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The Role of Double-Strand Break Repair Pathways at Functional and Dysfunctional Telomeres.
MedLine Citation:
PMID:  25228584     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Telomeres have evolved to protect the ends of linear chromosomes from the myriad of threats posed by the cellular DNA damage signaling and repair pathways. Mammalian telomeres have to block nonhomologous end joining (NHEJ), thus preventing chromosome fusions; they need to control homologous recombination (HR), which could change telomere lengths; they have to avoid activating the ATM (ataxia telangiectasia mutated) and ATR (ATM- and RAD3-related) kinase pathways, which could induce cell cycle arrest; and they have to protect chromosome ends from hyperresection. Recent studies of telomeres have provided insights into the mechanisms of NHEJ and HR, how these double-strand break (DSB) repair pathways can be thwarted, and how telomeres have co-opted DNA repair factors to help in the protection of chromosome ends. These aspects of telomere biology are reviewed here with particular emphasis on recombination, the main focus of this collection.
Authors:
Ylli Doksani; Titia de Lange
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-9-16
Journal Detail:
Title:  Cold Spring Harbor perspectives in biology     Volume:  -     ISSN:  1943-0264     ISO Abbreviation:  Cold Spring Harb Perspect Biol     Publication Date:  2014 Sep 
Date Detail:
Created Date:  2014-9-17     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101513680     Medline TA:  Cold Spring Harb Perspect Biol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014 Cold Spring Harbor Laboratory Press; all rights reserved.
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