热休克诱导的TRF2从端粒解离不会引发端粒依赖性DNA损伤反应。

Heat shock-induced dissociation of TRF2 from telomeres does not initiate a telomere-dependent DNA damage response.

作者信息

Petrova Nadezhda V, Velichko Artem K, Kantidze Omar L, Razin Sergey V

机构信息

Laboratory of Structural and Functional Organization of Chomosomes, Institute of Gene Biology, Russian Academy of Sciences, Moscow, Russia; Department of Molecular Biology, Lomonosov Moscow State University, Moscow, Russia.

出版信息

Cell Biol Int. 2014 May;38(5):675-81. doi: 10.1002/cbin.10252. Epub 2014 Feb 6.

DOI:10.1002/cbin.10252

PMID:24474557

Abstract

Telomeric repeat binding factor 2 (TRF2) is a well-studied shelterin complex subunit that plays a major role in the protection of chomosome ends and the prevention of the telomere-associated DNA damage response. We show that heat shock induces the dissociation of TRF2 from telomeres in human primary and cancer cell cultures. TRF2 is not simply degraded in response to heat shock, but redistributed thoughout the nucleoplasm. This TRF2 depletion/redistribution does not initiate the DNA damage response at chomosome termini.

摘要

端粒重复结合因子2（TRF2）是一种经过充分研究的端粒保护蛋白复合体亚基，在保护染色体末端以及预防端粒相关的DNA损伤反应中发挥着主要作用。我们发现，热休克可诱导人原代细胞和癌细胞培养物中端粒上的TRF2解离。TRF2并非简单地因热休克而降解，而是重新分布于整个核质中。这种TRF2的缺失/重新分布并未在染色体末端引发DNA损伤反应。