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人类癌细胞中突变型RPA的表达导致端粒缩短。

Expression of mutant RPA in human cancer cells causes telomere shortening.

作者信息

Kobayashi Yuka, Sato Koichiro, Kibe Tatsuya, Seimiya Hiroyuki, Nakamura Asako, Yukawa Masashi, Tsuchiya Eiko, Ueno Masaru

机构信息

Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Higashi-Hiroshima, Japan.

出版信息

Biosci Biotechnol Biochem. 2010;74(2):382-5. doi: 10.1271/bbb.90496. Epub 2010 Feb 7.

DOI:10.1271/bbb.90496
PMID:20139621
Abstract

Replication protein A (RPA) 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.

摘要

复制蛋白A(RPA)与DNA复制及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。在本研究中,我们发现人类细胞中突变型RPA70的表达导致端粒缩短,这表明RPA是人类癌细胞中端粒长度调控所必需的。

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