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端粒异染色质受损促进端粒的替代延长。

Compromised Telomeric Heterochromatin Promotes ALTernative Lengthening of Telomeres.

作者信息

Voon Hsiao P J, Collas Philippe, Wong Lee H

机构信息

Department of Biochemistry and Molecular Biology, The Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia.

Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, and Norwegian Center for Stem Cell Research, Oslo University Hospital, Oslo 0317, Norway.

出版信息

Trends Cancer. 2016 Mar;2(3):114-116. doi: 10.1016/j.trecan.2016.02.003. Epub 2016 Mar 4.

DOI:10.1016/j.trecan.2016.02.003

PMID:28741530

Abstract

Alternative lengthening of telomeres (ALT) is an enigmatic process that allows certain cancers to maintain telomeres in the absence of telomerase. ALT cancers are frequently defective for ATRX/DAXX, a chaperone complex that deposits histone variant H3.3 at telomeres. We propose that mutations in alpha thalassemia-mental retardation syndrome X-linked (ATRX)/death-domain associated protein (DAXX) prime ALT activation by disrupting telomeric heterochromatin.

摘要

端粒替代延长（ALT）是一个神秘的过程，它使某些癌症在缺乏端粒酶的情况下维持端粒长度。ALT癌症通常在ATRX/DAXX方面存在缺陷，ATRX/DAXX是一种伴侣蛋白复合体，可在端粒处沉积组蛋白变体H3.3。我们提出，X连锁的α地中海贫血-智力发育迟缓综合征（ATRX）/死亡结构域相关蛋白（DAXX）中的突变通过破坏端粒异染色质引发ALT激活。