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these observations demonstrate that Chk1 T378/T382 auto-phosphorylation within the KA1 domain is linked to kinase activation and rapid proteasomal degradation, and suggest a non-canonical mechanism of regulation.
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we report that WRN-deficient cells trigger an ATM signalling, which is responsible for CHK1 phosphorylation observed after prolonged Aph-induced replication perturbation
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CHEK1 inhibition targets breast cancer cells expressing higher levels of RNF126 by enhancing replication stress.
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Chk1 phosphorylates Src-S51 to fully induce Src kinase activity and phosphorylated Src promotes formation of actin patches and stabilizes chromatin bridges.
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Cellular conditions, especially cell density, influenced the target engagement of V158411 for Chk1.
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Targeting the ATR/CHK1 axis could result in reversing of drug resistance in small cell lung cancer.
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Inhibition of checkpoint kinase 1 following gemcitabine-mediated S phase arrest results in CDC7- and CDK2-dependent replication catastrophe.
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A pulse of gemcitabine and CHK1i followed by WEE1i durably suppressed tumor cell growth.
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The ATR-Chk1 and ATM-Chk2 signalings in male breast cancer (MBC).
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control of CHK1 localization between the nucleus and cytoplasm.
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Studies indicate mechanism for translocation of Tuberous Sclerosis Complex (TSC complex) protein to lysosomes in response to DNA damage, which depends on ATM and Rad3-related protein (ATR)/checkpoint kinase 1 (Chk1)-mediated rhoB GTP-binding protein (RhoB) phosphorylation and sumoylation.
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These results indicate that, under stressful conditions, maintained mTORC1 signaling in cancer cells promotes survival by suppressing endogenous DNA damage, and may control cell fate through the regulation of CHK1.
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Chk1 and 14-3-3 proteins cooperate to inactivate the transcriptional repressor functions of atypical E2F proteins. This mechanism might be of particular importance to cancer cells, since they are exposed frequently to DNA-damaging therapeutic reagents.
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Study provides evidence that expression of CHEK1 protein is high in breast tumors arising in Nigerian women and is associated with aggressive cancer phenotypes and is a prognostic marker.
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This study reports the crystal structure of the human Chk1 putative kinase-associated 1 (KA1) domain, demonstrating striking structural homology with other sequentially diverse KA1 domains. Separately purified Chk1 kinase and KA1 domains are intimately associated in solution, which results in inhibition of Chk1 kinase activity.
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The nuclear transcription factor Y subunit beta (NFYB)-E2F transcription factor 1 (E2F1) pathway displays a crucial role in the chemoresistance ofoxaliplatin-resistant colorectal cancer (OR-CRC) by inducing the expression and activation of checkpoint kinase 1 (CHK1), suggesting a possible therapeutic target for oxaliplatin resistance in CRC.
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Blocking apoptosis alone is insufficient to allow the subsequent outgrowth of primary B cells lacking CHK1 in vivo or B lymphoma lines in vitro, as these cells trigger p53- dependent cell cycle arrest in response to the accumulating DNA damage.
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Chk1 and Chk2 are significantly expressed in human sperm. In case of sperm DNA damage, up-regulated Chk1 expression may enhance sperm apoptosis and lead to asthenospermia, while increased Chk2 expression may inhibit spermatogenesis and result in oligospermia.
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CHK1 and CHK2 and their activated forms are frequently expressed in HGSC effusions, with higher expression following exposure to chemotherapy, and their expression is related to survival.
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expression of AURKA and CHEK1 was linked with detrimental outcome in patients. Our data describe a synthetic lethality interaction between CHEK1 and AURKA inhibitors with potential translation to the clinical setting