期刊
HUMAN MOLECULAR GENETICS
卷 13, 期 17, 页码 1919-1932出版社
OXFORD UNIV PRESS
DOI: 10.1093/hmg/ddh193
关键词
-
资金
- NCI NIH HHS [CA59268-06A1] Funding Source: Medline
- NIEHS NIH HHS [ES06096] Funding Source: Medline
- NINDS NIH HHS [NS-008900] Funding Source: Medline
In addition to increased DNA-strand exchange, a cytogenetic feature of cells lacking the RecQ-Iike BLM helicase is a tendency for telomeres to associate. We also report additional cellular and biochemical evidence for the role of BLM in telomere maintenance. BLM co-localizes and complexes with the telomere repeat protein TRF2 in cells that employ the recombination-mediated mechanism of telomere lengthening known as ALT (alternative lengthening of telomeres). BLM co-localizes with TRF2 in foci actively synthesizing DNA during late S and G(2)/M; co-localization increases in late S and G(2)/M when ALT is thought to occur. Additionally, TRF1 and TRF2 interact directly with BLM and regulate BLM unwinding activity in vitro. Whereas TRF2 stimulates BLM unwinding of telomeric and non-telomeric substrates, TRF1 inhibits BLM unwinding of telomeric substrates only. Finally, TRF2 stimulates BLM unwinding with equimolar concentrations of TRF1, but not when TRF1 is added in molar excess. These data suggest a function for BLM in recombination-mediated telomere lengthening and support a model for the coordinated regulation of BLM activity at telomeres by TRF1 and TRF2.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据