ALT— 端粒延长替代机制

doi:10.3724/SP.J.1005.2009.01185

遗传 ›› 2009, Vol. 31 ›› Issue (12): 1185-1191.doi: 10.3724/SP.J.1005.2009.01185

ALT— 端粒延长替代机制

吴晓明, 唐文如, 罗瑛

昆明理工大学生命科学与技术学院衰老与肿瘤分子遗传学实验室, 昆明 650224

收稿日期:2009-09-01 修回日期:2009-10-14 出版日期:2009-12-10 发布日期:2009-12-10
通讯作者: 罗瑛 E-mail:luoyingabc@yahoo.com
基金资助:
国家自然科学基金项目(编号：30771194, 30960152), 云南省科技计划项目(编号：2008C043M)和教育部新世纪优秀人才项目资助

ALT—Alternative lengthening of telomere

WU Xiao-Ming, TANG Wen-Ru, LUO Ying

Lab of Molecular Genetics of Aging and Tumor, Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming 650224, China

Received:2009-09-01 Revised:2009-10-14 Online:2009-12-10 Published:2009-12-10
Contact: LUO Ying E-mail:luoyingabc@yahoo.com

摘要/Abstract

摘要：

端粒长度和结构的稳定与肿瘤及衰老的发生密切相关, 端粒维持机制是细胞增殖的必要条件, 端粒维持机制的激活是肿瘤细胞演化过程中的一个重要环节。这种端粒维持机制可能是通过重新激活端粒酶, 使细胞快速增殖。在端粒酶失活或不足的情况下, 也存在着一种或多种维持和增加端粒长度的机制, 统称为端粒延长替代机制(Alterative lengthening of telomere, ALT)。其特点包括: 具有不均一的端粒长度, 存在与ALT相关的PML小体(APBs)以及同源重组增加。ALT细胞内存在的ALT相关蛋白及异常活跃的同源重组为ALT机制的激活和维持提供了可能。文章综述了ALT的特征性表型、与端粒酶的相关性及其可能的发生机制。对ALT机制的深入研究将有利于阐明衰老与肿瘤之间的辩证关系。

关键词: 端粒延长替代机制, 与ALT相关的PML小体, 同源重组, 端粒蛋白复合体, 端粒

Abstract:

The maintenance of the length and normal structure of telomeres is highly related to the development of senescence and tumorigenesis. The mechanisms of maintaining telomere are essential for cell growth and the reactivation of these mechanisms is an important step in tumor progression. The mechanism of telomere maintenance might be the reactivation of telomerase. In the case of telomerase deficiency, the mechanisms for maintaining the lengths of telomeres are referred to as alternative lengthening of telomere (ALT). The characteristics of the ALT cells include great heterogeneity of telomere size in individual cells, ALT-associated PML (promyelocytic leukemia) bodies, and evident homologous recombination. The ALT-related proteins and elevated homologous recombination found in ALT cells provide a possible mechanism for the alternative lengthening of telomere. The study of ALT provides a new view of crosstalk between senescence and tumori-genesis.

Key words: ALT, APBs, homologous recombination, shelterin, telomere

吴晓明，唐文如，罗瑛. ALT— 端粒延长替代机制[J]. 遗传, 2009, 31(12): 1185-1191.

TUN Xiao-Meng, TANG Wen-Ru, LUO Ying. ALT—Alternative lengthening of telomere[J]. HEREDITAS, 2009, 31(12): 1185-1191.

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ALT— 端粒延长替代机制

ALT—Alternative lengthening of telomere

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