Expression of Mutant RPA in Human Cancer Cells Causes Telomere Shortening
Expression of Mutant RPA in Human Cancer Cells Causes Telomere Shortening
复制标题
DOI：
10.1271/bbb.90496
复制
发表时间：
2010-02-01
影响因子：
1.6
通讯作者：
Ueno, Masaru
中科院分区：
文献类型：
--
作者：
Kobayashi, Yuka;Sato, Koichiro;Ueno, Masaru
复制蛋白 A (RIPA) 与 DNA 复制和其他过程中产生的单链 DNA 结合。 RPA 在端粒维持中的作用已在酵母中得到证实，但在端粒酶阳性的人类细胞中尚未得到证实。在这项研究中，我们发现人类细胞中突变体RPA70的表达导致端粒缩短，这表明RPA是人类癌细胞端粒长度调节所必需的。
Replication protein A (RIPA) binds to single-stranded DNA generated during DNA replication and other processes. The roles of RPA in telomere maintenance have been demonstrated in yeasts, but not in telomerase-positive human cells. In this study, we found that expression of mutant RPA70 in human cells caused telomere shortening, suggesting that RPA is required for telomere-length regulation in human cancer cells.