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Human CHEK2 Protein expressed in Wheat germ - ABIN1349305
Troncale, Barbet, Coulibaly, Henry, He, Barillot, Dubois, Hupé, de Koning: NormaCurve: a SuperCurve-based method that simultaneously quantifies and normalizes reverse phase protein array data. in PLoS ONE 2012
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present study aimed to molecularly define and determine the contribution of two rare, apparently novel CHEK2 Large Genomic Rearrangements, among Greek breast cancer patients.
CHEK2 Y390C mutation induced the drug resistance of triple negative breast cancer cells to chemotherapeutic drugs.
CHEK2 Germ Line Mutation is not associated with Familial and Sporadic Breast Cancer.
Chk1 (show CHEK1 Proteins) and Chk2 are significantly expressed in human sperm. In case of sperm DNA damage, up-regulated Chk1 (show CHEK1 Proteins) expression may enhance sperm apoptosis and lead to asthenospermia, while increased Chk2 expression may inhibit spermatogenesis and result in oligospermia.
CHK1 (show CHEK1 Proteins) 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.
first article to report that identical germline mutation of CHEK2 gene, p.R180C, exists in both NF1 (show NF1 Proteins) and NF2 (show NF2 Proteins) patients.
Results suggested that there was a correlation between mutation of the CHEK2 gene and gastric cancer.
Truncating variants in PALB2, ATM and CHEK2 , but not XRCC2 were associated with increased breast cancer risk.
our results identify a novel link between XRRA1 and the ATM (show ATM Proteins)/CHK1 (show CHEK1 Proteins)/2 pathway and suggest that XRRA1 is involved in a DNA damage response that drives radio- and chemoresistance by regulating the ATM (show ATM Proteins)/CHK1 (show CHEK1 Proteins)/2 pathway.
BRCA2 and CHEK2 play an important role in the genetic susceptibility to urinary tract cancers.
work reveals that simulated microgravity promotes the apoptotic response through a combined modulation of the Uev1A/TICAM/TRAF (show TRAF1 Proteins)/NF-kappaB (show NFKB1 Proteins)-regulated apoptosis and the p53 (show TP53 Proteins)/PCNA (show PCNA Proteins)- and ATM (show ATM Proteins)/ATR-Chk1 (show CHEK1 Proteins)/2-controlled DNA-damage response pathways.
Together, this study described the regulation of Chk2 expression through promoter methylation by Dnmt3b (show DNMT3B Proteins) 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 Proteins)-deficient spermatocytes also progress to an H1t (show HIST1H1T Proteins)-positive stage if ATM (show ATM Proteins) activity is attenuated by hypomorphic mutations in Mre11 (show MRE11A Proteins) or Nbs1 (show NBN Proteins) or by elimination of the ATM (show ATM Proteins)-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 Proteins) has central roles in the ubiquitylation of Chk2 and its turnover and in the regulation of its function.
Chk2 deficiency in Myc (show MYC Proteins) overexpressing lymphoma cells elicits a synergistic lethal response in combination with PARP (show PARP1 Proteins) inhibition.
Chk2/Cds (show ABHD5 Proteins) kinase operates at a switch between cell cycle arrest or apoptosis in response to genomic assaults.
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
, checkpoint kinase 2 L homeolog
, protein kinase Cds1