts to regulate the intracellular redox state and induces apoptosis by a pathway that is dependent on ROS production. Reactive Oxygen Species 134-137 tumor protein p53 Homo sapiens 27-30
8921985-12 1996 Recent studies have provided additional evidence that reactive oxygen species (ROS) and oxidative DNA damage may be involved in AFB1-induced p53 and ras mutations. Reactive Oxygen Species 54-77 tumor protein p53 Homo sapiens 141-144
8921985-12 1996 Recent studies have provided additional evidence that reactive oxygen species (ROS) and oxidative DNA damage may be involved in AFB1-induced p53 and ras mutations. Reactive Oxygen Species 79-82 tumor protein p53 Homo sapiens 141-144
34239689-0 2021 UNC5B Promotes Vascular Endothelial Cell Senescence via the ROS-Mediated P53 Pathway. Reactive Oxygen Species 60-63 tumor protein p53 Homo sapiens 73-76
30578154-9 2019 The up-regulated miRNAs were mainly enriched in pathways as GO:0000122-negative regulation of transcription from RNA polymerase II promoter, phosphatidylinositol phosphorylation, MAPK signaling pathway, and Ras signaling pathway, etc., while the down-regulated miRNAs were enriched in pathways as, response to reactive oxygen species, p53 signaling pathway, calcium signaling pathway, etc. Reactive Oxygen Species 310-333 tumor protein p53 Homo sapiens 335-338
34821461-4 2022 Moreover, the generation of tamoxifen resistance involved in apoptosis escape via a reactive oxygen species-regulated p53 signaling pathway. Reactive Oxygen Species 84-107 tumor protein p53 Homo sapiens 118-121
34785775-7 2022 Interestingly, ODN-induced p53 and Bax upregulation were modulated by the production of mitochondrial reactive oxygen species (ROS). Reactive Oxygen Species 102-125 tumor protein p53 Homo sapiens 27-30
34785775-7 2022 Interestingly, ODN-induced p53 and Bax upregulation were modulated by the production of mitochondrial reactive oxygen species (ROS). Reactive Oxygen Species 127-130 tumor protein p53 Homo sapiens 27-30
34785775-8 2022 Mitochondrial ROS scavengers prevented OTUB1-mediated p53 stabilization and Bax upregulation by ODN. Reactive Oxygen Species 14-17 tumor protein p53 Homo sapiens 54-57
34687773-7 2021 Taken together, CYN may induce ROS overproduction, leading to increased p53 expression and ultimately promoting VSMC apoptosis. Reactive Oxygen Species 31-34 tumor protein p53 Homo sapiens 72-75
34823034-14 2022 RESULTS: At 2-4 h after PDT treatment, ROS was dramatically elevated in lewis cells, DNA double-strand breaks (DDSB) occurred, as well as up-regulation of DDR proteins gamma-H2A.X, p-ATM, and p53. Reactive Oxygen Species 39-42 tumor protein p53 Homo sapiens 192-195
34628485-5 2022 Here, we show that p53 functions to support repair and recovery from CCl4-mediated liver damage, control reactive oxygen species (ROS) and limit the development of hepatocellular carcinoma (HCC), in part through the activation of a detoxification cytochrome P450, CYP2A5 (CYP2A6 in humans). Reactive Oxygen Species 105-128 tumor protein p53 Homo sapiens 19-22
34628485-5 2022 Here, we show that p53 functions to support repair and recovery from CCl4-mediated liver damage, control reactive oxygen species (ROS) and limit the development of hepatocellular carcinoma (HCC), in part through the activation of a detoxification cytochrome P450, CYP2A5 (CYP2A6 in humans). Reactive Oxygen Species 130-133 tumor protein p53 Homo sapiens 19-22
34506766-4 2021 We also found that the accumulation of reactive oxygen species (ROS) mediated A-24 induced apoptosis is p53-independent. Reactive Oxygen Species 39-62 tumor protein p53 Homo sapiens 104-107
34506766-4 2021 We also found that the accumulation of reactive oxygen species (ROS) mediated A-24 induced apoptosis is p53-independent. Reactive Oxygen Species 64-67 tumor protein p53 Homo sapiens 104-107
34181793-6 2021 Cell cycle arrest at G2 /M phase caused by surfactin was demonstrated through p53 and p21 accumulation combined p34cdc2 , phosphorylated p34cdc2 and cyclin B1 inhibition, which was regulated by NADPH oxidase-derived ROS. Reactive Oxygen Species 216-219 tumor protein p53 Homo sapiens 78-81
34886886-11 2021 CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells. Reactive Oxygen Species 199-202 tumor protein p53 Homo sapiens 51-54
34886886-11 2021 CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells. Reactive Oxygen Species 199-202 tumor protein p53 Homo sapiens 174-177
34928029-6 2021 The CPD regulates the expression levels of Caspase-3, p53, and Bcl-2 genes by increasing intracellular reactive oxygen species (ROS) levels and reducing mitochondrial membrane potential, which indicates that mitochondrial-mediated pathways are involved in apoptosis. Reactive Oxygen Species 103-126 tumor protein p53 Homo sapiens 54-57
34928029-6 2021 The CPD regulates the expression levels of Caspase-3, p53, and Bcl-2 genes by increasing intracellular reactive oxygen species (ROS) levels and reducing mitochondrial membrane potential, which indicates that mitochondrial-mediated pathways are involved in apoptosis. Reactive Oxygen Species 128-131 tumor protein p53 Homo sapiens 54-57
34676202-11 2021 In metformin-treated samples, the CEBPA, TP53 and USF1 transcription factors appeared to be involved in the regulation of several factors (SOD1, SOD2, CAT, GLRX, GSTP1) blocking ROS. Reactive Oxygen Species 178-181 tumor protein p53 Homo sapiens 41-45
34697746-8 2021 The viability, migration, and mitochondrial transmembrane potential of GC cells increased in association with decreased levels of ROS and mitochondrial apoptosis in the P53-silenced group. Reactive Oxygen Species 130-133 tumor protein p53 Homo sapiens 169-172
34144191-1 2021 Stabilization and activation of the p53 tumor suppressor are triggered in response to various cellular stresses, including DNA damaging agents and elevated Reactive Oxygen Species (ROS) like H2O2. Reactive Oxygen Species 156-179 tumor protein p53 Homo sapiens 36-39
34144191-1 2021 Stabilization and activation of the p53 tumor suppressor are triggered in response to various cellular stresses, including DNA damaging agents and elevated Reactive Oxygen Species (ROS) like H2O2. Reactive Oxygen Species 181-184 tumor protein p53 Homo sapiens 36-39
34405016-5 2021 Interestingly, massive accumulation of ROS inhibits tumor growth in two ways: (1) by blocking cancer cell proliferation by suppressing the proliferation signaling pathway, cell cycle, and the biosynthesis of nucleotides and ATP and (2) by inducing cancer cell death via activating endoplasmic reticulum stress-, mitochondrial-, and P53- apoptotic pathways and the ferroptosis pathway. Reactive Oxygen Species 39-42 tumor protein p53 Homo sapiens 332-335
34239689-11 2021 These findings suggest that UNC5B promotes endothelial cell senescence, potentially by activating the ROS-P53 pathway. Reactive Oxygen Species 102-105 tumor protein p53 Homo sapiens 106-109
35601652-3 2022 p53 activation in response to neurodegenerative stress is closely associated with the degeneration of dopaminergic neurons accompanied by mitochondrial dysfunction, reactive oxygen species (ROS) production, abnormal protein aggregation, and impairment of autophagy, and these pathogenic events have been implicated in the pathogenesis of PD. Reactive Oxygen Species 165-188 tumor protein p53 Homo sapiens 0-3
34131139-1 2021 Here, we identify iPLA2beta as a critical regulator for p53-driven ferroptosis upon reactive oxygen species (ROS)-induced stress. Reactive Oxygen Species 109-112 tumor protein p53 Homo sapiens 56-59
34131139-3 2021 We found that iPLA2beta-mediated detoxification of peroxidized lipids is sufficient to suppress p53-driven ferroptosis upon ROS-induced stress, even in GPX4-null cells. Reactive Oxygen Species 124-127 tumor protein p53 Homo sapiens 96-99
35395477-0 2022 Ultrasound-triggered reactive oxygen species effector nanoamplifier for enhanced combination therapy of mutant p53 tumors. Reactive Oxygen Species 21-44 tumor protein p53 Homo sapiens 111-114
35395477-2 2022 In this study, we built an ultrasound-triggered ROS damage nanoamplifier using a synergistic strategy consisting of ROS damage and decreased tumor self-protection capability to enhance the treatment efficacy of mutant p53 tumors. Reactive Oxygen Species 48-51 tumor protein p53 Homo sapiens 218-221
35395477-2 2022 In this study, we built an ultrasound-triggered ROS damage nanoamplifier using a synergistic strategy consisting of ROS damage and decreased tumor self-protection capability to enhance the treatment efficacy of mutant p53 tumors. Reactive Oxygen Species 116-119 tumor protein p53 Homo sapiens 218-221
35395477-5 2022 In addition, TH287 allies with ROS to eliminate the mutated p53 protein in tumor cells, thus reducing the self-protective capacity of tumor cells. Reactive Oxygen Species 31-34 tumor protein p53 Homo sapiens 60-63
35395477-7 2022 The construction of a ROS nanoamplifier not only provides an effective strategy for the treatment of mutant p53 tumors but also supplies an integrated platform for tumor diagnosis and therapy. Reactive Oxygen Species 22-25 tumor protein p53 Homo sapiens 108-111
35601652-3 2022 p53 activation in response to neurodegenerative stress is closely associated with the degeneration of dopaminergic neurons accompanied by mitochondrial dysfunction, reactive oxygen species (ROS) production, abnormal protein aggregation, and impairment of autophagy, and these pathogenic events have been implicated in the pathogenesis of PD. Reactive Oxygen Species 190-193 tumor protein p53 Homo sapiens 0-3
35107378-5 2022 Moreover, the expressions of HUWE1 and TRAF6 were significantly down-regulated during WSSV (White spot syndrome virus) infection, and therefore the ubiquitination of p53 was interrupted, leading to the activation of apoptosis and ROS (Reactive oxygen species) signals through p53 accumulation, which eventually suppressed viral invasion in mud crab. Reactive Oxygen Species 230-233 tumor protein p53 Homo sapiens 166-169
35513212-4 2022 The highly cytotoxic ROS was continuously produced via Fe2+-mediated and TA-assisted enhanced Fenton reaction as well as Ce6-induced photosensitive reaction, and meanwhile, the intratumoral upregulated p53 expression inactivated glutathione peroxidase 4 (GPX4) to suppress lipid peroxidation (LPO) resistance, thus resulting in amplified oxidative stress and intensified ferroptosis-apoptosis therapy. Reactive Oxygen Species 21-24 tumor protein p53 Homo sapiens 202-205
35398141-0 2022 Graphene oxide leads to mitochondrial-dependent apoptosis by activating ROS-p53-mPTP pathway in intestinal cells. Reactive Oxygen Species 72-75 tumor protein p53 Homo sapiens 76-79
35541904-5 2022 Significantly, SKI-V also provoked programmed necrosis cascade in cervical cancer cells, as it induced mitochondrial p53-cyclophilin-D-adenine nucleotide translocator-1 (ANT1) complexation, mitochondrial membrane potential collapse, reactive oxygen species production and the release of lactate dehydrogenase into the medium. Reactive Oxygen Species 233-256 tumor protein p53 Homo sapiens 117-120
34992144-0 2022 Small-molecule NSC59984 induces mutant p53 degradation through a ROS-ERK2-MDM2 axis in cancer cells. Reactive Oxygen Species 65-68 tumor protein p53 Homo sapiens 39-42
34992144-4 2022 We used a small-molecule NSC59984 to explore elimination of mutant p53 in cancer cells, and identified an inducible ROS-ERK2-MDM2 axis as a vulnerability for induction of mutant p53 degradation in cancer cells. Reactive Oxygen Species 116-119 tumor protein p53 Homo sapiens 67-70
34992144-4 2022 We used a small-molecule NSC59984 to explore elimination of mutant p53 in cancer cells, and identified an inducible ROS-ERK2-MDM2 axis as a vulnerability for induction of mutant p53 degradation in cancer cells. Reactive Oxygen Species 116-119 tumor protein p53 Homo sapiens 178-181
34992144-8 2022 High cellular ROS increases the efficacy of NSC59984 targeting mutant p53 degradation and anti-tumor effects. Reactive Oxygen Species 14-17 tumor protein p53 Homo sapiens 70-73
34992144-9 2022 Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells. Reactive Oxygen Species 78-81 tumor protein p53 Homo sapiens 29-32
34992144-9 2022 Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells. Reactive Oxygen Species 78-81 tumor protein p53 Homo sapiens 156-159
34992144-9 2022 Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells. Reactive Oxygen Species 208-211 tumor protein p53 Homo sapiens 29-32
34992144-9 2022 Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells. Reactive Oxygen Species 208-211 tumor protein p53 Homo sapiens 156-159
34992144-10 2022 Implications: An inducible ROS-ERK2-MDM2 axis exposes a vulnerability in mutant p53 stabilization and can be exploited by small molecule compounds to induce mutant p53 degradation for cancer therapy. Reactive Oxygen Species 27-30 tumor protein p53 Homo sapiens 80-83
34992144-10 2022 Implications: An inducible ROS-ERK2-MDM2 axis exposes a vulnerability in mutant p53 stabilization and can be exploited by small molecule compounds to induce mutant p53 degradation for cancer therapy. Reactive Oxygen Species 27-30 tumor protein p53 Homo sapiens 164-167
35107378-5 2022 Moreover, the expressions of HUWE1 and TRAF6 were significantly down-regulated during WSSV (White spot syndrome virus) infection, and therefore the ubiquitination of p53 was interrupted, leading to the activation of apoptosis and ROS (Reactive oxygen species) signals through p53 accumulation, which eventually suppressed viral invasion in mud crab. Reactive Oxygen Species 235-258 tumor protein p53 Homo sapiens 166-169
35107378-5 2022 Moreover, the expressions of HUWE1 and TRAF6 were significantly down-regulated during WSSV (White spot syndrome virus) infection, and therefore the ubiquitination of p53 was interrupted, leading to the activation of apoptosis and ROS (Reactive oxygen species) signals through p53 accumulation, which eventually suppressed viral invasion in mud crab. Reactive Oxygen Species 235-258 tumor protein p53 Homo sapiens 276-279
35107378-11 2022 Our findings revealed that p53 ubiquitination could affect ROS and apoptosis signals to cope with WSSV infection in mud crab, which firstly clarified the immunologic functions and mechanisms of p53 ubiquitination in invertebrates. Reactive Oxygen Species 59-62 tumor protein p53 Homo sapiens 27-30
35107378-11 2022 Our findings revealed that p53 ubiquitination could affect ROS and apoptosis signals to cope with WSSV infection in mud crab, which firstly clarified the immunologic functions and mechanisms of p53 ubiquitination in invertebrates. Reactive Oxygen Species 59-62 tumor protein p53 Homo sapiens 194-197
35107378-5 2022 Moreover, the expressions of HUWE1 and TRAF6 were significantly down-regulated during WSSV (White spot syndrome virus) infection, and therefore the ubiquitination of p53 was interrupted, leading to the activation of apoptosis and ROS (Reactive oxygen species) signals through p53 accumulation, which eventually suppressed viral invasion in mud crab. Reactive Oxygen Species 230-233 tumor protein p53 Homo sapiens 276-279
35085581-0 2022 Piperlongumine induces ROS mediated apoptosis by transcriptional regulation of SMAD4/P21/P53 genes and synergizes with doxorubicin in osteosarcoma cells. Reactive Oxygen Species 23-26 tumor protein p53 Homo sapiens 89-92
35266593-2 2022 Heat shock protein 90 (Hsp90) inhibitors are anti-inflammatory agents and P53 inducers, which reduce the production of reactive oxygen species (ROS) in a diverse variety of human tissues. Reactive Oxygen Species 119-142 tumor protein p53 Homo sapiens 74-77
35266593-2 2022 Heat shock protein 90 (Hsp90) inhibitors are anti-inflammatory agents and P53 inducers, which reduce the production of reactive oxygen species (ROS) in a diverse variety of human tissues. Reactive Oxygen Species 144-147 tumor protein p53 Homo sapiens 74-77