國家衛生研究院 NHRI:Item 3990099045/2697
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12189/12972 (94%)
造访人次 : 955523      在线人数 : 739
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/3990099045/2697


    题名: Characterization of novel transforming growth factor-beta type I receptors found in malignant pleural effusion tumor cells
    作者: Chen, KL;Liu, WH;Yang, YY;Leu, SJC;Shih, NY
    贡献者: National Institute of Cancer Research
    摘要: Background: Tumors expressing a transforming growth factor-beta type I receptor ( T beta RI) mutant with sequence deletions in a nine-alanine ( 9A) stretch of the signal peptide are reported to be highly associated with disease progression. Expression of this mutant could interfere with endogenous TGF beta signaling in the cell. However, little is known about the importance of the remaining part of the signal peptide on the cellular function of T beta RI. Results: We cloned and identified four new in-frame deletion variants of T beta RI, designated DM1 to DM4, in pleural effusion-derived tumor cells. Intriguingly, DM1 and DM2, with a small region truncated in the putative signal peptide of T beta RI, had a serious defect in their protein expression compared with that of the wild-type receptor. Using serial deletion mutagenesis, we characterized a region encoded by nucleotides 16 - 51 as a key element controlling T beta RI protein expression. Consistently, both DM1 and DM2 have this peptide deleted. Experiments using cycloheximde and MG132 further confirmed its indispensable role for the protein stability of T beta RI. In contrast, truncation of the 9A-stretch itself or a region downstream to the stretch barely affected T beta RI expression. However, variants lacking a region C-terminal to the stretch completely lost their capability to conduct TGF beta-induced transcriptional activation. Intriguingly, expression of DM3 in a cell sensitive to TGF beta made it significantly refractory to TGF beta-mediated growth inhibition. The effect of DM3 was to ablate the apoptotic event induced by TGF beta. Conclusion: We identified four new transcript variants of T beta RI in malignant effusion tumor cells and characterized two key elements controlling its protein stability and transcriptional activation. Expression of one of variants bestowed cancer cells with a growth advantage in the presence of TGF beta. These results highlight the potential roles of some naturally occurring T beta RI variants on the promotion of tumor malignancy.
    关键词: Biochemistry & Molecular Biology
    日期: 2007-08-17
    關聯: BMC Molecular Biology. 2007 Aug;8:Article number 72.
    Link to: http://dx.doi.org/10.1186/1471-2199-8-72
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000250032700001
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34848822904
    显示于类别:[施能耀] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    000250032700001.pdf611KbAdobe PDF765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