PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20637859-8 2010 Knockdown of either kinases significantly reduced ATM activation in response to etoposide treatment, and thereby attenuated phosphorylation of the ATM substrates, including the S139 of H2AX (gammaH2AX), p53 S15, and CHK2 T68. Etoposide 80-89 H2A.X variant histone Homo sapiens 185-189 20978201-4 2010 IR, doxorubicin, and etoposide induced the phosphorylation of H2A.X on Ser(139) (gammaH2AX) and DNA damage foci formation. Etoposide 21-30 H2A.X variant histone Homo sapiens 62-67 20921231-4 2010 During etoposide-induced apoptosis in Jurkat cells, the cleavage of MST1 directly corresponded with strong H2AX phosphorylation. Etoposide 7-16 H2A.X variant histone Homo sapiens 107-111 20921231-10 2010 Histone H2AX phosphorylation and DNA fragmentation were suppressed in MST1 knockdown Jurkat cells after etoposide treatment. Etoposide 104-113 H2A.X variant histone Homo sapiens 8-12 19516899-6 2009 By comparing the level of DSBs, H2AX phosphorylation and toxicity induced by etoposide and calicheamicin, we found that only 10% of etoposide-induced DSBs resulted in histone H2AX phosphorylation and toxicity. Etoposide 132-141 H2A.X variant histone Homo sapiens 32-36 19516899-6 2009 By comparing the level of DSBs, H2AX phosphorylation and toxicity induced by etoposide and calicheamicin, we found that only 10% of etoposide-induced DSBs resulted in histone H2AX phosphorylation and toxicity. Etoposide 132-141 H2A.X variant histone Homo sapiens 175-179 19516899-7 2009 There was a close match between toxicity and histone H2AX phosphorylation for calicheamicin and etoposide suggesting that the few etoposide-induced DSBs that activated H2AX phosphorylation were responsible for toxicity. Etoposide 96-105 H2A.X variant histone Homo sapiens 53-57 19516899-7 2009 There was a close match between toxicity and histone H2AX phosphorylation for calicheamicin and etoposide suggesting that the few etoposide-induced DSBs that activated H2AX phosphorylation were responsible for toxicity. Etoposide 96-105 H2A.X variant histone Homo sapiens 168-172 19516899-7 2009 There was a close match between toxicity and histone H2AX phosphorylation for calicheamicin and etoposide suggesting that the few etoposide-induced DSBs that activated H2AX phosphorylation were responsible for toxicity. Etoposide 130-139 H2A.X variant histone Homo sapiens 53-57 19516899-7 2009 There was a close match between toxicity and histone H2AX phosphorylation for calicheamicin and etoposide suggesting that the few etoposide-induced DSBs that activated H2AX phosphorylation were responsible for toxicity. Etoposide 130-139 H2A.X variant histone Homo sapiens 168-172 19516899-8 2009 CONCLUSIONS/SIGNIFICANCE: These results show that only 0.3% of all strand breaks produced by etoposide activate H2AX phosphorylation and suggests that over 99% of the etoposide induced DNA damage does not contribute to its toxicity. Etoposide 93-102 H2A.X variant histone Homo sapiens 112-116 19516899-8 2009 CONCLUSIONS/SIGNIFICANCE: These results show that only 0.3% of all strand breaks produced by etoposide activate H2AX phosphorylation and suggests that over 99% of the etoposide induced DNA damage does not contribute to its toxicity. Etoposide 167-176 H2A.X variant histone Homo sapiens 112-116 18285460-3 2008 The depletion of Rvb1 increases the amount and persistence of phosphorylation on chromatin-associated H2AX after the exposure of cells to UV irradiation or to mitomycin C, cisplatin, camptothecin, or etoposide, without increasing the amount of DNA damage. Etoposide 200-209 H2A.X variant histone Homo sapiens 102-106 17545612-4 2007 As evidenced by increased Ser(139)-phosphorylated histone H2AX (gammaH2AX), impaired Ku70 function diminished cellular capability to repair DNA DSBs induced by bleomycin, doxorubicin, and etoposide, thereby enhancing their cell-killing effect. Etoposide 188-197 H2A.X variant histone Homo sapiens 50-62 15304327-3 2004 We also studied etoposide-induced phosphorylation of histone H2AX (gamma-H2AX) in human cells in which PrxV activity was downregulated (knockdown, KD-clones) or compromised by overexpression of redox-negative (RD) protein. Etoposide 16-25 H2A.X variant histone Homo sapiens 53-65 17297310-0 2007 Induction of ATM activation, histone H2AX phosphorylation and apoptosis by etoposide: relation to cell cycle phase. Etoposide 75-84 H2A.X variant histone Homo sapiens 37-41 17297310-7 2007 The extent of etoposide-induced H2AX phosphorylation was partially reduced by N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species (ROS). Etoposide 14-23 H2A.X variant histone Homo sapiens 32-36 33941661-5 2021 VCP/p97 inhibition also reduces the etoposide-induced phosphorylation of histone H2AX, indicative of fewer DSBs . Etoposide 36-45 H2A.X variant histone Homo sapiens 73-85 12851679-3 2003 In this study, we show that radioresistant T98G glioblastoma cells can develop sensitivity to DNA damage induced by irradiation and etoposide as a result of the introduction of a DNA repair-associated histone, H2AX. Etoposide 132-141 H2A.X variant histone Homo sapiens 210-214 31855962-0 2019 Isobaric tags for relative and absolute quantitation-based quantitative proteomic analysis of X-linked inhibitor of apoptosis and H2AX in etoposide-induced renal cell carcinoma apoptosis. Etoposide 138-147 H2A.X variant histone Homo sapiens 130-134 26986476-8 2016 The results showed that knockdown of PTEN strongly antagonized ATM activation in response to etoposide treatment, and thereby reduced the phosphorylation level of ATM substrates, including H2AX, P53 and Chk2. Etoposide 93-102 H2A.X variant histone Homo sapiens 189-193 22739265-6 2012 In addition, etoposide induced p53 phosphorylation and H2AX foci formation in proliferating SH-SY5Y cells but failed to do so in differentiated SH-SY5Y cells. Etoposide 13-22 H2A.X variant histone Homo sapiens 55-59 23333390-6 2013 The steady and etoposide-induced phosphorylated H2AX (gamma-H2AX) were higher in PES1-silenced cells than in control cells. Etoposide 15-24 H2A.X variant histone Homo sapiens 48-52 23333390-6 2013 The steady and etoposide-induced phosphorylated H2AX (gamma-H2AX) were higher in PES1-silenced cells than in control cells. Etoposide 15-24 H2A.X variant histone Homo sapiens 54-64 23333390-7 2013 Besides, etoposide-induced gamma-H2AX persisted longer in PES1-silenced cells after removing the etoposide. Etoposide 9-18 H2A.X variant histone Homo sapiens 27-37 23333390-7 2013 Besides, etoposide-induced gamma-H2AX persisted longer in PES1-silenced cells after removing the etoposide. Etoposide 97-106 H2A.X variant histone Homo sapiens 27-37 23058634-3 2012 Indeed, we showed that etoposide could influence transcription and was able to activate DDR in resting human T cells by inducing phosphorylation of ATM and its substrates, H2AX and p53. Etoposide 23-32 H2A.X variant histone Homo sapiens 172-176 25875766-4 2015 Treatment of HuH7 cells with etoposide (25 muM, 30 min) or gamma irradiation (4 Gy) increased the phosphorylation of H2AX by 1.94 +- 0.13 and 2.0 +- 0.02 fold, respectively. Etoposide 29-38 H2A.X variant histone Homo sapiens 117-121