ATR signaling can drive cells into senescence in the absence of DNA breaks. - Wikidata - awgldk - TriplyDB

ATR signaling can drive cells into senescence in the absence of DNA breaks.

ATR signaling can drive cells into senescence in the absence of DNA breaks.

http://www.wikidata.org/entity/Q36411149

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Miz1 and HectH9 regulate the stability of the checkpoint protein, TopBP1 Targeting ATR and Chk1 kinases for cancer treatment: a new model for new (and old) drugs Common mechanisms of PIKK regulation Linking replication stress with heterochromatin formation Chromatin perturbations during the DNA damage response in higher eukaryotes Chemical strategies for development of ATR inhibitors Activation of the ATR kinase by the RPA-binding protein ETAA1 ETAA1 acts at stalled replication forks to maintain genome integrity ATR: an essential regulator of genome integrity A p53-mediated DNA damage response limits reprogramming to ensure iPS cell genomic integrity H2AX is required for cell cycle arrest via the p53/p21 pathway Persistent telomere damage induces bypass of mitosis and tetraploidy.Mitochondrial hyperfusion induced by loss of the fission protein Drp1 causes ATM-dependent G2/M arrest and aneuploidy through DNA replication stress Retinoblastoma loss modulates DNA damage response favoring tumor progression Akt/PKB suppresses DNA damage processing and checkpoint activation in late G2.Functional significance for a heterogenous ribonucleoprotein A18 signature RNA motif in the 3'-untranslated region of ataxia telangiectasia mutated and Rad3-related (ATR) transcript.Tumor suppression by p53: making cells senescent.Aging, cellular senescence, and cancer Akt: a double-edged sword in cell proliferation and genome stability.Cooperative functions of Chk1 and Chk2 reduce tumour susceptibility in vivo Interferon-β induces cellular senescence in cutaneous human papilloma virus-transformed human keratinocytes by affecting p53 transactivating activity Unfolded p53 in the pathogenesis of Alzheimer's disease: is HIPK2 the link?Absence of p53-dependent apoptosis leads to UV radiation hypersensitivity, enhanced immunosuppression and cellular senescence.RNAi screen of the protein kinome identifies checkpoint kinase 1 (CHK1) as a therapeutic target in neuroblastoma p53 governs telomere regulation feedback too, via TRF2.TRPM7 regulates quiescent/proliferative metabolic transitions in lymphocytes.Tethering DNA damage checkpoint mediator proteins topoisomerase IIbeta-binding protein 1 (TopBP1) and Claspin to DNA activates ataxia-telangiectasia mutated and RAD3-related (ATR) phosphorylation of checkpoint kinase 1 (Chk1)The tumor suppressor PML specifically accumulates at RPA/Rad51-containing DNA damage repair foci but is nonessential for DNA damage-induced fibroblast senescence.Modelling the onset of senescence at the G1/S cell cycle checkpoint.High levels of TopBP1 induce ATR-dependent shut-down of rRNA transcription and nucleolar segregation.Key role of dual specificity kinase TTK in proliferation and survival of pancreatic cancer cells.Caffeic acid phenethyl ester induced cell cycle arrest and growth inhibition in androgen-independent prostate cancer cells via regulation of Skp2, p53, p21Cip1 and p27Kip1.Molecular damage in cancer: an argument for mTOR-driven aging TOPBP1 regulates RAD51 phosphorylation and chromatin loading and determines PARP inhibitor sensitivity.Polygenic effects of common single-nucleotide polymorphisms on life span: when association meets causality.Inhibition of Chk1 with the small molecule inhibitor V158411 induces DNA damage and cell death in an unperturbed S-phase.S-phase-dependent p50/NF-кB1 phosphorylation in response to ATR and replication stress acts to maintain genomic stability The emerging role of nuclear architecture in DNA repair and genome maintenance.The ATR barrier to replication-born DNA damage.An autonomous chromatin/DNA-PK mechanism for localized DNA damage signaling in mammalian cells.

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ATR signaling can drive cells into senescence in the absence of DNA breaks.

http://www.wikidata.org/entity/Q36411149

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年學術文章

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2008年學術文章

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2008年學術文章

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ATR signaling can drive cells into senescence in the absence of DNA breaks.

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ATR signaling can drive cells into senescence in the absence of DNA breaks.

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type

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ATR signaling can drive cells into senescence in the absence of DNA breaks.

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ATR signaling can drive cells into senescence in the absence of DNA breaks.

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ATR signaling can drive cells into senescence in the absence of DNA breaks.

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ATR signaling can drive cells into senescence in the absence of DNA breaks.

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Genes & Development

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ATR signaling can drive cells into senescence in the absence of DNA breaks.

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P2093

Luis I Toledo

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

Matilde Murga

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

Oscar Fernandez-Capetillo

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

Paula Gutierrez-Martinez

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Rebeca Soria

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P2860

Linkage of ATM to cell cycle regulation by the Chk2 protein kinase

SMC1 is a downstream effector in the ATM/NBS1 branch of the human S-phase checkpoint

Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

Chk1 is an essential kinase that is regulated by Atr and required for the G(2)/M DNA damage checkpoint

Involvement of the cohesin protein, Smc1, in Atm-dependent and independent responses to DNA damage

Evidence for a lack of DNA double-strand break repair in human cells exposed to very low x-ray doses

Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis

ATM phosphorylates histone H2AX in response to DNA double-strand breaks

Histone H2AX is phosphorylated in an ATR-dependent manner in response to replicational stress

ATR/ATM-mediated phosphorylation of human Rad17 is required for genotoxic stress responses

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10.1101/GAD.452308

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3

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22

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