ATR and Chk1 suppress a caspase-3-dependent apoptotic response following DNA replication stress. - Test2 - elhamkhani - TriplyDB

ATR and Chk1 suppress a caspase-3-dependent apoptotic response following DNA replication stress.

ATR and Chk1 suppress a caspase-3-dependent apoptotic response following DNA replication stress.

http://www.wikidata.org/entity/Q33396987

about

Chk1 suppressed cell death Proapoptotic Bid mediates the Atr-directed DNA damage response to replicative stress Checkpoint kinase 1 in DNA damage response and cell cycle regulation Enhanced 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 apoptosis Human telomeres are hypersensitive to UV-induced DNA Damage and refractory to repair Ataxia 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-related DNA 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 temozolomide Targeting 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 inhibition The 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 regeneration DNA damage response is hijacked by human papillomaviruses to complete their life cycle Harnessing 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.

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P2860

ATR and Chk1 suppress a caspase-3-dependent apoptotic response following DNA replication stress.

http://www.wikidata.org/entity/Q33396987

description

2009 nî lūn-bûn

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2009 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2009 թվականի հունվարին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.

@ast

ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.

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type

label

ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.

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ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.

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prefLabel

ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.

@ast

ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.

@en

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ATR and Chk1 suppress a caspas ...... lowing DNA replication stress.

@en

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Katie Myers

http://www.w3.org/2001/XMLSchema#string

Mark Meuth

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Mary E Gagou

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Pedro Zuazua-Villar

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P2860

ATM phosphorylates p95/nbs1 in an S-phase checkpoint pathway

The ATM-Chk2-Cdc25A checkpoint pathway guards against radioresistant DNA synthesis

PUMA induces the rapid apoptosis of colorectal cancer cells

PUMA, a novel proapoptotic gene, is induced by p53

Activation of mammalian Chk1 during DNA replication arrest: a role for Chk1 in the intra-S phase checkpoint monitoring replication origin firing

Chk1 and p21 cooperate to prevent apoptosis during DNA replication fork stress

Selective Chk1 inhibitors differentially sensitize p53-deficient cancer cells to cancer therapeutics

Cell-cycle checkpoints and cancer

Aberrant cell cycle checkpoint function and early embryonic death in Chk1(-/-) mice

Rapid destruction of human Cdc25A in response to DNA damage

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