ATR and Chk1 suppress a caspase-3-dependent apoptotic response following DNA replication stress.
about
Chk1 suppressed cell deathProapoptotic Bid mediates the Atr-directed DNA damage response to replicative stressCheckpoint kinase 1 in DNA damage response and cell cycle regulationEnhanced H2AX phosphorylation, DNA replication fork arrest, and cell death in the absence of Chk1.Convergent transcription through a long CAG tract destabilizes repeats and induces apoptosisHuman telomeres are hypersensitive to UV-induced DNA Damage and refractory to repairAtaxia telangiectasia mutated- and Rad3-related kinase drives both the early and the late DNA-damage response to the monofunctional antitumour alkylator S23906.Impaired tissue growth is mediated by checkpoint kinase 1 (CHK1) in the integrated stress response.New insights into checkpoint kinase 1 in the DNA damage response signaling network.New insights into the link between DNA damage and apoptosis.Assessment of chk1 phosphorylation as a pharmacodynamic biomarker of chk1 inhibition.S phase entry causes homocysteine-induced death while ataxia telangiectasia and Rad3 related protein functions anti-apoptotically to protect neurons.DNA replication stress in CHK1-depleted tumour cells triggers premature (S-phase) mitosis through inappropriate activation of Aurora kinase B.The fork and the kinase: a DNA replication tale from a CHK1 perspective.Enhancement of hypoxia-activated prodrug TH-302 anti-tumor activity by Chk1 inhibition.Trovafloxacin-induced replication stress sensitizes HepG2 cells to tumor necrosis factor-alpha-induced cytotoxicity mediated by extracellular signal-regulated kinase and ataxia telangiectasia and Rad3-relatedDNA Damage and Repair Biomarkers in Cervical Cancer Patients Treated with Neoadjuvant Chemotherapy: An Exploratory Analysis.Repair of 3-methyladenine and abasic sites by base excision repair mediates glioblastoma resistance to temozolomideTargeting ATR in vivo using the novel inhibitor VE-822 results in selective sensitization of pancreatic tumors to radiation.DNA damage response in cisplatin-induced nephrotoxicity.A cell-based screen identifies ATR inhibitors with synthetic lethal properties for cancer-associated mutations.Repression of ATR pathway by miR-185 enhances radiation-induced apoptosis and proliferation inhibitionThe DNA-PK catalytic subunit regulates Bax-mediated excitotoxic cell death by Ku70 phosphorylation.Dual inactivation of Hus1 and p53 in the mouse mammary gland results in accumulation of damaged cells and impaired tissue regenerationDNA damage response is hijacked by human papillomaviruses to complete their life cycleHarnessing the complexity of DNA-damage response pathways to improve cancer treatment outcomes.DNA repair and cell cycle checkpoint defects as drivers and therapeutic targets in melanoma.Mismatch repair enhances convergent transcription-induced cell death at trinucleotide repeats by activating ATR.Screening analysis of ubiquitin ligases reveals G2E3 as a potential target for chemosensitizing cancer cells.DNA damage-induced S and G2/M cell cycle arrest requires mTORC2-dependent regulation of Chk1.CHK1 overexpression in T-cell acute lymphoblastic leukemia is essential for proliferation and survival by preventing excessive replication stress.Differential response of normal and malignant urothelial cells to CHK1 and ATM inhibitors.Inhibition of the checkpoint kinase Chk1 induces DNA damage and cell death in human Leukemia and Lymphoma cells.Excessive MET signaling causes acquired resistance and addiction to MET inhibitors in the MKN45 gastric cancer cell line.HMGA2 inhibits apoptosis through interaction with ATR-CHK1 signaling complex in human cancer cells.Cell cycle-tailored targeting of metastatic melanoma: Challenges and opportunities.DNA damage-induced CHK1 autophosphorylation at Ser296 is regulated by an intramolecular mechanism.Human embryonic stem cells fail to activate CHK1 and commit to apoptosis in response to DNA replication stress.A potent Chk1 inhibitor is selectively cytotoxic in melanomas with high levels of replicative stress.Efficacy of CHK inhibitors as single agents in MYC-driven lymphoma cells.
P2860
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P2860
ATR and Chk1 suppress a caspase-3-dependent apoptotic response following DNA replication stress.
description
2009 nî lūn-bûn
@nan
2009 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
name
ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.
@ast
ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.
@en
type
label
ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.
@ast
ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.
@en
prefLabel
ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.
@ast
ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.
@en
P2093
P2860
P1433
P1476
ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.
@en
P2093
Katie Myers
Mark Meuth
Mary E Gagou
Pedro Zuazua-Villar
P2860
P304
P356
10.1371/JOURNAL.PGEN.1000324
P50
P577
2009-01-02T00:00:00Z