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学科主题: 基础医学
题名:
TFDP3 inhibits E2F1-induced, p53-mediated apoptosis
作者: Tian, Chan; Lv, Dan; Qiao, Huan; Zhang, Jun; Yin, Yan-Hui; Qian, Xiao-Ping; Wang, Yu-Ping; Zhang, Yu; Chen, Wei-Feng
关键词: TFDP3 ; E2F1 ; DP ; apoptosis ; p53
刊名: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
发表日期: 2007-09-14
DOI: 10.1016/j.bbrc.2007.06.128
卷: 361, 期:1, 页:20-25
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Biophysics
研究领域[WOS]: Biochemistry & Molecular Biology ; Biophysics
关键词[WOS]: S-PHASE ENTRY ; E2F FAMILY ; CELL-CYCLE ; E2F-1-INDUCED APOPTOSIS ; DEREGULATED EXPRESSION ; DNA-SYNTHESIS ; P53 ; PROTEINS ; DP ; PROLIFERATION
英文摘要:

By dimerizing with E2F proteins, TFDP has profound influence on cellular E2F activities. While TFDPI and 2 enhance the DNA binding and the transcriptional activity of E2F, the newly identified member of the DP family, TFDP3 primarily functions as a negative regulator. To further characterize the inhibitory property of TFDP3, the present study specifically examined the modulatory role of TFDP3 on E2F1-induced cell death. HEK-293 cells underwent apoptosis following ectopic expression of E2F1. This effect was virtually abolished by co-transfection with TFDP3. In the meantime, the accumulation of p53 proteins and the increased expression of the proapoptotic molecules, including Bax, Puma, Noxa, and Bid were found to be suppressed. These data suggest a new mechanism for the regulation of E2F1-induced apoptosis and provide further evidence for the general involvement of TFDP3 in the regulation of E2F functions. (c) 2007 Elsevier Inc. All rights reserved.

语种: 英语
WOS记录号: WOS:000248659000004
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/53902
Appears in Collections:基础医学院_免疫学系_期刊论文

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作者单位: 1.Peking Univ, Hlth Sci Ctr, Dept Immunol, Beijing 100083, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Dept Pathol, Beijing 100871, Peoples R China

Recommended Citation:
Tian, Chan,Lv, Dan,Qiao, Huan,et al. TFDP3 inhibits E2F1-induced, p53-mediated apoptosis[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2007,361(1):20-25.
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