PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24477002-9 2014 Because somatic mutations in p53 occur late in tumor progression, antioxidants may accelerate the growth of early tumors or precancerous lesions in high-risk populations such as smokers and patients with chronic obstructive pulmonary disease who receive NAC to relieve mucus production. Acetylcysteine 254-257 tumor protein p53 Homo sapiens 29-32 24734887-7 2014 Furthermore, NAC significantly decreased cleaved caspase 3, p53 and renal epithelial tubular cell apoptosis. Acetylcysteine 13-16 tumor protein p53 Homo sapiens 60-63 24099794-1 2013 The successful clinical management of lung cancer is limited by frequent loss-of-function mutations in p53 which cooperates with chronic oxidant-stress induced adaptations in mercapturic acid pathway (MAP) which in turn regulates critical intracellular signaling cascades that determine therapeutic refractoriness. Acetylcysteine 175-191 tumor protein p53 Homo sapiens 103-106 23867003-8 2013 NAC induced p53 and reduced p65 protein expression through activation of PPARalpha. Acetylcysteine 0-3 tumor protein p53 Homo sapiens 12-15 23792775-5 2013 We found that NAC displayed a broad-spectrum chemoprotective activity against all three metals, including suppression of cytotoxicity, apoptosis, p53 activation, and HSP72 and HIF-1alpha upregulation. Acetylcysteine 14-17 tumor protein p53 Homo sapiens 146-149 23867003-9 2013 Silencing of p53 and overexpression of p65 blocked the effect of NAC on PDK1 promoter activity and protein expression. Acetylcysteine 65-68 tumor protein p53 Homo sapiens 13-16 23867003-10 2013 CONCLUSION: Our results show that NAC inhibits PDK1 expression through PPARalpha-mediated induction of p53 and inhibition of p65 protein expression. Acetylcysteine 34-37 tumor protein p53 Homo sapiens 103-106 23124852-5 2013 After scavenging ROS with N-acetylcysteine, Wnt/beta-catenin signaling-induced MSC aging was significantly attenuated and the DNA damage and the expression of p16(INK4A), p53, and p21 were reduced in MSCs. Acetylcysteine 26-42 tumor protein p53 Homo sapiens 171-174 23128467-0 2013 N-acetylcysteine potentiates doxorubicin-induced ATM and p53 activation in ovarian cancer cells. Acetylcysteine 0-16 tumor protein p53 Homo sapiens 57-60 23841076-5 2013 Similarly, pretreatment with the antioxidant N-acetyl-cysteine (NAC) markedly inhibited both the autophagy and the apoptosis triggered by DHA, indicating that mitochondrial ROS mediate the cytotoxicity of DHA in mutant p53 cells. Acetylcysteine 45-62 tumor protein p53 Homo sapiens 219-222 23841076-5 2013 Similarly, pretreatment with the antioxidant N-acetyl-cysteine (NAC) markedly inhibited both the autophagy and the apoptosis triggered by DHA, indicating that mitochondrial ROS mediate the cytotoxicity of DHA in mutant p53 cells. Acetylcysteine 64-67 tumor protein p53 Homo sapiens 219-222 23128467-9 2013 Pretreatment of CaOV3 cells with antioxidant N-acetylcysteine (NAC), but not pyrrolidine dithiocarbamate (PDTC) potentiates doxorubicin-induced phosphorylation of p53 and ATM. Acetylcysteine 45-61 tumor protein p53 Homo sapiens 187-190 23128467-9 2013 Pretreatment of CaOV3 cells with antioxidant N-acetylcysteine (NAC), but not pyrrolidine dithiocarbamate (PDTC) potentiates doxorubicin-induced phosphorylation of p53 and ATM. Acetylcysteine 63-66 tumor protein p53 Homo sapiens 187-190 22982566-4 2012 However, hypoxia further increased the susceptibility of mutant p53 breast cancer SKBR3 cells to lower PRIMA-1 levels, possibly through oxidative stress since this was counteracted by N-acetylcysteine. Acetylcysteine 184-200 tumor protein p53 Homo sapiens 64-67 22294162-5 2012 N-acetylcysteine, a reactive oxygen species scavenger, not only blocked the oridonin-induced increase in hydrogen peroxide and glutathione depletion, but also blocked apoptosis and senescence induced by oridonin, as evidenced by the decrease in Annexin V and senescence-associated beta-galactosidase- positive cells and the inhibition of oridonin-induced upregulation of p53 and p16 and downregulation of c-Myc. Acetylcysteine 0-16 tumor protein p53 Homo sapiens 371-374 22509835-4 2012 A decrease in the p53 protein with increased protein ubiquitination was detected in QUE/As(+3)-treated HaCaT cells, and this was prevented by the addition of NAC. Acetylcysteine 158-161 tumor protein p53 Homo sapiens 18-21 22537194-8 2012 We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line. Acetylcysteine 139-158 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. Acetylcysteine 139-158 tumor protein p53 Homo sapiens 188-191 22085531-8 2012 Importantly, the ROS scavenger N-acetylcysteine (NAC) could inhibited LPS-induced autophagy and knockdown of p8 by RNA interference inhibited the autophagy, p53 protein level increase, the translocation of p53 into nuclei and the ROS level increase induced by LPS in HUVECs. Acetylcysteine 49-52 tumor protein p53 Homo sapiens 157-160 22283740-6 2012 The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS. Acetylcysteine 18-35 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. Acetylcysteine 18-35 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. Acetylcysteine 37-40 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. Acetylcysteine 37-40 tumor protein p53 Homo sapiens 122-125 20653475-6 2010 CONCLUSIONS: NAC prevents the increased expression levels of p53 and CASP8 induced by long-term maintained hypoxia. Acetylcysteine 13-16 tumor protein p53 Homo sapiens 61-64 19626645-10 2009 Additionally, the antioxidant N-acetyl-L-cysteine could obviously abrogate p53 stabilization triggered by oroxylin A. Acetylcysteine 30-49 tumor protein p53 Homo sapiens 75-78 20171194-7 2010 NAC subsequently inhibited BEL-induced activation of p38 and p53 in LNCaP cells. Acetylcysteine 0-3 tumor protein p53 Homo sapiens 61-64 19202565-6 2009 Scavenging of DADS-induced ROS by N-acetyl cysteine or reduced glutathione inhibited cell cycle arrest, apoptosis and p53 activation by DADS. Acetylcysteine 34-51 tumor protein p53 Homo sapiens 118-121 18719315-3 2008 Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well. Acetylcysteine 145-162 tumor protein p53 Homo sapiens 85-88 18718914-8 2008 Pretreatment with antioxidant N-acetylcysteine prevented the p53 accumulation, the phosphorylations of JNK and p38 MAPK, the inhibition of NF-kappaB activity, as well as the apoptosis induced by 15d-PGJ(2). Acetylcysteine 30-46 tumor protein p53 Homo sapiens 61-64 18847491-12 2008 Moreover, NAC or U0126 pretreatment significantly attenuated Triphala-induced p53 transcriptional activity. Acetylcysteine 10-13 tumor protein p53 Homo sapiens 78-81 18719315-3 2008 Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well. Acetylcysteine 145-162 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. Acetylcysteine 145-162 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. Acetylcysteine 164-167 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. Acetylcysteine 164-167 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. Acetylcysteine 164-167 tumor protein p53 Homo sapiens 260-263 10585590-5 2000 Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity. Acetylcysteine 84-100 tumor protein p53 Homo sapiens 133-136 17289842-9 2007 In EDCs treated with a recombinant adenovirus expressing superoxide dismutase or N-acetyl-cysteine (but not catalase), the p53-Bax pathway activated by oxLDL was blocked, and apoptosis was prevented. Acetylcysteine 81-98 tumor protein p53 Homo sapiens 123-126 16872365-5 2006 Because the tumour suppressor p53 (tumour protein p53) is known to induce transcription of genes associated with cell response to oxidative stress, we have compared the intensity of constitutive H2AX phosphorylation, and the effect of N-acetyl-L-cysteine on it, in cells with different tumour protein p53 status. Acetylcysteine 235-254 tumor protein p53 Homo sapiens 30-33 15496615-6 2005 Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC. Acetylcysteine 209-212 tumor protein p53 Homo sapiens 31-34 15496615-6 2005 Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC. Acetylcysteine 209-212 tumor protein p53 Homo sapiens 127-130 15496615-7 2005 In p53-negative SKOV3 cells, cisplatin toxicity and NAC chemoprotection remained effective, suggesting that chemoprotection may be mediated through both p53-dependent and -independent pathways. Acetylcysteine 52-55 tumor protein p53 Homo sapiens 3-6 16400524-8 2005 NAC treatment also restored cell cycle progression inhibited by rk-2 and down-regulated p53 and nuclear p21(Waf1/Cip1) expression induced by rk-2.These data suggest that rk-2 induces the BCE cell cycle arrest at G(0)-G(1) phase through inhibition of the cyclin D1/CDK4 complex caused by increase of ROS generation and nuclear cyclin-dependent kinase inhibitors. Acetylcysteine 0-3 tumor protein p53 Homo sapiens 88-91 10951577-7 2000 The antioxidant N-acetylcysteine and the Cu/Zn superoxide dismutase inhibitor diethyldithiocarbamic acid abolished the hypoxia-induced increases in ROS and p53 levels. Acetylcysteine 16-32 tumor protein p53 Homo sapiens 156-159 18645026-7 2008 Pretreatment with an antioxidant (N-acetylcysteine) or a c-Jun NH(2)-terminal kinase inhibitor (SP600125) effectively prevented Andro-induced p53 activation and DR4 up-regulation and eventually blocked the Andro-induced sensitization on TRAIL-induced apoptosis. Acetylcysteine 34-50 tumor protein p53 Homo sapiens 142-145 15489221-10 2004 In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways. Acetylcysteine 73-89 tumor protein p53 Homo sapiens 177-180 15489221-10 2004 In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways. Acetylcysteine 73-89 tumor protein p53 Homo sapiens 182-185 10777712-7 2000 The antioxidant and GSH precursor N-acetyl-l-cysteine favored Bcl-2 at the expense of Bax/p53, whereas pyrrolidine dithiocarbamate induced Bax against Bcl-2, with mild effect on p53. Acetylcysteine 34-53 tumor protein p53 Homo sapiens 90-93 10585590-5 2000 Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity. Acetylcysteine 84-100 tumor protein p53 Homo sapiens 273-276 10585590-5 2000 Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity. Acetylcysteine 102-105 tumor protein p53 Homo sapiens 133-136 10585590-5 2000 Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity. Acetylcysteine 102-105 tumor protein p53 Homo sapiens 273-276 10585590-5 2000 Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity. Acetylcysteine 258-261 tumor protein p53 Homo sapiens 133-136 9563490-7 1998 N-Acetylcysteine elevated p53 expression posttranscriptionally by increasing the rate of p53 mRNA translation rather than by altering the protein stability. Acetylcysteine 0-16 tumor protein p53 Homo sapiens 26-29 10935502-0 1999 p53-independent inhibition of proliferation and p21(WAF1/Cip1)-modulated induction of cell death by the antioxidants N-acetylcysteine and vitamin E. Acetylcysteine 117-133 tumor protein p53 Homo sapiens 0-3 10935502-5 1999 The antioxidants, N-acetylcysteine (NAC) and vitamin E either inhibited proliferation in a p53-independent manner without affecting cell viability or induced cell death. Acetylcysteine 18-34 tumor protein p53 Homo sapiens 91-94 10935502-5 1999 The antioxidants, N-acetylcysteine (NAC) and vitamin E either inhibited proliferation in a p53-independent manner without affecting cell viability or induced cell death. Acetylcysteine 36-39 tumor protein p53 Homo sapiens 91-94 9563490-7 1998 N-Acetylcysteine elevated p53 expression posttranscriptionally by increasing the rate of p53 mRNA translation rather than by altering the protein stability. Acetylcysteine 0-16 tumor protein p53 Homo sapiens 89-92 8743957-6 1996 Pretreatment of cells with N-acetylcysteine, an agent known to counteract oxidative stress, attenuates the cellular p53 response to ultraviolet light by reducing the number of cells with high p53 levels but does not affect the response to ionizing radiation. Acetylcysteine 27-43 tumor protein p53 Homo sapiens 116-119 9535218-4 1998 Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein. Acetylcysteine 12-28 tumor protein p53 Homo sapiens 187-190 9257692-5 1997 Simulated solar UV radiation increased p53, and agents that scavenge active oxygen species, N-acetylcysteine, ascorbate and alpha-tocopherol, inhibited the increase. Acetylcysteine 92-108 tumor protein p53 Homo sapiens 39-42 8743957-6 1996 Pretreatment of cells with N-acetylcysteine, an agent known to counteract oxidative stress, attenuates the cellular p53 response to ultraviolet light by reducing the number of cells with high p53 levels but does not affect the response to ionizing radiation. Acetylcysteine 27-43 tumor protein p53 Homo sapiens 192-195 34447990-5 2021 On the other hand, treatment with the antioxidant N-acetylcysteine (NAC) increased glutathione concentration, decreased basal H2O2 production, p53 levels and sensitivity to AA treatment in the XPC-null back to the levels found in XPC-wt cells. Acetylcysteine 50-66 tumor protein p53 Homo sapiens 143-146 34447990-5 2021 On the other hand, treatment with the antioxidant N-acetylcysteine (NAC) increased glutathione concentration, decreased basal H2O2 production, p53 levels and sensitivity to AA treatment in the XPC-null back to the levels found in XPC-wt cells. Acetylcysteine 68-71 tumor protein p53 Homo sapiens 143-146 31995555-8 2020 Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC). Acetylcysteine 215-218 tumor protein p53 Homo sapiens 87-90 34681647-9 2021 Compound 6c-induced DNA damage was characterized by comet assay, p53 phosphorylation, and gammaH2A.X, which was diminished by pretreatment with NAC. Acetylcysteine 144-147 tumor protein p53 Homo sapiens 65-68 35215995-9 2022 The ROS scavenger N-acetyl-l-cysteine (NAC) and the p53 specific inhibitor Pifithrin-alpha (PFT-alpha) suppressed PEDV-induced apoptosis and impeded viral replication, suggesting that ROS and p53 play an important role in PEDV-induced apoptosis and viral replication. Acetylcysteine 39-42 tumor protein p53 Homo sapiens 192-195 33781788-6 2021 Pre-treatment with N-acetylcysteine (NAC, a ROS scavenger) demonstrated that reactive oxygen species (ROS) mediated T-17-induced p53-independent apoptosis. Acetylcysteine 19-35 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. Acetylcysteine 37-40 tumor protein p53 Homo sapiens 129-132 32864863-8 2021 Total p53 protein level increase was observed by 24 hours in HCT-116 upon NAC pre-treatment. Acetylcysteine 74-77 tumor protein p53 Homo sapiens 6-9 32905825-5 2020 On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells. Acetylcysteine 89-108 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. Acetylcysteine 89-108 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. Acetylcysteine 110-113 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. Acetylcysteine 110-113 tumor protein p53 Homo sapiens 189-192 31959867-7 2020 NAC treatment prolonged the lifespan and ameliorated pulmonary dysfunction and SAPF by downregulating TIME signaling more than p16INK4a deletion by inhibiting oxidative stress and DNA damage and promoting ubiquitin-proteasome degradation of p16INK4a and p53. Acetylcysteine 0-3 tumor protein p53 Homo sapiens 254-257 35065218-6 2022 Pre-treatment with NAC was efficient to prevent cell damage at lower Cl2 concentrations in part by averting the formation of apoptotic-like bodies and increasing the expression of the anti-apoptotic proteins clusterin and phosphorylated tumour protein p53(S46). Acetylcysteine 19-22 tumor protein p53 Homo sapiens 252-255 33139577-4 2020 As a result, Akt3-expressing cells activate the DNA damage response pathway, express high levels of p53 and its direct transcriptional target miR-34, and exhibit a proliferation defect, which is rescued by the antioxidant N-acetylcysteine. Acetylcysteine 222-238 tumor protein p53 Homo sapiens 100-103 31945496-11 2020 Interestingly, mutation of redox sensitive cysteine residues at 124, 141 and 182 position in p53 significantly reduces mal C plus NAC mediated sensitization of cancer cells. Acetylcysteine 130-133 tumor protein p53 Homo sapiens 93-96 31995555-8 2020 Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC). Acetylcysteine 196-213 tumor protein p53 Homo sapiens 87-90 31812668-4 2020 We demonstrate that mutant p53 induces MnSOD expression, which is recovered by the ROS scavenger N-acetyl-l-cysteine. Acetylcysteine 97-116 tumor protein p53 Homo sapiens 27-30 31752383-11 2019 Furthermore, NAC could alleviate p53 and the p53 upregulated modulator of apoptosis (PUMA) expression induced by TRAIL and ASH. Acetylcysteine 13-16 tumor protein p53 Homo sapiens 33-36 31752383-11 2019 Furthermore, NAC could alleviate p53 and the p53 upregulated modulator of apoptosis (PUMA) expression induced by TRAIL and ASH. Acetylcysteine 13-16 tumor protein p53 Homo sapiens 45-48 30318520-6 2018 The restoration of the mitochondrial uncoupling protein 2 (UCP2) expression, as well as the addition of the radical scavenger N-acetyl-L-cysteine, reversed the oncogenic effects of mutant p53 as cellular hyper-proliferation, antiapoptotic effect, and resistance to drugs. Acetylcysteine 126-145 tumor protein p53 Homo sapiens 188-191 30865562-6 2019 Blocking ROS generation by N-acetylcysteine (NAC) or overexpressing constitutively active AKT vector (CA-AKT) inhibited HMS-incurred p53 mitochondrial translocation and promoted its nuclear targeting. Acetylcysteine 27-43 tumor protein p53 Homo sapiens 133-136 30447351-0 2019 N-acetylcysteine ameliorates cisplatin-induced renal senescence and renal interstitial fibrosis through sirtuin1 activation and p53 deacetylation. Acetylcysteine 0-16 tumor protein p53 Homo sapiens 128-131 30447351-10 2019 N-acetylcysteine (NAC), an antioxidant, attenuated premature senescence and decreased renal fibrosis, and its effects were dependent on sirtuin1 (SIRT1) activation and p53 deacetylation. Acetylcysteine 0-16 tumor protein p53 Homo sapiens 168-171 30447351-10 2019 N-acetylcysteine (NAC), an antioxidant, attenuated premature senescence and decreased renal fibrosis, and its effects were dependent on sirtuin1 (SIRT1) activation and p53 deacetylation. Acetylcysteine 18-21 tumor protein p53 Homo sapiens 168-171 30865562-6 2019 Blocking ROS generation by N-acetylcysteine (NAC) or overexpressing constitutively active AKT vector (CA-AKT) inhibited HMS-incurred p53 mitochondrial translocation and promoted its nuclear targeting. Acetylcysteine 45-48 tumor protein p53 Homo sapiens 133-136 30483736-4 2019 Treatment with N-acetyl-L-cysteine reversed these effects, restoring the MTP and attenuated ROS production and p53 expression. Acetylcysteine 15-34 tumor protein p53 Homo sapiens 111-114 29668110-8 2018 Pre-incubation with ROS scavenger N-acetyl-l-cysteine preserved AR and PSA abundance, markedly reduced ISC-4-induced apoptosis and attenuated p53 Ser phosphorylation, p21Cip1, and p-H2A.X. Acetylcysteine 34-53 tumor protein p53 Homo sapiens 142-145 27633119-7 2016 Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK. Acetylcysteine 41-44 tumor protein p53 Homo sapiens 64-67 30011295-6 2018 Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins. Acetylcysteine 36-52 tumor protein p53 Homo sapiens 204-207 29392716-5 2018 Antioxidant (N-acetyl-L-cysteine, NAC) treatment in vitro not only quantitatively and functionally improved BM MSCs derived from PT patients through down-regulation of the p38 (also termed MAPK14) and p53 (also termed TP53) pathways but also partially rescued the impaired ability of BM MSCs to support megakaryocytopoiesis. Acetylcysteine 13-32 tumor protein p53 Homo sapiens 201-204 29392716-5 2018 Antioxidant (N-acetyl-L-cysteine, NAC) treatment in vitro not only quantitatively and functionally improved BM MSCs derived from PT patients through down-regulation of the p38 (also termed MAPK14) and p53 (also termed TP53) pathways but also partially rescued the impaired ability of BM MSCs to support megakaryocytopoiesis. Acetylcysteine 13-32 tumor protein p53 Homo sapiens 218-222 28653879-5 2017 In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. Acetylcysteine 207-223 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. Acetylcysteine 207-223 tumor protein p53 Homo sapiens 228-232 28653879-5 2017 In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. Acetylcysteine 207-223 tumor protein p53 Homo sapiens 228-232 28653879-6 2017 N-acetylcysteine prevented phosphorylation of P53 protein that had been induced by doxorubicin. Acetylcysteine 0-16 tumor protein p53 Homo sapiens 46-49 26756900-10 2016 Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation. Acetylcysteine 62-78 tumor protein p53 Homo sapiens 133-136 27620489-6 2016 The levels of p53 in YD8 and H460 cells decreased in a Cd concentration-dependent manner, which was inhibited by pretreatment with N-acetylcysteine. Acetylcysteine 131-147 tumor protein p53 Homo sapiens 14-17 26934645-7 2016 Moreover, N-acetylcysteine (reactive oxygen species scavenger) blocked the SK inhibitor-induced increase in p21 and p53 expression but had no effect on the proteasomal degradation of SK1a. Acetylcysteine 10-26 tumor protein p53 Homo sapiens 116-119 27270209-11 2016 Pretreatment with N-acetylcysteine decreases phosphorylation of p53 in citral-treated ECC-1 and OVCAR-3. Acetylcysteine 18-34 tumor protein p53 Homo sapiens 64-67 26152521-9 2016 Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells. Acetylcysteine 41-58 tumor protein p53 Homo sapiens 208-211 26936454-7 2016 Furthermore, CA generated reactive oxygen species (ROS), and pretreatment with ROS scavenger N-acetyl cysteine (NAC) abrogated CA-induced cleavage of PARP and expression of p53. Acetylcysteine 93-110 tumor protein p53 Homo sapiens 173-176 26936454-7 2016 Furthermore, CA generated reactive oxygen species (ROS), and pretreatment with ROS scavenger N-acetyl cysteine (NAC) abrogated CA-induced cleavage of PARP and expression of p53. Acetylcysteine 112-115 tumor protein p53 Homo sapiens 173-176 26859482-12 2016 DC cell culture supplemented with N-acetylcysteine, or alternatively grown in low oxygen, afforded significant proliferative benefits (proliferation: maximum 2-fold increase; NAC: 5-fold p53 decrease; low oxygen: maximum 3.5-fold p53 decrease). Acetylcysteine 34-50 tumor protein p53 Homo sapiens 187-190 26859482-12 2016 DC cell culture supplemented with N-acetylcysteine, or alternatively grown in low oxygen, afforded significant proliferative benefits (proliferation: maximum 2-fold increase; NAC: 5-fold p53 decrease; low oxygen: maximum 3.5-fold p53 decrease). Acetylcysteine 34-50 tumor protein p53 Homo sapiens 230-233 26859482-12 2016 DC cell culture supplemented with N-acetylcysteine, or alternatively grown in low oxygen, afforded significant proliferative benefits (proliferation: maximum 2-fold increase; NAC: 5-fold p53 decrease; low oxygen: maximum 3.5-fold p53 decrease). Acetylcysteine 175-178 tumor protein p53 Homo sapiens 187-190 25607831-8 2015 Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells. Acetylcysteine 18-35 tumor protein p53 Homo sapiens 163-166 26264138-7 2015 The growth inhibitory effect of P53 was partially reversed by the antioxidant N-acetylcysteine. Acetylcysteine 78-94 tumor protein p53 Homo sapiens 32-35 26408691-4 2015 Treatment of tumor cells with the antioxidant N-acetylcysteine was able to prevent Zn(2+)-induced apoptosis, as well as the increase of p53 and FAS ligand protein induced by zinc. Acetylcysteine 46-62 tumor protein p53 Homo sapiens 136-139 25607831-8 2015 Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells. Acetylcysteine 37-40 tumor protein p53 Homo sapiens 163-166 25369051-9 2014 Crucially, administration of N-acetylcysteine, a ROS scavenger, abrogated the effect of PA-2 on p53 acetylation and mitochondria translocation, thus identifying RONS as proximal molecules mediating the anticancer effect of PA-2. Acetylcysteine 29-45 tumor protein p53 Homo sapiens 96-99