Sensitivity of cells to ATR and CHK1 inhibitors requires hyperactivation of CDK2 rather than endogen...
Sensitivity of cells to ATR and CHK1 inhibitors requires hyperactivation of CDK2 rather than endogenous replication stress or ATM dysfunction
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London: Nature Publishing Group UK
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English
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London: Nature Publishing Group UK
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DNA damage activates cell cycle checkpoint proteins ATR and CHK1 to arrest cell cycle progression, providing time for repair and recovery. Consequently, inhibitors of ATR (ATRi) and CHK1 (CHK1i) enhance damage-induced cell death. Intriguingly, both CHK1i and ATRi alone elicit cytotoxicity in some cell lines. Sensitivity has been attributed to endog...
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Sensitivity of cells to ATR and CHK1 inhibitors requires hyperactivation of CDK2 rather than endogenous replication stress or ATM dysfunction
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TN_cdi_doaj_primary_oai_doaj_org_article_5351eae2b961433688e264c109fd09cc
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https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_5351eae2b961433688e264c109fd09cc
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ISSN
2045-2322
E-ISSN
2045-2322
DOI
10.1038/s41598-021-86490-x