据近期一篇发表于EMBO Journal的研究报告称，Stowers研究所的研究人员发现一种名为hRAP1的蛋白在细胞中能够阻止染色体末端与DNA断裂位点融合，从而起到保护染色体的末端的功能。
染色体末端(也称端粒)发生错误融合将导致基因组不稳定，从而导致癌症发生。这项研究表明，在人类癌症预防中，RAP1发挥着极其重要的作用。
据研究人员Jay Sarthy介绍，自然地保护染色体末端的损耗和融合能延长人的寿命和减少癌症的患病风险。该蛋白保护染色体末端的功能将给科学家提供一种延缓衰老和癌症的新靶标。
将hRAP1作为一种重要的染色体末端保护因子，对研究人员理解DNA修复过程非常重要。该课题组打算继续致力于研究在DNA修复过程中，hRAP1是如何保护端粒的。（生物谷Bioon.com）
生物谷推荐原始出处：
The EMBO Journal advance online publication 17 September 2009; doi:10.1038/emboj.2009.275
Human RAP1 inhibits non-homologous end joining at telomeres
Jay Sarthy1,2, Nancy S Bae1, Jonathan Scrafford1 and Peter Baumann1,3
1 Stowers Institute for Medical Research, Kansas City, MO, USA
2 Department of Molecular Biosciences, University of Kansas, Lawrence, KS, USA
3 Department of Molecular and Integrative Physiology, Kansas University Medical Center, Kansas City, KS, USA
Telomeres, the nucleoprotein structures at the ends of linear chromosomes, promote genome stability by distinguishing chromosome termini from DNA double-strand breaks (DSBs). Cells possess two principal pathways for DSB repair: homologous recombination and non-homologous end joining (NHEJ). Several studies have implicated TRF2 in the protection of telomeres from NHEJ, but the underlying mechanism remains poorly understood. Here, we show that TRF2 inhibits NHEJ, in part, by recruiting human RAP1 to telomeres. Heterologous targeting of hRAP1 to telomeric DNA was sufficient to bypass the need for TRF2 in protecting telomeric DNA from NHEJ in vitro. On expanding these studies in cells, we find that recruitment of hRAP1 to telomeres prevents chromosome fusions caused by the loss of TRF2/hRAP1 from chromosome ends despite activation of a DNA damage response. These results provide the first evidence that hRAP1 inhibits NHEJ at mammalian telomeres and identify hRAP1 as a mediator of genome stability.
