viability assays atrt cell line chla 02 atrt Search Results


viability assays atrt cell line chla 02 atrt  (ATCC)
93
ATCC viability assays atrt cell line chla 02 atrt
Viability Assays Atrt Cell Line Chla 02 Atrt, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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atr6-001  (Federation of European Neuroscience Societies)
90
Federation of European Neuroscience Societies atr6-001
Atr6 001, supplied by Federation of European Neuroscience Societies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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azd6738; atri  (AstraZeneca ltd)
90
AstraZeneca ltd azd6738; atri
Azd6738; Atri, supplied by AstraZeneca ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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atr inhibitor ve821  (Axon Medchem LLC)
90
Axon Medchem LLC atr inhibitor ve821
PD-L1 upregulation requires <t>ATM/ATR/Chk1</t> activity after DSBs. a ATM kinase activity is required for PD-L1 upregulation after IR. U2OS cells were treated with a specific ATMi 15 min prior to IR, Etp, CPT or APH treatment. PD-L1 was examined 48 h after 10 Gy or the addition of 500 nM Etp, 50 nM CPT or 500 nM APH. b NBS1 depletion attenuates ATM auto-phosphorylation, which results in less PD-L1 upregulation. U2OS cells were exposed to NBS1 siRNA. ATM S1981 auto-phosphorylation was examined 30 min after 5 or 10 Gy (left panel). PD-L1 was examined 48 h after 5 or 10 Gy (right panel). c ATM kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were harvested with or without ATMi after IR. PD-L1 mRNA was examined 48 h after 5 or 10 Gy. d ATR and Chk1 kinase activities are required for PD-L1 upregulation after IR. PD-L1 in U2OS cells was examined 48 h after 5 or 10 Gy with or without <t>ATRi</t> or Chk1i (UCN-01). e The Chk1 dependence was confirmed by another Chk1 inhibitor. PD-L1 in U2OS cells was examined 48 h after 10 Gy with or without Chk1i (MK8776). f Chk1 kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were exposed to IR with or without Chk1i (UCN-01 or MK8776). PD-L1 mRNA was examined 48 h after 10 Gy. g Chk1 kinase activity is required for the upregulation of cell-surface PD-L1 after IR. PD-L1 in U2OS, H1299, DU145 cells was examined by flow cytometry at 48 h after 10 Gy with or without Chk1i (UCN-01 or MK8776). Statistical significance was examined compared with non-treated cells. Error bars represent the s.d. of three independent experiments ( c , f , g ). Statistical significance was determined using Student’s two-tailed t -test. * P < 0.05, ** P < 0.01, *** P < 0.001
Atr Inhibitor Ve821, supplied by Axon Medchem LLC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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atri atr-kinase inhibitor ii  (Merck KGaA)
90
Merck KGaA atri atr-kinase inhibitor ii
PD-L1 upregulation requires <t>ATM/ATR/Chk1</t> activity after DSBs. a ATM kinase activity is required for PD-L1 upregulation after IR. U2OS cells were treated with a specific ATMi 15 min prior to IR, Etp, CPT or APH treatment. PD-L1 was examined 48 h after 10 Gy or the addition of 500 nM Etp, 50 nM CPT or 500 nM APH. b NBS1 depletion attenuates ATM auto-phosphorylation, which results in less PD-L1 upregulation. U2OS cells were exposed to NBS1 siRNA. ATM S1981 auto-phosphorylation was examined 30 min after 5 or 10 Gy (left panel). PD-L1 was examined 48 h after 5 or 10 Gy (right panel). c ATM kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were harvested with or without ATMi after IR. PD-L1 mRNA was examined 48 h after 5 or 10 Gy. d ATR and Chk1 kinase activities are required for PD-L1 upregulation after IR. PD-L1 in U2OS cells was examined 48 h after 5 or 10 Gy with or without <t>ATRi</t> or Chk1i (UCN-01). e The Chk1 dependence was confirmed by another Chk1 inhibitor. PD-L1 in U2OS cells was examined 48 h after 10 Gy with or without Chk1i (MK8776). f Chk1 kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were exposed to IR with or without Chk1i (UCN-01 or MK8776). PD-L1 mRNA was examined 48 h after 10 Gy. g Chk1 kinase activity is required for the upregulation of cell-surface PD-L1 after IR. PD-L1 in U2OS, H1299, DU145 cells was examined by flow cytometry at 48 h after 10 Gy with or without Chk1i (UCN-01 or MK8776). Statistical significance was examined compared with non-treated cells. Error bars represent the s.d. of three independent experiments ( c , f , g ). Statistical significance was determined using Student’s two-tailed t -test. * P < 0.05, ** P < 0.01, *** P < 0.001
Atri Atr Kinase Inhibitor Ii, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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cell titer-glo  (Promega)
90
Promega cell titer-glo
PD-L1 upregulation requires <t>ATM/ATR/Chk1</t> activity after DSBs. a ATM kinase activity is required for PD-L1 upregulation after IR. U2OS cells were treated with a specific ATMi 15 min prior to IR, Etp, CPT or APH treatment. PD-L1 was examined 48 h after 10 Gy or the addition of 500 nM Etp, 50 nM CPT or 500 nM APH. b NBS1 depletion attenuates ATM auto-phosphorylation, which results in less PD-L1 upregulation. U2OS cells were exposed to NBS1 siRNA. ATM S1981 auto-phosphorylation was examined 30 min after 5 or 10 Gy (left panel). PD-L1 was examined 48 h after 5 or 10 Gy (right panel). c ATM kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were harvested with or without ATMi after IR. PD-L1 mRNA was examined 48 h after 5 or 10 Gy. d ATR and Chk1 kinase activities are required for PD-L1 upregulation after IR. PD-L1 in U2OS cells was examined 48 h after 5 or 10 Gy with or without <t>ATRi</t> or Chk1i (UCN-01). e The Chk1 dependence was confirmed by another Chk1 inhibitor. PD-L1 in U2OS cells was examined 48 h after 10 Gy with or without Chk1i (MK8776). f Chk1 kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were exposed to IR with or without Chk1i (UCN-01 or MK8776). PD-L1 mRNA was examined 48 h after 10 Gy. g Chk1 kinase activity is required for the upregulation of cell-surface PD-L1 after IR. PD-L1 in U2OS, H1299, DU145 cells was examined by flow cytometry at 48 h after 10 Gy with or without Chk1i (UCN-01 or MK8776). Statistical significance was examined compared with non-treated cells. Error bars represent the s.d. of three independent experiments ( c , f , g ). Statistical significance was determined using Student’s two-tailed t -test. * P < 0.05, ** P < 0.01, *** P < 0.001
Cell Titer Glo, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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elyra 7 microscope  (Carl Zeiss)
90
Carl Zeiss elyra 7 microscope
PD-L1 upregulation requires <t>ATM/ATR/Chk1</t> activity after DSBs. a ATM kinase activity is required for PD-L1 upregulation after IR. U2OS cells were treated with a specific ATMi 15 min prior to IR, Etp, CPT or APH treatment. PD-L1 was examined 48 h after 10 Gy or the addition of 500 nM Etp, 50 nM CPT or 500 nM APH. b NBS1 depletion attenuates ATM auto-phosphorylation, which results in less PD-L1 upregulation. U2OS cells were exposed to NBS1 siRNA. ATM S1981 auto-phosphorylation was examined 30 min after 5 or 10 Gy (left panel). PD-L1 was examined 48 h after 5 or 10 Gy (right panel). c ATM kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were harvested with or without ATMi after IR. PD-L1 mRNA was examined 48 h after 5 or 10 Gy. d ATR and Chk1 kinase activities are required for PD-L1 upregulation after IR. PD-L1 in U2OS cells was examined 48 h after 5 or 10 Gy with or without <t>ATRi</t> or Chk1i (UCN-01). e The Chk1 dependence was confirmed by another Chk1 inhibitor. PD-L1 in U2OS cells was examined 48 h after 10 Gy with or without Chk1i (MK8776). f Chk1 kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were exposed to IR with or without Chk1i (UCN-01 or MK8776). PD-L1 mRNA was examined 48 h after 10 Gy. g Chk1 kinase activity is required for the upregulation of cell-surface PD-L1 after IR. PD-L1 in U2OS, H1299, DU145 cells was examined by flow cytometry at 48 h after 10 Gy with or without Chk1i (UCN-01 or MK8776). Statistical significance was examined compared with non-treated cells. Error bars represent the s.d. of three independent experiments ( c , f , g ). Statistical significance was determined using Student’s two-tailed t -test. * P < 0.05, ** P < 0.01, *** P < 0.001
Elyra 7 Microscope, supplied by Carl Zeiss, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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elyra 7 microscope - by Bioz Stars, 2026-07
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atrt-tyr  (CH Instruments)
90
CH Instruments atrt-tyr
PD-L1 upregulation requires <t>ATM/ATR/Chk1</t> activity after DSBs. a ATM kinase activity is required for PD-L1 upregulation after IR. U2OS cells were treated with a specific ATMi 15 min prior to IR, Etp, CPT or APH treatment. PD-L1 was examined 48 h after 10 Gy or the addition of 500 nM Etp, 50 nM CPT or 500 nM APH. b NBS1 depletion attenuates ATM auto-phosphorylation, which results in less PD-L1 upregulation. U2OS cells were exposed to NBS1 siRNA. ATM S1981 auto-phosphorylation was examined 30 min after 5 or 10 Gy (left panel). PD-L1 was examined 48 h after 5 or 10 Gy (right panel). c ATM kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were harvested with or without ATMi after IR. PD-L1 mRNA was examined 48 h after 5 or 10 Gy. d ATR and Chk1 kinase activities are required for PD-L1 upregulation after IR. PD-L1 in U2OS cells was examined 48 h after 5 or 10 Gy with or without <t>ATRi</t> or Chk1i (UCN-01). e The Chk1 dependence was confirmed by another Chk1 inhibitor. PD-L1 in U2OS cells was examined 48 h after 10 Gy with or without Chk1i (MK8776). f Chk1 kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were exposed to IR with or without Chk1i (UCN-01 or MK8776). PD-L1 mRNA was examined 48 h after 10 Gy. g Chk1 kinase activity is required for the upregulation of cell-surface PD-L1 after IR. PD-L1 in U2OS, H1299, DU145 cells was examined by flow cytometry at 48 h after 10 Gy with or without Chk1i (UCN-01 or MK8776). Statistical significance was examined compared with non-treated cells. Error bars represent the s.d. of three independent experiments ( c , f , g ). Statistical significance was determined using Student’s two-tailed t -test. * P < 0.05, ** P < 0.01, *** P < 0.001
Atrt Tyr, supplied by CH Instruments, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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blocking buffer 1% w/v bsa, 22.52mg/ml glycine, 0.1%v/vtween20,and1000xdilutedmurinernase inhibitor indpbs  (AmericanBio Inc)
90
AmericanBio Inc blocking buffer 1% w/v bsa, 22.52mg/ml glycine, 0.1%v/vtween20,and1000xdilutedmurinernase inhibitor indpbs
PD-L1 upregulation requires <t>ATM/ATR/Chk1</t> activity after DSBs. a ATM kinase activity is required for PD-L1 upregulation after IR. U2OS cells were treated with a specific ATMi 15 min prior to IR, Etp, CPT or APH treatment. PD-L1 was examined 48 h after 10 Gy or the addition of 500 nM Etp, 50 nM CPT or 500 nM APH. b NBS1 depletion attenuates ATM auto-phosphorylation, which results in less PD-L1 upregulation. U2OS cells were exposed to NBS1 siRNA. ATM S1981 auto-phosphorylation was examined 30 min after 5 or 10 Gy (left panel). PD-L1 was examined 48 h after 5 or 10 Gy (right panel). c ATM kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were harvested with or without ATMi after IR. PD-L1 mRNA was examined 48 h after 5 or 10 Gy. d ATR and Chk1 kinase activities are required for PD-L1 upregulation after IR. PD-L1 in U2OS cells was examined 48 h after 5 or 10 Gy with or without <t>ATRi</t> or Chk1i (UCN-01). e The Chk1 dependence was confirmed by another Chk1 inhibitor. PD-L1 in U2OS cells was examined 48 h after 10 Gy with or without Chk1i (MK8776). f Chk1 kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were exposed to IR with or without Chk1i (UCN-01 or MK8776). PD-L1 mRNA was examined 48 h after 10 Gy. g Chk1 kinase activity is required for the upregulation of cell-surface PD-L1 after IR. PD-L1 in U2OS, H1299, DU145 cells was examined by flow cytometry at 48 h after 10 Gy with or without Chk1i (UCN-01 or MK8776). Statistical significance was examined compared with non-treated cells. Error bars represent the s.d. of three independent experiments ( c , f , g ). Statistical significance was determined using Student’s two-tailed t -test. * P < 0.05, ** P < 0.01, *** P < 0.001
Blocking Buffer 1% W/V Bsa, 22.52mg/Ml Glycine, 0.1%V/Vtween20,And1000xdilutedmurinernase Inhibitor Indpbs, supplied by AmericanBio Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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blocking buffer 1% w/v bsa, 22.52mg/ml glycine, 0.1%v/vtween20,and1000xdilutedmurinernase inhibitor indpbs - by Bioz Stars, 2026-07
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atrn  (Sino Biological)
93
Sino Biological atrn
PD-L1 upregulation requires <t>ATM/ATR/Chk1</t> activity after DSBs. a ATM kinase activity is required for PD-L1 upregulation after IR. U2OS cells were treated with a specific ATMi 15 min prior to IR, Etp, CPT or APH treatment. PD-L1 was examined 48 h after 10 Gy or the addition of 500 nM Etp, 50 nM CPT or 500 nM APH. b NBS1 depletion attenuates ATM auto-phosphorylation, which results in less PD-L1 upregulation. U2OS cells were exposed to NBS1 siRNA. ATM S1981 auto-phosphorylation was examined 30 min after 5 or 10 Gy (left panel). PD-L1 was examined 48 h after 5 or 10 Gy (right panel). c ATM kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were harvested with or without ATMi after IR. PD-L1 mRNA was examined 48 h after 5 or 10 Gy. d ATR and Chk1 kinase activities are required for PD-L1 upregulation after IR. PD-L1 in U2OS cells was examined 48 h after 5 or 10 Gy with or without <t>ATRi</t> or Chk1i (UCN-01). e The Chk1 dependence was confirmed by another Chk1 inhibitor. PD-L1 in U2OS cells was examined 48 h after 10 Gy with or without Chk1i (MK8776). f Chk1 kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were exposed to IR with or without Chk1i (UCN-01 or MK8776). PD-L1 mRNA was examined 48 h after 10 Gy. g Chk1 kinase activity is required for the upregulation of cell-surface PD-L1 after IR. PD-L1 in U2OS, H1299, DU145 cells was examined by flow cytometry at 48 h after 10 Gy with or without Chk1i (UCN-01 or MK8776). Statistical significance was examined compared with non-treated cells. Error bars represent the s.d. of three independent experiments ( c , f , g ). Statistical significance was determined using Student’s two-tailed t -test. * P < 0.05, ** P < 0.01, *** P < 0.001
Atrn, supplied by Sino Biological, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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atrn - by Bioz Stars, 2026-07
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azd6738  (Selleck Chemicals)
93
Selleck Chemicals azd6738
TNBC cell line sensitivity to DDR small molecule inhibitors. (A) Cells continuously exposed to ATM inhibitor KU-55933 (ATMi). (B) Cells continuously exposed to ATR inhibitor <t>AZD6738</t> (ATRi). (C) Cells continuously exposed to CHK1/2 inhibitor prexasertib (LY2606368). (D) Cells continuously exposed to DNA-PK inhibitor NU7062. (E) IC 50 values for DDR inhibitors. DDR, DNA damage response; TNBC, triple negative breast cancer.
Azd6738, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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atr inhibitor az20  (Selleck Chemicals)
94
Selleck Chemicals atr inhibitor az20
TNBC cell line sensitivity to DDR small molecule inhibitors. (A) Cells continuously exposed to ATM inhibitor KU-55933 (ATMi). (B) Cells continuously exposed to ATR inhibitor <t>AZD6738</t> (ATRi). (C) Cells continuously exposed to CHK1/2 inhibitor prexasertib (LY2606368). (D) Cells continuously exposed to DNA-PK inhibitor NU7062. (E) IC 50 values for DDR inhibitors. DDR, DNA damage response; TNBC, triple negative breast cancer.
Atr Inhibitor Az20, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


PD-L1 upregulation requires ATM/ATR/Chk1 activity after DSBs. a ATM kinase activity is required for PD-L1 upregulation after IR. U2OS cells were treated with a specific ATMi 15 min prior to IR, Etp, CPT or APH treatment. PD-L1 was examined 48 h after 10 Gy or the addition of 500 nM Etp, 50 nM CPT or 500 nM APH. b NBS1 depletion attenuates ATM auto-phosphorylation, which results in less PD-L1 upregulation. U2OS cells were exposed to NBS1 siRNA. ATM S1981 auto-phosphorylation was examined 30 min after 5 or 10 Gy (left panel). PD-L1 was examined 48 h after 5 or 10 Gy (right panel). c ATM kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were harvested with or without ATMi after IR. PD-L1 mRNA was examined 48 h after 5 or 10 Gy. d ATR and Chk1 kinase activities are required for PD-L1 upregulation after IR. PD-L1 in U2OS cells was examined 48 h after 5 or 10 Gy with or without ATRi or Chk1i (UCN-01). e The Chk1 dependence was confirmed by another Chk1 inhibitor. PD-L1 in U2OS cells was examined 48 h after 10 Gy with or without Chk1i (MK8776). f Chk1 kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were exposed to IR with or without Chk1i (UCN-01 or MK8776). PD-L1 mRNA was examined 48 h after 10 Gy. g Chk1 kinase activity is required for the upregulation of cell-surface PD-L1 after IR. PD-L1 in U2OS, H1299, DU145 cells was examined by flow cytometry at 48 h after 10 Gy with or without Chk1i (UCN-01 or MK8776). Statistical significance was examined compared with non-treated cells. Error bars represent the s.d. of three independent experiments ( c , f , g ). Statistical significance was determined using Student’s two-tailed t -test. * P < 0.05, ** P < 0.01, *** P < 0.001

Journal: Nature Communications

Article Title: DNA double-strand break repair pathway regulates PD-L1 expression in cancer cells

doi: 10.1038/s41467-017-01883-9

Figure Lengend Snippet: PD-L1 upregulation requires ATM/ATR/Chk1 activity after DSBs. a ATM kinase activity is required for PD-L1 upregulation after IR. U2OS cells were treated with a specific ATMi 15 min prior to IR, Etp, CPT or APH treatment. PD-L1 was examined 48 h after 10 Gy or the addition of 500 nM Etp, 50 nM CPT or 500 nM APH. b NBS1 depletion attenuates ATM auto-phosphorylation, which results in less PD-L1 upregulation. U2OS cells were exposed to NBS1 siRNA. ATM S1981 auto-phosphorylation was examined 30 min after 5 or 10 Gy (left panel). PD-L1 was examined 48 h after 5 or 10 Gy (right panel). c ATM kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were harvested with or without ATMi after IR. PD-L1 mRNA was examined 48 h after 5 or 10 Gy. d ATR and Chk1 kinase activities are required for PD-L1 upregulation after IR. PD-L1 in U2OS cells was examined 48 h after 5 or 10 Gy with or without ATRi or Chk1i (UCN-01). e The Chk1 dependence was confirmed by another Chk1 inhibitor. PD-L1 in U2OS cells was examined 48 h after 10 Gy with or without Chk1i (MK8776). f Chk1 kinase activity is required for the upregulation of PD-L1 mRNA expression. U2OS cells were exposed to IR with or without Chk1i (UCN-01 or MK8776). PD-L1 mRNA was examined 48 h after 10 Gy. g Chk1 kinase activity is required for the upregulation of cell-surface PD-L1 after IR. PD-L1 in U2OS, H1299, DU145 cells was examined by flow cytometry at 48 h after 10 Gy with or without Chk1i (UCN-01 or MK8776). Statistical significance was examined compared with non-treated cells. Error bars represent the s.d. of three independent experiments ( c , f , g ). Statistical significance was determined using Student’s two-tailed t -test. * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: In addition, 10 μM ATM inhibitor (ATMi) (KU55933; Merck Chemicals), 10 μM ATR inhibitor (ATRi) (VE821; Axon Medchem), Chk1 inhibitor (100 nM UCN-01; Calbiochem or 50 nM MK8776; AdooQ Bioscience) was added at 30 min prior to DNA damage induction.

Techniques: Activity Assay, Phospho-proteomics, Expressing, Flow Cytometry, Two Tailed Test

TNBC cell line sensitivity to DDR small molecule inhibitors. (A) Cells continuously exposed to ATM inhibitor KU-55933 (ATMi). (B) Cells continuously exposed to ATR inhibitor AZD6738 (ATRi). (C) Cells continuously exposed to CHK1/2 inhibitor prexasertib (LY2606368). (D) Cells continuously exposed to DNA-PK inhibitor NU7062. (E) IC 50 values for DDR inhibitors. DDR, DNA damage response; TNBC, triple negative breast cancer.

Journal: Therapeutic Advances in Medical Oncology

Article Title: Exploiting DNA repair defects in triple negative breast cancer to improve cell killing

doi: 10.1177/1758835920958354

Figure Lengend Snippet: TNBC cell line sensitivity to DDR small molecule inhibitors. (A) Cells continuously exposed to ATM inhibitor KU-55933 (ATMi). (B) Cells continuously exposed to ATR inhibitor AZD6738 (ATRi). (C) Cells continuously exposed to CHK1/2 inhibitor prexasertib (LY2606368). (D) Cells continuously exposed to DNA-PK inhibitor NU7062. (E) IC 50 values for DDR inhibitors. DDR, DNA damage response; TNBC, triple negative breast cancer.

Article Snippet: For coexposure experiments, MDA-231 cells were exposed to DMSO vehicle control, doxorubicin, and 10 μM KU-55933 (ATM inhibitor, ATMi), 1 μM AZD6738 (ATR inhibitor, ATRi), 5 μM NU7026 (DNAPK inhibitor, DNAPKi), or 10 nM prexasertib (LY2606368, Selleck Chemicals).

Techniques: