據近期一篇發表於EMBO Journal的研究報告稱，Stowers研究所的研究人員發現一種名為hRAP1的蛋白在細胞中能夠阻止染色體末端與DNA斷裂位點融合，從而起到保護染色體的末端的功能。
染色體末端(也稱端粒)發生錯誤融合將導致基因組不穩定，從而導致癌症發生。這項研究表明，在人類癌症預防中，RAP1發揮著極其重要的作用。
據研究人員Jay Sarthy介紹，自然地保護染色體末端的損耗和融合能延長人的壽命和減少癌症的患病風險。該蛋白保護染色體末端的功能將給科學家提供一種延緩衰老和癌症的新靶標。
將hRAP1作為一種重要的染色體末端保護因子，對研究人員理解DNA修復過程非常重要。該課題組打算繼續致力於研究在DNA修復過程中，hRAP1是如何保護端粒的。（生物谷Bioon.com）
生物谷推薦原始出處：
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.