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Results confirm the predicted multiplicative relationship between CHEK2*1100delC and the common low-penetrance susceptibility variants for breast cancer.
Results show that Chk2 expression is regulated by 14-3-3s in G2-M arrest for non-homologous end joining repair probably via PARP1 (show PARP1 ELISA Kits).
Results indicate that CHEK2 possesses non-cell-autonomous tumor suppressor functions, and present the Chk2 protein as an important mediator in the functional interplay between breast carcinomas and their stromal fibroblasts through repressing the expression/secretion of SDF-1 (show CXCL12 ELISA Kits) and IL-6 (show IL6 ELISA Kits).
variants in CHEK2 were associated with moderate risks of breast cancer.
In this paper, we describe an extension to the BOADICEA model to incorporate the effects of intermediate risk variants for breast cancer, specifically loss of function mutations in the three genes for which the evidence for association is clearest and the risk estimates most precise: PALB2 (show PALB2 ELISA Kits), CHEK2 and ATM (show ATM ELISA Kits)
SIAH2 (show SIAH2 ELISA Kits) regulates CHK2 basal turnover, with important consequences on cell-cycle control and on the ability of hypoxia to alter the DNA damage-response pathway in cancer cells.
MCM2 (show MCM2 ELISA Kits)-MCM6 (show MCM6 ELISA Kits) complex is required for CHK2 chromatin loading and its phosphorylation to DNA damage response in squamous cell carcinoma cells.
On the basis of analyses of approximately 87,000 controls and patients with breast cancer from population- and hospital-based studies, our best estimate for the relative risk of invasive breast cancer for carriers of the 1100delC mutation in CHEK2, compared with noncarriers, was 2.26 (95% CI, 1.90 to 2.69).
the G2 damage checkpoint prevents stable recruitment of the chromosome-packaging-machinery components condensin complex (show SMC4 ELISA Kits) I and II onto the chromatin even in the presence of an active Cdk1 (show CDK1 ELISA Kits).
data suggest that cancer risks reported for founder mutations may be generalizable to all CHEK2 + s, particularly for breast cancer
work reveals that simulated microgravity promotes the apoptotic response through a combined modulation of the Uev1A/TICAM/TRAF (show TRAF1 ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits)-regulated apoptosis and the p53 (show TP53 ELISA Kits)/PCNA (show PCNA ELISA Kits)- and ATM (show ATM ELISA Kits)/ATR (show ATR ELISA Kits)-Chk1 (show CHEK1 ELISA Kits)/2-controlled DNA-damage response pathways.
Together, this study described the regulation of Chk2 expression through promoter methylation by Dnmt3b (show DNMT3B ELISA Kits) and also presented a novel role of Chk2 during neuronal differentiation, which is independent of its previously known function in DNA damage response.
We conclude that Chk2 regulates renal 25-hydroxyvitamin D 1alpha-hydroxylase expression thereby impacting on calcium and phosphate metabolism.
TRIP13 (show TRIP13 ELISA Kits)-deficient spermatocytes also progress to an H1t (show HIST1H1T ELISA Kits)-positive stage if ATM (show ATM ELISA Kits) activity is attenuated by hypomorphic mutations in Mre11 (show MRE11A ELISA Kits) or Nbs1 (show NBN ELISA Kits) or by elimination of the ATM (show ATM ELISA Kits)-effector kinase CHK2
Results represent the first demonstration of a role for CHK2 in the in vivo signaling of dysfunctional telomeres.
DNA-PK/Chk2 signaling induces centrosome amplification upon long-term HU treatment, therefore increasing our insight into tumor recurrence after initial chemotherapy.
Results demonstrate that Chk2 plays important roles in regulating cell cycle progression during female meiosis and early embryo development.
These data establish CHK2 as essential for DNA damage surveillance in female meiosis and indicate that the oocyte DNA double-strand breaks damage response primarily involves a pathway hierarchy in which ataxia telangiectasia and Rad3-related (ATR) signals to CHK2, which then activates p53 and p63.
Findings indicate that PIRH2 (show RCHY1 ELISA Kits) has central roles in the ubiquitylation of Chk2 and its turnover and in the regulation of its function.
Chk2 deficiency in Myc (show MYC ELISA Kits) overexpressing lymphoma cells elicits a synergistic lethal response in combination with PARP (show PARP1 ELISA Kits) inhibition.
In response to DNA damage and replication blocks, cell cycle progression is halted through the control of critical cell cycle regulators. The protein encoded by this gene is a cell cycle checkpoint regulator and putative tumor suppressor. It contains a forkhead-associated protein interaction domain essential for activation in response to DNA damage and is rapidly phosphorylated in response to replication blocks and DNA damage. When activated, the encoded protein is known to inhibit CDC25C phosphatase, preventing entry into mitosis, and has been shown to stabilize the tumor suppressor protein p53, leading to cell cycle arrest in G1. In addition, this protein interacts with and phosphorylates BRCA1, allowing BRCA1 to restore survival after DNA damage. Mutations in this gene have been linked with Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53. Also, mutations in this gene are thought to confer a predisposition to sarcomas, breast cancer, and brain tumors. This nuclear protein is a member of the CDS1 subfamily of serine/threonine protein kinases. Several transcript variants encoding different isoforms have been found for this gene.
CHK2 checkpoint homolog
, cds1 homolog
, checkpoint-like protein CHK2
, serine/threonine-protein kinase Chk2
, protein kinase CHK2
, checkpoint and tumor suppressor protein 2
, Cds1 homolog
, Rad53 homolog
, protein kinase Chk2
, CHK2 checkpoint homolog (S. pombe)
, serine/threonine-protein kinase Chk2-like
, serine/threonine-protein kinase chk2
, blue cone photoreceptor pigment
, blue-sensitive opsin
, opsin CHK-2