A selective requirement for 53BP1 in the biological response to genomic instability induced by Brca1 deficiency - Wikidata - awgldk - TriplyDB

A selective requirement for 53BP1 in the biological response to genomic instability induced by Brca1 deficiency

A selective requirement for 53BP1 in the biological response to genomic instability induced by Brca1 deficiency

http://www.wikidata.org/entity/Q28256846

about

BRCA1 is an essential regulator of heart function and survival following myocardial infarction 53BP1 loss rescues BRCA1 deficiency and is associated with triple-negative and BRCA-mutated breast cancers Writers, Readers, and Erasers of Histone Ubiquitylation in DNA Double-Strand Break Repair Role of Deubiquitinating Enzymes in DNA Repair Fine-tuning the ubiquitin code at DNA double-strand breaks: deubiquitinating enzymes at work 53BP1: pro choice in DNA repair BRCA1, a 'complex' protein involved in the maintenance of genomic stability DNA double-strand break repair pathway choice and cancer Repair of strand breaks by homologous recombination PARP inhibitors and more Aberrant autolysosomal regulation is linked to the induction of embryonic senescence: differential roles of Beclin 1 and p53 in vertebrate Spns1 deficiency 53BP1 mediates productive and mutagenic DNA repair through distinct phosphoprotein interactions.p53 transactivation and the impact of mutations, cofactors and small molecules using a simplified yeast-based screening system Palb2 synergizes with Trp53 to suppress mammary tumor formation in a model of inherited breast cancer The RNF8/RNF168 ubiquitin ligase cascade facilitates class switch recombination Double strand break repair functions of histone H2AX Expanded roles of the Fanconi anemia pathway in preserving genomic stability 53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks RIF1 is essential for 53BP1-dependent nonhomologous end joining and suppression of DNA double-strand break resection.The yin-yang of DNA damage response: roles in tumorigenesis and cellular senescence.53BP1 and the LINC Complex Promote Microtubule-Dependent DSB Mobility and DNA Repair Veliparib Alone or in Combination with Mitomycin C in Patients with Solid Tumors With Functional Deficiency in Homologous Recombination Repair.USP28 is recruited to sites of DNA damage by the tandem BRCT domains of 53BP1 but plays a minor role in double-strand break metabolism.PARP3 affects the relative contribution of homologous recombination and nonhomologous end-joining pathways.Crosstalk between the DNA damage response, histone modifications and neovascularisation.CtIP-mediated resection is essential for viability and can operate independently of BRCA1.Origin of chromosomal translocations in lymphoid cancer.BRCA1 and BRCA2: breast/ovarian cancer susceptibility gene products and participants in DNA double-strand break repair.miR-182-mediated downregulation of BRCA1 impacts DNA repair and sensitivity to PARP inhibitors.Regulation of DNA cross-link repair by the Fanconi anemia/BRCA pathway BRCA1 modulates the autophosphorylation status of DNA-PKcs in S phase of the cell cycle.Pathway choice in DNA double strand break repair: observations of a balancing act.Loss of ATM kinase activity leads to embryonic lethality in mice Cockayne syndrome group B protein regulates DNA double-strand break repair and checkpoint activation.BRCA1, PARP, and 53BP1: conditional synthetic lethality and synthetic viability.The role of ATM in the deficiency in nonhomologous end-joining near telomeres in a human cancer cell line.UbcH7 regulates 53BP1 stability and DSB repair The AID-induced DNA damage response in chromatin.The 53BP1 homolog in C. elegans influences DNA repair and promotes apoptosis in response to ionizing radiation HCoDES reveals chromosomal DNA end structures with single-nucleotide resolution

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P2860

A selective requirement for 53BP1 in the biological response to genomic instability induced by Brca1 deficiency

http://www.wikidata.org/entity/Q28256846

description

2009 nî lūn-bûn

@nan

2009 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2009年の論文

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2009年論文

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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

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name

A selective requirement for 53 ...... ty induced by Brca1 deficiency

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A selective requirement for 53 ...... ty induced by Brca1 deficiency

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A selective requirement for 53 ...... ty induced by Brca1 deficiency

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type

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A selective requirement for 53 ...... ty induced by Brca1 deficiency

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A selective requirement for 53 ...... ty induced by Brca1 deficiency

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A selective requirement for 53 ...... ty induced by Brca1 deficiency

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prefLabel

A selective requirement for 53 ...... ty induced by Brca1 deficiency

@ast

A selective requirement for 53 ...... ty induced by Brca1 deficiency

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A selective requirement for 53 ...... ty induced by Brca1 deficiency

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J.MOLCEL.2009.06.037

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A selective requirement for 53 ...... ty induced by Brca1 deficiency

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Andre Nussenzweig

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Chu-Xia Deng

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J Julie Wu

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Jie Liu

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Junjie Chen

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Liu Cao

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Longyue L Cao

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Rui-Hong Wang

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Samuel F Bunting

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Tie-Nan Peng

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P2860

A biomarker that identifies senescent human cells in culture and in aging skin in vivo

Structural basis for the methylation state-specific recognition of histone H4-K20 by 53BP1 and Crb2 in DNA repair

Two faces of p53: aging and tumor suppression

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

DNA damage-induced activation of p53 by the checkpoint kinase Chk2

Methylated lysine 79 of histone H3 targets 53BP1 to DNA double-strand breaks

Targeted mutations of breast cancer susceptibility gene homologs in mice: lethal phenotypes of Brca1, Brca2, Brca1/Brca2, Brca1/p53, and Brca2/p53 nullizygous embryos

Genomic instability in mice lacking histone H2AX

Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours

Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions

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