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Human CHEK1 Protein expressed in Baculovirus infected Insect Cells - ABIN457519
Larsen, Rampalli, Burns, Brunette, Dilworth, Megeney: Caspase 3/caspase-activated DNase promote cell differentiation by inducing DNA strand breaks. dans Proceedings of the National Academy of Sciences of the United States of America 2010
PM2.5 exposure strongly induced the activation of the ATR (ATR (Montrer ANTXR1 Protéines) serine/threonine kinase (Montrer TLK2 Protéines))-CHEK1/CHK1 (checkpoint kinase 1) axis, which subsequently triggered TP53 (Montrer TP53 Protéines)-dependent autophagy and VEGFA (Montrer VEGFA Protéines) production in Beas-2B cells.
BRCA1 downregulation combined with CHK1 inhibition induced excessive amounts of DNA damage, resulting in an inability to complete the S-phase. Therefore, we suggest CHK1 inhibition as a strategy for targeting BRCA1- or CDK12 (Montrer CRKRS Protéines)-deficient tumors.
PLAUR (Montrer PLAUR Protéines) to be essential for activation of Checkpoint kinase 1 (CHK1); maintenance of cell cycle arrest after DNA damage in a TP53 (Montrer TP53 Protéines)-dependent manner; expression, nuclear import and recruitment to DNA-damage foci of RAD51 (Montrer RAD51 Protéines) recombinase (Montrer RAG1 Protéines), the principal protein involved in the homologous recombination repair pathway.
Results unveil a new aspect of PERK (Montrer EIF2AK3 Protéines) function and previously unknown roles for Claspin and Chk1 as negative regulators of DNA replication in the absence of genotoxic stress.
The findings reveal ATXN3 (Montrer ATXN3 Protéines) to be a novel deubiquitinase of Chk1, providing a new mechanism of Chk1 stabilization in genome integrity maintenance.
Small molecule ATR (Montrer ANTXR1 Protéines) and Chk1 inhibitors potently sensitize lymphoma cells to UVA radiation and induce a prominent apoptotic response
These findings demonstrate an unsuspected requirement for a balanced nucleotide pool for optimal Chk1 activation both in unchallenged cells and in response to genotoxic stress.
ATR (Montrer ANTXR1 Protéines) inhibition potentiated Chk1 inhibitor induced replication stress and cytotoxicity via the abrogation of ATR (Montrer ANTXR1 Protéines)-dependent feedback activation of Chk1 induced by Chk1 inhibitor generated replication stress in tumor cell lines.
CHK1 overexpression is associated with T-cell and Hodgkin Lymphoma.
Date show that when Wee1 (Montrer WEE1 Protéines) alone is inhibited, Chk1 suppresses CDC45 (Montrer CDC45 Protéines) loading and thereby limits the extent of unscheduled replication initiation and subsequent S-phase DNA damage, despite very high CDK (Montrer CDK4 Protéines)-activity.
Inhibition of Drf1 (Montrer DBF4B Protéines) is the primary mechanism by which Chk1 blocks cell-cycle progression in the early embryo and is an essential function of Chk1 at the blastula-to-gastrula stage of development.
The study analyzes the role of Chk1 in the replication program in sperm nuclei replicating in Xenopus egg extracts by a combination of experimental and modelling approaches.
ATR-Chk1 DDR pathway appears to be dispensable for the preferential association of REV1 to MMC-damaged chromatin.
Results show that Chk1 negatively regulates the Treslin-mediated loading of Cdc45 (Montrer CDC45 Protéines) onto chromatin and thereby serves to antagonize the initiation of replication.
The MRN complex, in particular the nuclease (Montrer DCLRE1C Protéines) activity of Mre11 (Montrer MRE11A Protéines), plays an important role in the activation of Chk1 in response to stalled replication forks.
DNA polymerase kappa (Montrer POLK Protéines)-dependent DNA synthesis at stalled replication forks is important for CHK1 activation.
APE2 (Montrer APEX2 Protéines) associates with Chk1; a serine residue (S86) in the Chk1-binding motif of APE2 (Montrer APEX2 Protéines) is essential for Chk1 phosphorylation, indicating a Claspin-like but distinct role for APE2 (Montrer APEX2 Protéines) in ATR-Chk1 signaling.
Data show that the death pathway is independent of ERK (Montrer MAPK1 Protéines) but relies on activating Bad phosphorylation through the control of both kinases Cdk1 (Montrer CDK1 Protéines) and JNK (Montrer MAPK8 Protéines).
Findings reveal that XH2AX has a specific role in anterior neural formation of Xenopus, which is mediated through phosphorylation of XH2AX at Thr (Montrer TRH Protéines)(16) by Chk1.
mechanism of Chk1 activation at the DNA replication checkpoint
During neurogenesis, cortical neurons became protected from S-phase Chk1 pathway activation by the DNA methyltransferase (Montrer DNMT1 Protéines) Dnmt1 (Montrer DNMT1 Protéines), and underwent cell death after S-phase progression.
work reveals that simulated microgravity promotes the apoptotic response through a combined modulation of the Uev1A/TICAM/TRAF (Montrer TRAF1 Protéines)/NF-kappaB (Montrer NFKB1 Protéines)-regulated apoptosis and the p53 (Montrer TP53 Protéines)/PCNA (Montrer PCNA Protéines)- and ATM (Montrer ATM Protéines)/ATR-Chk1/2-controlled DNA-damage response pathways.
Chk1(-/-) MEFs exhibited the absence of double-strand breaks, yet cells showed delayed DNA damage recovery with pan-nuclear immunostaining pattern of Histone H2AX.
RAD9 (Montrer RAD9A Protéines) has a prominent role in the ATR-Chk1 pathway that is necessary for successful formation of the damage-sensing complex and DNA damage checkpoint signaling.
Acute inactivation of E4F1 (Montrer E4F1 Protéines) in these cells results in CHK1-dependent checkpoint deficiency and multiple mitochondrial dysfunctions that lead to increased ROS (Montrer ROS1 Protéines) production, energy stress, and inhibition of de novo pyrimidine synthesis
Altogether, our results classify E4F1 (Montrer E4F1 Protéines) as a master regulator of CHK1 activity that ensures high fidelity of DNA replication, thus safeguarding genome stability.
Heterozygous loss of Chk1 in a Wnt (Montrer WNT2 Protéines)-driven background resulted in an increase in DNA damage and apoptosis and accelerated both tumour development and progression.
PAR, supplied by PARP1, interacts with Chk1 via a novel PAR-binding regulatory (PbR) motif in Chk1, independent of ATR and its activity
ATM (Montrer ATM Protéines) (pSer-1981)-Chk1 (pSer-345) cascade might have mediated G2/M cell cycle arrest to allowed time to facilitate sperm-derived DNA damage repair in mouse zygotes fertilized with oxygen-stressed sperm.
High level of phospho-Chk1 is associated with skin tumors.
The Chk1 directly phosphorylates eNOS (Montrer NOS3 Protéines) Ser (Montrer SIGLEC1 Protéines)(1179) in response to UV irradiation, which is dependent on Hsp90 (Montrer HSP90 Protéines) interaction.
The protein encoded by this gene belongs to the Ser/Thr protein kinase family. It is required for checkpoint mediated cell cycle arrest in response to DNA damage or the presence of unreplicated DNA. This protein acts to integrate signals from ATM and ATR, two cell cycle proteins involved in DNA damage responses, that also associate with chromatin in meiotic prophase I. Phosphorylation of CDC25A protein phosphatase by this protein is required for cells to delay cell cycle progression in response to double-strand DNA breaks. Several alternatively spliced transcript variants have been found for this gene.
CHK1 checkpoint homolog
, Serine/threonine-protein kinase Chk1-like protein
, serine/threonine-protein kinase Chk1
, serine/threonine-protein kinase chk1
, Checkpoint, S. pombe, homolog of, 1
, cell cycle checkpoint kinase
, checkpoint kinase-1
, Chk1 checkpoint kinase
, checkpoint kinase 1 homolog
, rad27 homolog
, integral membrane protein 1