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jsp.display-item.identifier=請使用永久網址來引用或連結此文件:
https://tkuir.lib.tku.edu.tw/dspace/handle/987654321/61771
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题名: | The N-terminal domain of EBNA1 acts as a suppressor of the HER2/neu oncogene |
作者: | Liu, Jah-yao;Chuang, Tzu-chao;Way, Tzong-der;Tsai, Tzung-chieh;Hu, Chih-lin;Liu, Guang-yaw;Wang, Shan-shue;Chung, Jing-gung;Kao, Ming-ching |
贡献者: | 淡江大學化學學系 |
关键词: | HER2/neu;EBV;EBNA1;Cell cycle;Gene therapy |
日期: | 2009-01-18 |
上传时间: | 2011-10-15 23:38:50 (UTC+8) |
出版者: | Shannon: Elsevier Ireland Ltd |
摘要: | HER2/neu oncogene-mediated malignancy is clearly associated with various human cancers. Therefore, HER2/neu targeting is an effective approach to cancer therapy. We have previously demonstrated that Epstein–Barr virus nuclear antigen-1 (EBNA1) can suppress HER2/neu oncogene expression, although EBNA1 itself has oncogenic potential. Here, we found that the N-terminal domain of EBNA1 alone, named EBNA1-NT, which contains the N-terminal region of amino acid residues 1–86 of EBNA1, is required and sufficient to suppress HER2/neu oncogene expression at the transcriptional level. Furthermore, in EBNA1-NT-transfected HER2/neu-overexpressing cells, we found EBNA1-NT could down-regulate the endogenous production of p185HER2/neu, lower transformation ability, sensitize paclitaxel-induced apoptosis and decrease tumorigenic potential. These data suggest that EBNA1-NT may act as a repressor of the HER2/neu oncogene. |
關聯: | Cancer Letters 273(2), pp.273-280 |
DOI: | 10.1016/j.canlet.2008.08.013 |
显示于类别: | [化學學系暨研究所] 期刊論文
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