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: | , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
3 April 2015
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| 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 |
| 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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