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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 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.
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.
first article to report that identical germline mutation of CHEK2 gene, p.R180C, exists in both NF1 and NF2 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/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.
BRCA2 and CHEK2 play an important role in the genetic susceptibility to urinary tract cancers.
Checkpoint kinase 2 (Chk2) inhibition suppressed C-terminal acetylation of p53 and delayed the induction of p53-target genes under heat stress (HS). Chk2 inhibition failed to inhibit apoptosis induced by HS, indicating that Chk2 was dispensable for p53-dependent apoptosis under HS. Chk2 inhibition abrogated G2/M arrest and promoted cell death induced by HS in cells with p53 defects.
The inhibition CHK2 expression reduced detachment-induced apoptosis but did not influence the ability of cells to migrate and invade, which illustrates that CHK2 could inhibit tumor progression and metastatic potential by enhancing anoikis.
These data suggest that the CHEK2 c.1100delC mutation is associated with an increased risk for MBC in the Finnish population.
Data suggest that mediator complex subunit 1 (Med1/TRAP220) is a target for checkpoint kinase 2 (Chk2)-mediated phosphorylation and may play a role in cellular DNA damage responses by mediating proper induction of gene transcription upon DNA damage.
this report conceives a novel strategy of Twist1 suppression through Chk2 induction, which prevents metastatic dissemination and promotes premature senescence in p53-defective invasive cancer cells.
we have provided evidence in this study that hepatocarcinogenesis with lagging chromosomes elicits the expression of DNA damage response protein Chk2. Thus, the overexpression of Chk2 and its mislocalisation within structures of the mitotic spindle contribute to sustain cell division and chromosomes missegregation.
PI3K kinase activity is necessary for maintaining 4E-BP1 stability. Our results also suggest 4E-BP1 a novel biological role of regulating cell cycle G2 checkpoint in responding to IR stress in association with controlling CHK2 phosphorylation
Data show that the checkpoint kinase 1/2 (Chk1/Chk2) inhibitor prexasertib (LY2606368) inhibits cell viability in B-/T-ALL cell lines.
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.
Chk2/Cds 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