PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20959117-3 2011 Using MCF-7 cells, we observed that doxorubicin treatment triggered autophosphorylation of ATM on serine 1981 and the ATM-dependent activation of its downstream effectors p53, Chk2, and SMC1. Doxorubicin 36-47 checkpoint kinase 2 Homo sapiens 176-180 25535901-2 2014 By using BJ human fibroblasts, HCT116 colorectal cancer cells and HeLa cervical cancer cells, we further detailed phosphorylation kinetics of Chk2 under treatment with neocarcinostatin (NCS) or doxorubicin (Dox). Doxorubicin 207-210 checkpoint kinase 2 Homo sapiens 142-146 21624350-7 2011 Thus, gammaH2AX((S139)) foci formation remained higher than the control, and an increase in CHK2((T68)) phosphorylation was observed by ALCAP2 and 7 treatments suggested that, these compounds can be potential therapeutics against tumor cell growth because of their unique DNA damaging abilities additional to enzyme inhibition similar to those of doxorubicin. Doxorubicin 347-358 checkpoint kinase 2 Homo sapiens 92-96 31759252-9 2019 Activation of DNA damage response pathways (ATM, Chk1, and Chk2) are decreased at 24 hours DOX-treatment in MMTV-PyMT;ApcMin/+ cells compared to control cells, but show activation at earlier time points. Doxorubicin 91-94 checkpoint kinase 2 Homo sapiens 59-63 20526748-1 2010 Cisplatin and doxorubicin are widely used anticancer drugs that cause DNA damage, which activates the ATM-Chk2-p53 pathway in cancer cells. Doxorubicin 14-25 checkpoint kinase 2 Homo sapiens 106-110 19996108-3 2010 We report that TIM is likewise essential for ATM-dependent Chk2-mediated signaling of doxorubicin-induced DNA double strand breaks. Doxorubicin 86-97 checkpoint kinase 2 Homo sapiens 59-63 19453842-7 2009 When doxorubicin was administered, Chk2 activation was induced in KB cell, but not in pulp cells. Doxorubicin 5-16 checkpoint kinase 2 Homo sapiens 35-39 19453842-10 2009 Moreover, in case of KB cell, cell death was increased and activation of Chk2 was increased in doxorubicin dose-dependent. Doxorubicin 95-106 checkpoint kinase 2 Homo sapiens 73-77 16150728-6 2005 Camptothecin and adriamycin also reduce the amount of chromatin-associated Chk2. Doxorubicin 17-27 checkpoint kinase 2 Homo sapiens 75-79 15489221-7 2004 Doxorubicin treatment also stimulated ATM autophosphorylation on serine 1981 and the ATM-dependent phosphorylation of numerous effectors in the ATM-signaling pathway, including Nbs1 (Ser(343)), SMC1 (Ser(957)), Chk1 (Ser(317) and Ser(345)), and Chk2 (Ser(33/35) and Thr(68)). Doxorubicin 0-11 checkpoint kinase 2 Homo sapiens 245-249 11741320-0 2001 Etoposide and adriamycin but not genistein can activate the checkpoint kinase Chk2 independently of ATM/ATR. Doxorubicin 14-24 checkpoint kinase 2 Homo sapiens 78-82 11741320-1 2001 We have investigated the effects of three unrelated topoisomerase 2 inhibitors, genistein, adriamycin, and etoposide, on phosphorylation/activation of the checkpoint kinase Chk2 in normal or ATM-deficient (ATM-) human fibroblasts and in cells overexpressing a catalytically inactive ATR kinase. Doxorubicin 91-101 checkpoint kinase 2 Homo sapiens 173-177 11741320-2 2001 We demonstrate that genistein activates Chk2 in a strictly ATM-dependent manner, whereas etoposide and adriamycin can trigger Chk2 activation in long-term cultures of ATM- cells. Doxorubicin 103-113 checkpoint kinase 2 Homo sapiens 126-130 15707569-0 2005 The relative contribution of CHK1 and CHK2 to Adriamycin-induced checkpoint. Doxorubicin 46-56 checkpoint kinase 2 Homo sapiens 38-42 15707569-2 2005 Adriamycin-induced DNA damage checkpoint activates ATM and ATR, which could in turn inhibit the cell cycle engine through either CHK1 or CHK2. Doxorubicin 0-10 checkpoint kinase 2 Homo sapiens 137-141 15707569-3 2005 In this study, we characterized whether CHK1 or CHK2 is required for Adriamycin-induced checkpoint. Doxorubicin 69-79 checkpoint kinase 2 Homo sapiens 48-52 15707569-4 2005 We found that both CHK1 and CHK2 were phosphorylated after Adriamycin treatment. Doxorubicin 59-69 checkpoint kinase 2 Homo sapiens 28-32 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. Doxorubicin 120-131 checkpoint kinase 2 Homo sapiens 254-258 30405800-7 2018 Furthermore, DOX resulted in increased alterations in DNA damage-related proteins such as p-ATM, p-Chk2, p-p53, p21 and gammaH2AX, but not p16. Doxorubicin 13-16 checkpoint kinase 2 Homo sapiens 99-103 30665195-5 2019 In contrast, breast cells were more resistant and showed more Chk2 activation in response to doxorubicin. Doxorubicin 93-104 checkpoint kinase 2 Homo sapiens 62-66 30405800-8 2018 Notably, the combination of dinaciclib and DOX inhibited cell growth and promoted senescence by transforming the suppressive effects of the ATM/Chk2/p53/p21 signaling pathway and enhancing the p16 signaling pathway. Doxorubicin 43-46 checkpoint kinase 2 Homo sapiens 144-148 29316526-4 2018 A potentiation effect of the synthesized Chk2 inhibitors was also investigated using the genotoxic anticancer drugs cisplatin and doxorubicin on breast carcinoma, (ER+) cell line (MCF-7). Doxorubicin 130-141 checkpoint kinase 2 Homo sapiens 41-45 29775409-5 2018 Exposure to a low dose of doxorubicin (Doxo) induced similar DNA damage and DNA damage response (DDR) as measured by RAD50 and MRE11 expression, checkpoint kinase 2 activation, and gammaH2A.X recruitment at DNA strand breaks in both cell groups, indicating that silence of p53-TAD does not affect the DDR mechanism upstream of p53. Doxorubicin 26-37 checkpoint kinase 2 Homo sapiens 145-164 29775409-5 2018 Exposure to a low dose of doxorubicin (Doxo) induced similar DNA damage and DNA damage response (DDR) as measured by RAD50 and MRE11 expression, checkpoint kinase 2 activation, and gammaH2A.X recruitment at DNA strand breaks in both cell groups, indicating that silence of p53-TAD does not affect the DDR mechanism upstream of p53. Doxorubicin 39-43 checkpoint kinase 2 Homo sapiens 145-164 27888802-6 2016 Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker). Doxorubicin 34-37 checkpoint kinase 2 Homo sapiens 127-131 27403577-0 2016 The Effect of Caffeine and chk2 Inhibitor on Doxorubicin-Induced Cellular Senescence in MCF-7 Cells. Doxorubicin 45-56 checkpoint kinase 2 Homo sapiens 27-31 27403577-12 2016 Our findings demonstrate that low-dose doxorubicin induced senescence via the activation of ATM, -chk2, and -p21 pathways, while inhibition of ATM and chk2 cannot consider as a new target for sensitization of MCF-7 cells to doxorubicin. Doxorubicin 39-50 checkpoint kinase 2 Homo sapiens 98-102 27403577-3 2016 We investigated the effect of caffeine and chk2 inhibitor on doxorubicin induced senescence in MCF-7 cells. Doxorubicin 61-72 checkpoint kinase 2 Homo sapiens 43-47 25683911-11 2015 Treatment of melanoma cells with an inhibitor of Chk2 upstream kinase ATM and doxorubicin almost completely abolishes G0-G1 arrest. Doxorubicin 78-89 checkpoint kinase 2 Homo sapiens 49-53 25478729-0 2015 Alternation of adriamycin penetration kinetics in MCF-7 cells from 2D to 3D culture based on P-gp expression through the Chk2/p53/NF-kappaB pathway. Doxorubicin 15-25 checkpoint kinase 2 Homo sapiens 121-125