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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
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DNA alkylation damage leads to ATR-Chk1 activation in cancer cells and ATR-Chk1 activation mitigates replication stress caused by mismatch repair-dependent processing of DNA damage.
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Expression levels of phosphorylated cdc25A (p-cdc25A) and phosphorylated Chk1 (p-Chk1), belonging to the ATR pathway, were decreased by treatment with Dclk1 inhibitor LRRK2-IN-1 (LRRK), indicating Dclk1 involvement in the ATR pathway
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these data demonstrate that prexasertib is a specific inhibitor of CHK1 in neuroblastoma and leads to DNA damage and cell death in preclinical models of this devastating pediatric malignancy.
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our results identify a novel link between XRRA1 and the ATM/CHK1/2 pathway and suggest that XRRA1 is involved in a DNA damage response that drives radio- and chemoresistance by regulating the ATM/CHK1/2 pathway.
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results show that HGF was involved in regulating Chk1 phosphorylation, and further demonstrate that AKT activity was responsible for this HGF-induced Chk1 phosphorylation.
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Chk1 was linked to DNA damage response bypass by suppressing JNK activation following oxidative stress, promoting cell cycle progression despite DNA damage.
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inhibition of Chk1 can potentiate activity of nucleoside analogs in TP53-mutated B-lymphoid cells
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Data show that protein phosphatase-1 alpha (PP1alpha) is required to maintain checkpoint kinase 1 (CHK1) in a dephosphorylated state and for the accelerated replication fork progression in Spi1/PU.1 transcription factor-overexpressing cells.
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Following DNA damage, addition of the TLK1 inhibitor, THD, or overexpression of NEK1-T141A mutant impaired ATR and Chk1 activation, indicating the existence of a TLK1>NEK1>ATR>Chk1 pathway. Indeed, overexpression of the NEK1-T141A mutant resulted in an altered cell cycle response after exposure of cells to oxidative stress, including bypass of G1 arrest and implementation of an intra S-phase checkpoint.
