Laboratory of Cell Cycle Regulation, Department of Gene Mechanisms, Graduate School of Biostudies, Kyoto University,Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
J Biochem. 2011 Jan;149(1):5-14. doi: 10.1093/jb/mvq119. Epub 2010 Oct 11.
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.
无限增殖的细胞需要获得端粒 DNA 维持机制，以抵抗通过多次复制和线性染色体分离导致的可能缩短。大多数人类癌细胞表达端粒酶，而其他细胞则利用端粒的替代性延长（ALT）途径来延长端粒 DNA。有人认为，ALT 依赖于端粒重复 DNA 之间的重组。然而，分子细节仍然未知。最近的研究提供了 ALT 细胞表型所必需的端粒 DNA 和基因的特殊结构的证据。ALT 途径的分子模型应该得到验证，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。
