端粒：并非所有断裂都是相同的。

Telomeres: not all breaks are equal.

作者信息

Purdy Amanda, Su Tin Tin

机构信息

Molecular, Cellular and Developmental Biology, 347UCB, University of Colorado, Boulder, Colorado, USA.

出版信息

Curr Biol. 2004 Aug 10;14(15):R613-4. doi: 10.1016/j.cub.2004.07.042.

DOI:10.1016/j.cub.2004.07.042

PMID:15296775

Abstract

ATM, Rad50 and Mre11 have been shown to prevent telomere fusion in Drosophila, thereby extending the protective role of DNA damage checkpoint proteins to non-canonical telomeres formed without telomerase. How do these proteins help chromosomal termini escape fusion through 'repair' while promoting repair of induced DNA breaks?

摘要

已证明，ATM、Rad50和Mre11可防止果蝇中的端粒融合，从而将DNA损伤检查点蛋白的保护作用扩展至在没有端粒酶的情况下形成的非典型端粒。这些蛋白质如何在促进诱导性DNA断裂修复的同时，通过“修复”帮助染色体末端避免融合？