No DDRama at chromosome ends: TRF2 takes centre stage

Telomeres are nucleoprotein structures capping the natural termini of eukaryotic linear chromosomes. Telomeres possess an inherent ability to circumvent the activation of a full-blown DNA damage response (DDR), and hence fusion reactions, by limiting inappropriate double-strand break (DSB) repair an...

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Hauptverfasser: Feuerhahn, Sascha (VerfasserIn) , Chen, Liuh-yow (VerfasserIn) , Luke, Brian (VerfasserIn) , Porro, Antonio (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 3 April 2015
In: Trends in biochemical sciences
Year: 2015, Jahrgang: 40, Heft: 5, Pages: 275-285
ISSN:1362-4326
DOI:10.1016/j.tibs.2015.03.003
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.tibs.2015.03.003
Verlag, lizenzpflichtig, Volltext: http://www.sciencedirect.com/science/article/pii/S0968000415000419
Volltext
Verfasserangaben:Sascha Feuerhahn, Liuh-yow Chen, Brian Luke, and Antonio Porro

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520 |a Telomeres are nucleoprotein structures capping the natural termini of eukaryotic linear chromosomes. Telomeres possess an inherent ability to circumvent the activation of a full-blown DNA damage response (DDR), and hence fusion reactions, by limiting inappropriate double-strand break (DSB) repair and processing activities at eukaryotic chromosome ends. A telomere-specific protein complex, termed shelterin, has a crucial function in safeguarding and securing telomere integrity. Within this complex, TRF2 has emerged as the key player, dictating different states of telomere protection during the replicative lifespan of a cell. How TRF2 prevents activation of DSB repair activities at functional telomeres has now been extensively investigated. In this review we aim at exploring the complex and multi-faceted mechanisms underlying the TRF2-mediated protection of eukaryotic chromosome ends. 
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