Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1. - Wikidata - wikimedia - TriplyDB

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

http://www.wikidata.org/entity/Q34262604

about

Role of Deubiquitinating Enzymes in DNA Repair Relative contribution of four nucleases, CtIP, Dna2, Exo1 and Mre11, to the initial step of DNA double-strand break repair by homologous recombination in both the chicken DT40 and human TK6 cell lines Regulation of pairing between broken DNA-containing chromatin regions by Ku80, DNA-PKcs, ATM, and 53BP1 Inhibiting DNA-PKcs in a non-homologous end-joining pathway in response to DNA double-strand breaks.Synthetic viability genomic screening defines Sae2 function in DNA repair.Regulators of homologous recombination repair as novel targets for cancer treatment.Smarcal1 promotes double-strand-break repair by nonhomologous end-joining.Impaired 53BP1/RIF1 DSB mediated end-protection stimulates CtIP-dependent end resection and switches the repair to PARP1-dependent end joining in G1.53BP1 Protects against CtIP-Dependent Capture of Ectopic Chromosomal Sequences at the Junction of Distant Double-Strand Breaks.Repair Pathway Choices and Consequences at the Double-Strand Break The DNA resection protein CtIP promotes mammary tumorigenesis.Single-stranded DNA oligomers stimulate error-prone alternative repair of DNA double-strand breaks through hijacking Ku protein.Efficient Rejoining of DNA Double-Strand Breaks despite Increased Cell-Killing Effectiveness following Spread-Out Bragg Peak Carbon-Ion Irradiation.The control of DNA repair by the cell cycle.A Process of Resection-Dependent Nonhomologous End Joining Involving the Goddess Artemis.Nek1 Regulates Rad54 to Orchestrate Homologous Recombination and Replication Fork Stability.Coordinated nuclease activities counteract Ku at single-ended DNA double-strand breaks.DNA Double-Strand Break Resection Occurs during Non-homologous End Joining in G1 but Is Distinct from Resection during Homologous Recombination.The ubiquitin ligase APC/C(Cdh1) puts the brakes on DNA-end resection.DNA repair with a hefty price tag.Screening of Pesticides with the Potential of Inducing DSB and Successive Recombinational Repair.DNA non-homologous end-joining enters the resection arena.Repair of DNA double-strand breaks by mammalian alternative end-joining pathways.Identification of DNA double strand breaks at chromosome boundaries along the track of particle irradiation.Biased genome editing using the local accumulation of DSB repair molecules system TDP1 suppresses mis-joining of radiomimetic DNA double-strand breaks and cooperates with Artemis to promote optimal nonhomologous end joining

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Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

http://www.wikidata.org/entity/Q34262604

description

2014 nî lūn-bûn

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2014 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2014年の論文

@ja

2014年論文

@yue

2014年論文

@zh-hant

2014年論文

@zh-hk

2014年論文

@zh-mo

2014年論文

@zh-tw

2014年论文

@wuu

name

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

@ast

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

@en

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

@nl

type

label

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

@ast

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

@en

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

@nl

prefLabel

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

@ast

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

@en

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.

@nl

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Journal of Cell Biology

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Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1

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Jiadong Wang

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Julia Künzel

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

Junjie Chen

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

Lin Feng

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

Markus Löbrich

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

Monika Steinlage

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

Nodar Makharashvili

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

Olivia Barton

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

Penny A Jeggo

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

Ronja Diemer-Biehs

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

P2860

A probability-based approach for high-throughput protein phosphorylation analysis and site localization

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

Polo-like kinase 3 is required for entry into S phase

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

CDK targets Sae2 to control DNA-end resection and homologous recombination

The DNA-damage response in human biology and disease

Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications

Radiation exposure from CT scans in childhood and subsequent risk of leukaemia and brain tumours: a retrospective cohort study

Human CtIP promotes DNA end resection

ATM and Artemis promote homologous recombination of radiation-induced DNA double-strand breaks in G2

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877-894

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scholarly article

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10.1083/JCB.201401146

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7

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206

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2014-09-01T00:00:00Z

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266264957

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25267294

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4178966

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