Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair. - Wikidata - wikimedia - TriplyDB

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

http://www.wikidata.org/entity/Q34883924

about

Telomere dysfunction and chromosome instability Antigenic variation and the generation of diversity in malaria parasites Telomere Biology-Insights into an Intriguing Phenomenon.Telomere proteins POT1, TRF1 and TRF2 augment long-patch base excision repair in vitro.Advances in the molecular design of potential anticancer agents via targeting of human telomeric DNA.The role of ATM in the deficiency in nonhomologous end-joining near telomeres in a human cancer cell line.Targeted DNA damage at individual telomeres disrupts their integrity and triggers cell death.De Novo ring chromosome 11 and non-reciprocal translocation of 11p15.3-pter to 21qter in a patient with congenital heart disease Mechanisms of telomere loss and their consequences for chromosome instability.Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks.TERRA, hnRNP A1, and DNA-PKcs Interactions at Human Telomeres.Sister chromatid telomere fusions, but not NHEJ-mediated inter-chromosomal telomere fusions, occur independently of DNA ligases 3 and 4.Homologous recombination-dependent repair of telomeric DSBs in proliferating human cells.Telomere-Internal Double-Strand Breaks Are Repaired by Homologous Recombination and PARP1/Lig3-Dependent End-Joining Telomere dysfunction and its role in haematological cancer.The role of telomere length modulation in delayed chromosome instability induced by ionizing radiation in human primary fibroblasts.Differences in the recruitment of DNA repair proteins at subtelomeric and interstitial I-SceI endonuclease-induced DNA double-strand breaks.Mild Telomere Dysfunction as a Force for Altering the Adaptive Potential of Subtelomeric Genes.

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P2860

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

http://www.wikidata.org/entity/Q34883924

description

2011 nî lūn-bûn

@nan

2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի ապրիլին հրատարակված գիտական հոդված

@hy

2011年の論文

@ja

2011年論文

@yue

2011年論文

@zh-hant

2011年論文

@zh-hk

2011年論文

@zh-mo

2011年論文

@zh-tw

2011年论文

@wuu

name

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

@ast

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

@en

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

@nl

type

label

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

@ast

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

@en

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

@nl

prefLabel

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

@ast

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

@en

Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

@nl

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P356

J.DNAREP.2011.03.001

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Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.

@en

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Douglas Miller

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Gloria E Reynolds

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Jeremy M Stark

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John P Murnane

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Ricardo Mejia

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P2860

Alternative-NHEJ is a mechanistically distinct pathway of mammalian chromosome break repair

Both telomeric and non-telomeric DNA damage are determinants of mammalian cellular senescence

Ku regulates the non-homologous end joining pathway choice of DNA double-strand break repair in human somatic cells

Cell-cycle-regulated association of RAD50/MRE11/NBS1 with TRF2 and human telomeres

A RAP1/TRF2 complex inhibits nonhomologous end-joining at human telomeric DNA ends

Control of human telomere length by TRF1 and TRF2

ATM damage response and XLF repair factor are functionally redundant in joining DNA breaks

The telomeric protein TRF2 binds the ATM kinase and can inhibit the ATM-dependent DNA damage response

TRF2 Protects Human Telomeres from End-to-End Fusions

IgH class switching and translocations use a robust non-classical end-joining pathway

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536-544

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scholarly article

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10.1016/J.DNAREP.2011.03.001

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5

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3084351

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