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Alternative lengthening of telomeres pathway: Recombination-mediated telomere maintenance mechanism in human cells

机译:端粒途径的替代性延长:重组介导的人类细胞端粒维持机制

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摘要

Unlimitedly proliferating cells need to acquire the telomere DNA maintenance mechanism, to counteract possible shortening through multiple rounds of replication and segregation of linear chromosomes. Most human cancer cells express telomerase whereas the other cells utilize the alternative lengthening of telomeres (ALT) pathway to elongate telomere DNA. It is suggested that ALT depends on the recombination between telomere repetitive DNAs. However, the molecular details remain unknown. Recent studies have provided evidence of special structures of telomere DNA and genes essential for the phenotypes of ALT cells. The molecular models of the ALT pathway should be validated to elucidate recombination-mediated telomere maintenance and promote the applications to anti-cancer therapy.
机译:无限增殖的细胞需要获得端粒DNA维持机制,以通过线性染色体的多轮复制和分离来抵消可能的缩短。大多数人类癌细胞表达端粒酶,而其他细胞则利用端粒(ALT)路径的替代性延长来延长端粒DNA。提示ALT取决于端粒重复DNA之间的重组。但是,分子细节仍然未知。最近的研究提供了端粒DNA的特殊结构和ALT细胞表型必不可少的基因的证据。 ALT途径的分子模型应经过验证,以阐明重组介导的端粒维持并促进其在抗癌治疗中的应用。

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