PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26055704-5 2015 In addition, CPT-treated hMSH5-deficient cells exhibit aberrant activation of Chk1 and Chk2 kinases and therefore abnormal cell cycle progression. Camptothecin 13-16 checkpoint kinase 1 Homo sapiens 78-82 33536335-3 2021 We found that inactivation of Ataxia Telangiectasia- and Rad3-related (ATR), CHK1, BRCA2, and RPA1 overcome chemoresistance to camptothecin (CPT) in SLFN11-KO cells. Camptothecin 127-139 checkpoint kinase 1 Homo sapiens 77-81 33529438-6 2021 In combination with cytotoxic chemotherapy such as gemcitabine or camptothecin, Chk1 inhibition increased cytoplasmic dsDNA compared to the cytotoxic alone but attenuated the cytotoxic chemotherapy-induced increase in IRF1 protein and STAT1 phosphorylation through inhibition of nuclear RelB translocation. Camptothecin 66-78 checkpoint kinase 1 Homo sapiens 80-84 27634334-6 2016 Chemical and cytotoxic induction of replication stress, through aphidicolin, gemcitabine, camptothecin or hydroxyurea exposure, activates transcription of APOBEC3B via an ATR/Chk1-dependent pathway in vitro. Camptothecin 90-102 checkpoint kinase 1 Homo sapiens 175-179 31713291-8 2020 Moreover, prolonged replication stress induced by hydroxyurea or camptothecin resulted in a reduction of Chk1 protein levels, which was rescued by HUWE1 knockdown. Camptothecin 65-77 checkpoint kinase 1 Homo sapiens 105-109 26068472-4 2015 In response to camptothecin-mediated DNA DSBs, CHK1 and RPA2 phosphorylation, which are hallmarks of HR activation, was abrogated in SERBP1-depleted cells. Camptothecin 15-27 checkpoint kinase 1 Homo sapiens 47-51 18339864-2 2008 Here, we found that the Hsp72-depleted cells show defect in phosphorylation and activation of the protein kinase Chk1 by genotoxic stresses, such as UVC irradiation or camptothecin. Camptothecin 168-180 checkpoint kinase 1 Homo sapiens 113-117 25253693-3 2014 Inhibition of Gli1 in tumor cells induced replication stress-mediated DNA damage response, attenuated their clonogenic potential, abrogated camptothecin (CPT)-induced Chk1 phosphorylation, and potentiated its cytotoxicity. Camptothecin 140-152 checkpoint kinase 1 Homo sapiens 167-171 25253693-3 2014 Inhibition of Gli1 in tumor cells induced replication stress-mediated DNA damage response, attenuated their clonogenic potential, abrogated camptothecin (CPT)-induced Chk1 phosphorylation, and potentiated its cytotoxicity. Camptothecin 154-157 checkpoint kinase 1 Homo sapiens 167-171 19716789-5 2009 Further, we show that low levels of Fbx6 and consequent impairment of replication stress-induced Chk1 degradation are associated with cancer cell resistance to the chemotherapeutic agent, camptothecin. Camptothecin 188-200 checkpoint kinase 1 Homo sapiens 97-101 19060337-2 2009 A systematic screening of the protein kinase small interfering RNA library reveals that Chk1 and ataxia telangiectasia-mutated (ATM) and Rad3-related (ATR) are the main kinases responsible for intra-S-phase checkpoint upon topoisomerase I inhibitor camptothecin-induced DNA damage. Camptothecin 249-261 checkpoint kinase 1 Homo sapiens 88-92 19060337-6 2009 In cells deficient in both Chk1 and p53, Cdc25A down-regulation upon camptothecin-induced DNA damage is completely abolished, leading to severe defects in cell cycle checkpoints and remarkable cell death in mitosis. Camptothecin 69-81 checkpoint kinase 1 Homo sapiens 27-31 18566216-6 2008 Using RNA interference, we further showed that Chk2 was essential to G(2)-M arrest, whereas Chk1 was mainly required for HR repair in CPT-treated HCT116 cells. Camptothecin 134-137 checkpoint kinase 1 Homo sapiens 92-96 24915421-9 2014 WJ35435 was less effective than camptothecin and etoposide in inducing the phosphorylation and activation of Chk1, Chk2 and RPA32 which were crucial coordinators in DNA repair pathway, indicating a low DNA repair activity to WJ35435 action. Camptothecin 32-44 checkpoint kinase 1 Homo sapiens 109-113 24996846-9 2014 CONCLUSIONS: Our results suggest that Chk1 phosphorylation could be a useful biomarker for monitoring inhibition of Chk1 activity in clinical trials involving a range of V158411-chemotherapy combinations and gammaH2AX induction as a predictor of potentiation in combinations containing gemcitabine or camptothecin. Camptothecin 301-313 checkpoint kinase 1 Homo sapiens 38-42 24996846-9 2014 CONCLUSIONS: Our results suggest that Chk1 phosphorylation could be a useful biomarker for monitoring inhibition of Chk1 activity in clinical trials involving a range of V158411-chemotherapy combinations and gammaH2AX induction as a predictor of potentiation in combinations containing gemcitabine or camptothecin. Camptothecin 301-313 checkpoint kinase 1 Homo sapiens 116-120 20042274-9 2010 Thus, depending on the biological context, the camptothecin activated ATM-Chk2 or ATR-Chk1 pathways, both having a protective role. Camptothecin 47-59 checkpoint kinase 1 Homo sapiens 86-90 18566216-0 2008 Chk1 and Chk2 are differentially involved in homologous recombination repair and cell cycle arrest in response to DNA double-strand breaks induced by camptothecins. Camptothecin 150-163 checkpoint kinase 1 Homo sapiens 0-4 17935989-3 2007 These compounds significantly sensitize tumor cells to the DNA-damaging antitumor agent doxorubicin in a cell-based assay and efficiently abrogate the doxorubicin-induced G2/M and camptothecin-induced S checkpoints, indicating that the potent biological activities of these compounds are mechanism-based through Chk1 inhibition. Camptothecin 180-192 checkpoint kinase 1 Homo sapiens 312-316 17352464-5 2007 Compounds 5b, 5c, 5f, 15, 16d, 17g, 17h, 17k, 18d, and 22 were identified as ideal Chk1 inhibitors, which showed little or no single-agent activity but significantly potentiate the cytotoxicities of the DNA-damaging antitumor agents doxorubicin and camptothecin. Camptothecin 249-261 checkpoint kinase 1 Homo sapiens 83-87 17544271-6 2007 These compounds significantly potentiate the cytotoxicity of DNA-damaging antitumor agents in a cell-based assay and efficiently abrogate the doxorubicin-induced G2/M and the camptothecin-induced S checkpoints, suggesting that their potent biological activities are mechanism-based through Chk1 inhibition. Camptothecin 175-187 checkpoint kinase 1 Homo sapiens 290-294 17986860-7 2007 In human colon carcinoma cells treated with the topoisomerase I inhibitor camptothecin, DNA replication is inhibited both at the level of initiation and at the level of elongation through a Chk1-dependent checkpoint mechanism. Camptothecin 74-86 checkpoint kinase 1 Homo sapiens 190-194 17352464-6 2007 These novel Chk1 inhibitors abrogate the doxorubicin-induced G2 and camptothecin-induced S checkpoint arrests, confirming that their potent biological activities are mechanism-based through Chk1 inhibition. Camptothecin 68-80 checkpoint kinase 1 Homo sapiens 12-16 17352464-6 2007 These novel Chk1 inhibitors abrogate the doxorubicin-induced G2 and camptothecin-induced S checkpoint arrests, confirming that their potent biological activities are mechanism-based through Chk1 inhibition. Camptothecin 68-80 checkpoint kinase 1 Homo sapiens 190-194 16603354-3 2006 These compounds are potent cell permeable CHK-1 inhibitors and showed synergistic effect with a DNA-damaging agent, camptothecin. Camptothecin 116-128 checkpoint kinase 1 Homo sapiens 42-47 16928871-0 2006 The Chk1/Cdc25A pathway as activators of the cell cycle in neuronal death induced by camptothecin. Camptothecin 85-97 checkpoint kinase 1 Homo sapiens 4-8 16928871-12 2006 Importantly, expression of wild-type Chk1, but not kinase-dead Chk1, inhibits the camptothecin-induced increase in Cdc25A activity. Camptothecin 82-94 checkpoint kinase 1 Homo sapiens 37-41 16928813-7 2006 Our result showed that only the down-regulation of Chk1, but not of Chk2 or MK2, abrogated camptothecin- or 5-fluorouracil-induced S-phase arrest or doxorubicin-induced G(2)-phase arrest. Camptothecin 91-103 checkpoint kinase 1 Homo sapiens 51-55 16137618-5 2005 Treatment of cells with the anticancer agent camptothecin (CPT) triggers Chk1 destruction, which blocks recovery from drug-induced S phase arrest and leads to cell death. Camptothecin 45-57 checkpoint kinase 1 Homo sapiens 73-77 16407843-6 2006 The cell cycle checkpoint abrogator and Chk1/Chk2 inhibitor 7-hydroxystaurosporine (UCN-01) also increases camptothecin-induced gammaH2AX formation and inhibits camptothecin-induced p21(CDKN1A) upregulation in HCT116 wt cells. Camptothecin 107-119 checkpoint kinase 1 Homo sapiens 40-44 16407843-6 2006 The cell cycle checkpoint abrogator and Chk1/Chk2 inhibitor 7-hydroxystaurosporine (UCN-01) also increases camptothecin-induced gammaH2AX formation and inhibits camptothecin-induced p21(CDKN1A) upregulation in HCT116 wt cells. Camptothecin 161-173 checkpoint kinase 1 Homo sapiens 40-44 16137618-5 2005 Treatment of cells with the anticancer agent camptothecin (CPT) triggers Chk1 destruction, which blocks recovery from drug-induced S phase arrest and leads to cell death. Camptothecin 59-62 checkpoint kinase 1 Homo sapiens 73-77 16137618-7 2005 Proteolysis of activated Chk1 may promote checkpoint termination under normal conditions, and may play an important role in the cytotoxic effects of CPT and related anticancer drugs. Camptothecin 149-152 checkpoint kinase 1 Homo sapiens 25-29 15608676-2 2005 We have previously shown that inhibition of Chk1 sensitizes tumor cells to topoisomerase inhibitors such as camptothecin and doxorubicin through abrogation of cell-cycle arrest (S or G2/M checkpoints). Camptothecin 108-120 checkpoint kinase 1 Homo sapiens 44-48 15699047-5 2005 Colony forming assays demonstrated that down-regulation of ATR or Chk1 sensitized cells to SN-38 and camptothecin. Camptothecin 101-113 checkpoint kinase 1 Homo sapiens 66-70 15665856-4 2005 Abrogation of Chk1 function with small interfering RNA or chemical antagonists inhibits HRR, leading to persistent unrepaired DNA double-strand breaks (DSBs) and cell death after replication inhibition with hydroxyurea or DNA-damage caused by camptothecin. Camptothecin 243-255 checkpoint kinase 1 Homo sapiens 14-18 11980637-0 2002 Ku affects the ataxia and Rad 3-related/CHK1-dependent S phase checkpoint response after camptothecin treatment. Camptothecin 89-101 checkpoint kinase 1 Homo sapiens 40-44 35430566-8 2022 SLFN12 over-expression decreased CHK1 and CHK2 phosphorylation after treatment with the DNA damaging agent camptothecin (CPT). Camptothecin 107-119 checkpoint kinase 1 Homo sapiens 33-37 35430566-8 2022 SLFN12 over-expression decreased CHK1 and CHK2 phosphorylation after treatment with the DNA damaging agent camptothecin (CPT). Camptothecin 121-124 checkpoint kinase 1 Homo sapiens 33-37