PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30867794-4 2019 Supporting the in vivo data, immunohistochemical staining of tumor masses from mice treated with AvidinOX, bCet and cisplatin exhibited the highest tumor cell damage and the lowest angiogenic activity among all treatment groups, measured as the number of gamma-H2A.X and cleaved caspase-3-positive cells, and vascular endothelial growth factor-C and platelet and endothelial cell adhesion molecule 1-positive cells, respectively. Cisplatin 116-125 H2A.X variant histone Mus musculus 255-266 26019260-7 2015 Here we show that cisplatin induces germ cell damage through inhibition of p53-dependent DNA repair mechanisms involving gamma-H2AX and ataxia telangiectasia mutated protein kinase. Cisplatin 18-27 H2A.X variant histone Mus musculus 121-180 28057599-8 2017 The in vivo effects of aspirin plus sorafenib on cisplatin therapy were also confirmed in resistant HNC xenograft models, in terms of growth inhibition, GSH depletion, and increased gammaH2AX formation and apoptosis in tumors. Cisplatin 49-58 H2A.X variant histone Mus musculus 182-191 21593482-5 2011 UV irradiation or cisplatin treatment of 2-cell embryos in the G(2) phase of the cell cycle caused DNA damage as defined by increased phosphorylation of the H2A histone family, member X (H2AFX; previously H2AX) variant. Cisplatin 18-27 H2A.X variant histone Mus musculus 157-185 23784839-8 2013 Finally, exposure of spermatocytes to double strand break DNA-damaging agents such as cisplatin, bleomycin or etoposide also induced ATR relocalization and intense H2AX phosphorylation and led to anomalies in synaptonemal assembly. Cisplatin 86-95 H2A.X variant histone Mus musculus 164-168 25387467-7 2014 When comparing cisplatin and PIFA-treated tumours with cisplatin alone treated tumours we found overall less gammaH2AX, a measure for DNA damage. Cisplatin 15-24 H2A.X variant histone Mus musculus 109-118 25387467-7 2014 When comparing cisplatin and PIFA-treated tumours with cisplatin alone treated tumours we found overall less gammaH2AX, a measure for DNA damage. Cisplatin 55-64 H2A.X variant histone Mus musculus 109-118 24571982-6 2014 Interestingly, the gamma-H2AX signal was localized to telomeres after treatment with bleomycin, cisplatin, and 4OOH-CPA, but not etoposide. Cisplatin 96-105 H2A.X variant histone Mus musculus 19-29 21593482-5 2011 UV irradiation or cisplatin treatment of 2-cell embryos in the G(2) phase of the cell cycle caused DNA damage as defined by increased phosphorylation of the H2A histone family, member X (H2AFX; previously H2AX) variant. Cisplatin 18-27 H2A.X variant histone Mus musculus 187-192 21593482-5 2011 UV irradiation or cisplatin treatment of 2-cell embryos in the G(2) phase of the cell cycle caused DNA damage as defined by increased phosphorylation of the H2A histone family, member X (H2AFX; previously H2AX) variant. Cisplatin 18-27 H2A.X variant histone Mus musculus 205-209 19738461-3 2009 The cytotoxicity of cisplatin and beta-lap alone or in combination against FSaII fibrosarcoma cells of C3H mice in vitro was determined with a clonogenic survival assay and assessment of gamma-H2AX foci formation, a hallmark of DNA double-strand breaks. Cisplatin 20-29 H2A.X variant histone Mus musculus 187-197 18927497-5 2008 MEFs lacking Puralpha also showed enhanced H2AX phosphorylation in response to cisplatin. Cisplatin 79-88 H2A.X variant histone Mus musculus 43-47 18162465-6 2008 We show that ATR is specifically activated during cisplatin treatment and co-localizes with H2AX, forming nuclear foci at the site of DNA damage. Cisplatin 50-59 H2A.X variant histone Mus musculus 92-96 33168727-5 2020 Moreover, although p-gamma-H2AX foci formation was elevated and ATR expression was low in single agent cisplatin-treated cells, the opposite was true in cells treated with cisplatin/JH-RE-06. Cisplatin 172-181 H2A.X variant histone Mus musculus 21-31