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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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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.
Checkpoint kinase 2 (Chk2) inhibition suppressed C-terminal acetylation of p53 (show TP53 Proteins) and delayed the induction of p53 (show TP53 Proteins)-target genes under heat stress (HS). Chk2 inhibition failed to inhibit apoptosis induced by HS, indicating that Chk2 was dispensable for p53 (show TP53 Proteins)-dependent apoptosis under HS. Chk2 inhibition abrogated G2/M arrest and promoted cell death induced by HS in cells with p53 (show TP53 Proteins) 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 (show MED1 Proteins)) 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 (show TWIST1 Proteins) suppression through Chk2 induction, which prevents metastatic dissemination and promotes premature senescence in p53 (show TP53 Proteins)-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 (show PIK3CA Proteins) kinase activity is necessary for maintaining 4E-BP1 (show EIF4EBP1 Proteins) stability. Our results also suggest 4E-BP1 (show EIF4EBP1 Proteins) a novel biological role of regulating cell cycle G2 checkpoint in responding to IR stress in association with controlling CHK2 phosphorylation
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