Study the role of TLE2 in v-Src-mediated transformation

碩士 === 國立成功大學 === 藥理學研究所 === 95 === Two isoforms, i.e. p97Eps8 and p68Eps8, were detected in many cultured cell lines by Eps8 antibody. Our previous studies indicated that p97Eps8 participates in v-Src-mediated tumorigenesis. To characterize Eps8-mediated signal transduction, we previously identifie...

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Main Authors: Shang-hsien Chen, 陳尚賢
Other Authors: Tzeng-horng Leu
Format: Others
Language:zh-TW
Published: 2007
Online Access:http://ndltd.ncl.edu.tw/handle/11522555162784762073
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spelling ndltd-TW-095NCKU55500142015-10-13T14:16:32Z http://ndltd.ncl.edu.tw/handle/11522555162784762073 Study the role of TLE2 in v-Src-mediated transformation 研究TLE2在v-Src所調控的細胞轉型中扮演的角色 Shang-hsien Chen 陳尚賢 碩士 國立成功大學 藥理學研究所 95 Two isoforms, i.e. p97Eps8 and p68Eps8, were detected in many cultured cell lines by Eps8 antibody. Our previous studies indicated that p97Eps8 participates in v-Src-mediated tumorigenesis. To characterize Eps8-mediated signal transduction, we previously identified TLE2 (transducin-like enhancer of split 2) as one of its associated proteins by yeast-two hybrid screening. Further studies indicated that TLE2, as well as both Eps8 isoforms, was overexpressed in v-Src transformed IV5 cells. Interestingly, decreased expression of TLE2 was detected in Eps8-attenuated IV5 cells suggested its involvement in Eps8-mediated signal transduction. To study the role of TLE2 in cell proliferation and transformation, we transiently expressed tle2 into NIH3T3 cells or Eps8 overexpressing human kidney 293T cells. We found TLE2 overexpression could inhibit their anchorage-independent growth in soft agar. These findings suggested that TLE2 might be able to interact with Eps8 and inhibit the transforming ability of Eps8. Tzeng-horng Leu 呂增宏 2007 學位論文 ; thesis 60 zh-TW
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description 碩士 === 國立成功大學 === 藥理學研究所 === 95 === Two isoforms, i.e. p97Eps8 and p68Eps8, were detected in many cultured cell lines by Eps8 antibody. Our previous studies indicated that p97Eps8 participates in v-Src-mediated tumorigenesis. To characterize Eps8-mediated signal transduction, we previously identified TLE2 (transducin-like enhancer of split 2) as one of its associated proteins by yeast-two hybrid screening. Further studies indicated that TLE2, as well as both Eps8 isoforms, was overexpressed in v-Src transformed IV5 cells. Interestingly, decreased expression of TLE2 was detected in Eps8-attenuated IV5 cells suggested its involvement in Eps8-mediated signal transduction. To study the role of TLE2 in cell proliferation and transformation, we transiently expressed tle2 into NIH3T3 cells or Eps8 overexpressing human kidney 293T cells. We found TLE2 overexpression could inhibit their anchorage-independent growth in soft agar. These findings suggested that TLE2 might be able to interact with Eps8 and inhibit the transforming ability of Eps8.
author2 Tzeng-horng Leu
author_facet Tzeng-horng Leu
Shang-hsien Chen
陳尚賢
author Shang-hsien Chen
陳尚賢
spellingShingle Shang-hsien Chen
陳尚賢
Study the role of TLE2 in v-Src-mediated transformation
author_sort Shang-hsien Chen
title Study the role of TLE2 in v-Src-mediated transformation
title_short Study the role of TLE2 in v-Src-mediated transformation
title_full Study the role of TLE2 in v-Src-mediated transformation
title_fullStr Study the role of TLE2 in v-Src-mediated transformation
title_full_unstemmed Study the role of TLE2 in v-Src-mediated transformation
title_sort study the role of tle2 in v-src-mediated transformation
publishDate 2007
url http://ndltd.ncl.edu.tw/handle/11522555162784762073
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AT chénshàngxián yánjiūtle2zàivsrcsuǒdiàokòngdexìbāozhuǎnxíngzhōngbànyǎndejiǎosè
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