ALT— 端粒延长替代机制

doi:10.3724/SP.J.1005.2009.01185

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

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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

Abstract

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

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—Alternative lengthening of telomere

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