The interaction of CtIP and Nbs1 connects CDK and ATM to regulate HR-mediated double-strand break repair. - Wikidata - awgldk - TriplyDB

The interaction of CtIP and Nbs1 connects CDK and ATM to regulate HR-mediated double-strand break repair.

The interaction of CtIP and Nbs1 connects CDK and ATM to regulate HR-mediated double-strand break repair.

http://www.wikidata.org/entity/Q34611192

about

DNA Damage Signalling and Repair Inhibitors: The Long-Sought-After Achilles' Heel of Cancer BRCA1 and CtIP Are Both Required to Recruit Dna2 at Double-Strand Breaks in Homologous Recombination Protein kinase C-η controls CTLA-4-mediated regulatory T cell function.Phosphorylation of EXO1 by CDKs 1 and 2 regulates DNA end resection and repair pathway choice.CtIP maintains stability at common fragile sites and inverted repeats by end resection-independent endonuclease activity.End resection at double-strand breaks: mechanism and regulation.Off-Line Multidimensional Liquid Chromatography and Auto Sampling Result in Sample Loss in LC/LC-MS/MS.Productive replication of human papillomavirus 31 requires DNA repair factor Nbs1.Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.Homologous recombination is a primary pathway to repair DNA double-strand breaks generated during DNA rereplication RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand Breaks.Regulators of homologous recombination repair as novel targets for cancer treatment.SV40 utilizes ATM kinase activity to prevent non-homologous end joining of broken viral DNA replication products DNA end resection is needed for the repair of complex lesions in G1-phase human cells.Phosphorylation of Sae2 Mediates Forkhead-associated (FHA) Domain-specific Interaction and Regulates Its DNA Repair Function.Two separable functions of Ctp1 in the early steps of meiotic DNA double-strand break repair EXO1 is critical for embryogenesis and the DNA damage response in mice with a hypomorphic Nbs1 allele.Impaired 53BP1/RIF1 DSB mediated end-protection stimulates CtIP-dependent end resection and switches the repair to PARP1-dependent end joining in G1.CtIP-Specific Roles during Cell Reprogramming Have Long-Term Consequences in the Survival and Fitness of Induced Pluripotent Stem Cells NBS1 Phosphorylation Status Dictates Repair Choice of Dysfunctional Telomeres.Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks.Repair Pathway Choices and Consequences at the Double-Strand Break Controlling DNA-end resection: a new task for CDKs.Sharpening the ends for repair: mechanisms and regulation of DNA resection.Tetratricopeptide repeat factor XAB2 mediates the end resection step of homologous recombination Mechanism and regulation of DNA end resection in eukaryotes Disease-associated MRE11 mutants impact ATM/ATR DNA damage signaling by distinct mechanisms.Triapine disrupts CtIP-mediated homologous recombination repair and sensitizes ovarian cancer cells to PARP and topoisomerase inhibitors.The Elephant and the Blind Men: Making Sense of PARP Inhibitors in Homologous Recombination Deficient Tumor Cells.CtIP/Ctp1/Sae2, molecular form fit for function.Augmented HR Repair Mediates Acquired Temozolomide Resistance in Glioblastoma.USP4 Auto-Deubiquitylation Promotes Homologous Recombination.Cyclin D1 promotes BRCA2-Rad51 interaction by restricting cyclin A/B-dependent BRCA2 phosphorylation.Hereditary breast and ovarian cancer: new genes in confined pathways.miR-19, a component of the oncogenic miR-17∼92 cluster, targets the DNA-end resection factor CtIP.Catalytic and noncatalytic roles of the CtIP endonuclease in double-strand break end resection The control of DNA repair by the cell cycle.New factors in mammalian DNA repair-the chromatin connection.Cell cycle-dependent control of homologous recombination.Homologous Recombination Repair Factors Rad51 and BRCA1 Are Necessary for Productive Replication of Human Papillomavirus 31.

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The interaction of CtIP and Nbs1 connects CDK and ATM to regulate HR-mediated double-strand break repair.

http://www.wikidata.org/entity/Q34611192

description

2013 nî lūn-bûn

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2013 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2013 թվականի փետրվարին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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name

The interaction of CtIP and Nb ...... ed double-strand break repair.

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The interaction of CtIP and Nb ...... ed double-strand break repair.

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The interaction of CtIP and Nb ...... ed double-strand break repair.

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The interaction of CtIP and Nb ...... ed double-strand break repair.

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The interaction of CtIP and Nb ...... ed double-strand break repair.

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The interaction of CtIP and Nb ...... ed double-strand break repair.

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The interaction of CtIP and Nb ...... ed double-strand break repair.

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The interaction of CtIP and Nb ...... ed double-strand break repair.

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The interaction of CtIP and Nb ...... ed double-strand break repair.

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JOURNAL.PGEN.1003277

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The interaction of CtIP and Nb ...... ed double-strand break repair.

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Catherine C L Wong

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David J Chen

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Hailong Wang

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John R Yates

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Lan N Truong

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

Linda Z Shi

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

Longchuan Chen

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

Michael W Berns

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

Patty Yi-Hwa Hwang

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Qingyuan Zhu

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

P2860

The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway

Nuclear localization and cell cycle-specific expression of CtIP, a protein that associates with the BRCA1 tumor suppressor

Functional link of BRCA1 and ataxia telangiectasia gene product in DNA damage response

BLM-DNA2-RPA-MRN and EXO1-BLM-RPA-MRN constitute two DNA end resection machineries for human DNA break repair

MDC1 directly binds phosphorylated histone H2AX to regulate cellular responses to DNA double-strand breaks

A divalent FHA/BRCT-binding mechanism couples the MRE11-RAD50-NBS1 complex to damaged chromatin

DNA end resection by CtIP and exonuclease 1 prevents genomic instability

DNA damage-induced cell cycle checkpoint control requires CtIP, a phosphorylation-dependent binding partner of BRCA1 C-terminal domains

N terminus of CtIP is critical for homologous recombination-mediated double-strand break repair

Nibrin, a novel DNA double-strand break repair protein, is mutated in Nijmegen breakage syndrome

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10.1371/JOURNAL.PGEN.1003277

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2013-02-28T00:00:00Z

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