國家衛生研究院 NHRI:Item 3990099045/3319
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12145/12927 (94%)
造访人次 : 914942      在线人数 : 1408
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧：
  • 您可在西文检索词汇前后加上"双引号"，以获取较精准的检索结果
  • 若欲以作者姓名搜寻，建议至进阶搜寻限定作者字段，可获得较完整数据
    •  进阶搜寻
    主页 ‧ 登入 ‧ 上传 ‧ 说明 ‧ 关于NHRI ‧ 管理 到手机版


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/3319


    题名: Human DNA polymerase eta activity and translocation is regulated by phosphorylation
    作者: Chen, YW;Cleaver, JE;Hatahet, Z;Honkanen, RE;Chang, JY;Yen, Y;Chou, KM
    贡献者: National Institute of Cancer Research
    摘要: Human DNA polymerase ? (pol ?) can replicate across UV-induced pyrimidine dimers, and defects in the gene encoding pol ? result in a syndrome called xeroderma pigmentosum variant (XP-V). XP-V patients are prone to the development of cancer in sun-exposed areas, and cells derived from XP-V patients demonstrate increased sensitivity to UV radiation and a higher mutation rate compared with wild-type cells. pol ? has been shown to replicate across a wide spectrum of DNA lesions introduced by environmental or chemotherapeutic agents, or during nucleotide starvation, suggesting that the biological roles for pol ? are not limited to repair of UV-damaged DNA. The high error rate of pol ? requires that its intracellular activity be tightly regulated. Here, we show that the phosphorylation of pol ? increased after UV irradiation, and that treatment with caffeine, siRNA against ATR, or an inhibitor of PKC (calphostin C), reduced the accumulation of pol ? at stalled replication forks after UV irradiation or treatment with cisplatin and gemcitabine. Site-specific mutagenesis (S587A and T617A) of pol ? at two putative PKC phosphorylation sites located in the protein-protein interaction domain prevented nuclear foci formation induced by UV irradiation or treatment with gemcitabine/cisplatin. In addition, XP-V cell lines stably expressing either the S587A or T617A mutant form of pol ? were more sensitive to UV radiation and gemcitabine/cisplatin than control cells expressing wild-type pol ?. These results suggest that phosphorylation is one mechanism by which the cellular activity of pol ? is regulated. ?2008 by The National Academy of Sciences of the USA.
    日期: 2008-10-28
    關聯: Proceedings of the National Academy of Sciences of the United States of America. 2008 Oct 28;105(43):16578-16583.
    Link to: http://dx.doi.org/10.1073/pnas.0808589105
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0027-8424&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000260913500033
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=55949125726
    显示于类别:[張俊彥] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    SCP55949125726.pdf705KbAdobe PDF647检视/开启


    在NHRI中所有的数据项都受到原著作权保护.

    TAIR相关文章

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈