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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. dans PLoS ONE 2012
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Among 13 early-onset breast cancer, Cowden-like and Li-Fraumeni-like syndromes Norwegian patients, gene panel sequencing identified a potentially pathogenic variant in CHEK2 that affects a canonical RNA splicing signal.
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.
work reveals that simulated microgravity promotes the apoptotic response through a combined modulation of the Uev1A/TICAM/TRAF/NF-kappaB-regulated apoptosis and the p53/PCNA- and ATM/ATR-Chk1/2-controlled DNA-damage response pathways.
Together, this study described the regulation of Chk2 expression through promoter methylation by Dnmt3b 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-deficient spermatocytes also progress to an H1t-positive stage if ATM activity is attenuated by hypomorphic mutations in Mre11 or Nbs1 or by elimination of the ATM-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 has central roles in the ubiquitylation of Chk2 and its turnover and in the regulation of its function.
Chk2 deficiency in Myc overexpressing lymphoma cells elicits a synergistic lethal response in combination with PARP inhibition.
Point mutation at the Nbs1 Threonine 278 site does not affect mouse development, but compromises the Chk2 and Smc1 phosphorylation after DNA damage.
data indicate that an important role for Chk2 is maintaining lymphocyte development and that dual inactivation of Chk2 and Mus81 remarkably inhibits cancer
Loss of ATM/Chk2/p53 pathway components accelerates tumor development and contributes to radiation resistance in gliomas.
Results suggest that the Chk1/2 double mutation leads to a high level of spontaneous DNA damage, but fails to eliminate cells with damaged DNA, which may ultimately increase cancer susceptibility independently of senescence.
Results indicate that CHK2 mediates the induction of senescence in fibroblasts, but is dispensable for the induction of telomere dysfunction checkpoints at the stem and progenitor cell level in vivo.
Ron overexpression on a Chk2*1100 deletion background accelerates the development of mammary tumors.
Study show that mice carrying the variant CHEK2*1100delC allele not only are at an elevated risk for the development of cancer but also that this risk can be further increased as a result of environmental exposure.
role of Chk2 in p53-dependent apoptotic response
Chk2 regulates apoptosis in both an ataxia telangiectasia mutated (ATM)-dependent and an ATM-independent manner
results show that Chk2 plays a critical role in p53 function in response to IR by regulating its transcriptional activity as well as its stability
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