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[端粒替代延长]

[ALT--alternative lengthening of telomere].

作者信息

Wu Xiao-Ming, Tang Wen-Ru, Luo Ying

机构信息

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

出版信息

Yi Chuan. 2009 Dec;31(12):1185-91.

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 tumorigenesis.

摘要

端粒长度和正常结构的维持与衰老及肿瘤发生发展密切相关。维持端粒的机制对细胞生长至关重要,而这些机制的重新激活是肿瘤进展的重要步骤。端粒维持机制可能是端粒酶的重新激活。在端粒酶缺乏的情况下,维持端粒长度的机制被称为端粒替代延长(ALT)。ALT细胞的特征包括单个细胞中端粒大小的高度异质性、ALT相关的早幼粒细胞白血病(PML)小体以及明显的同源重组。ALT细胞中发现的ALT相关蛋白和升高的同源重组为端粒替代延长提供了一种可能的机制。对ALT的研究为衰老与肿瘤发生之间的相互作用提供了新的视角。

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