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Latent membrane protein 1 encoded by Epstein-Barr virus modulates directly and synchronously cyclin D1 and p16 by newly forming a c-Jun/Jun B heterodimer in nasopharyngeal carcinoma cell line

  1. Author:
    Song, X.
    Tao, Y. G.
    Zeng, L.
    Deng, X. Y.
    Lee, L. M.
    Gong, J. P.
    Wu, Q.
    Cao, Y.

  2. Author Address

    Cent S Univ, Canc Res Inst, Xiangya Sch Med, Changsha 410078, Peoples R China. Wayne State Univ, Dept Pathol, Sch Med, Detroit, MI 48201 USA. NCI, SAIC Frederick, Lab Mol Technol, Frederick, MD 21702 USA. Tongji Med Univ, Tongji Hosp, Mol Med Ctr, Wuhan 430030, Peoples R China. Xiamen Univ, Sch Life Sci, Key Lab, Minist Educ Cell Biol & Tumor Cell Engn, Xiamen 361005, Peoples R China Cao, Y, Cent S Univ, Canc Res Inst, Xiangya Sch Med, 88 Rd Xiangya, Changsha 410078, Peoples R China
    1. Year: 2005
    2. Date: NOV
  2. Journal: Virus Research
    1. 113
    2. 2
    3. Pages: 89-99
  4. Type of Article: Article
  1. Abstract:

    Recently we confirmed that latent membrane protein 1 (LMP1) encoded by Epstein-Barr virus (EBV) accelerates a newly forming active c-Jun/Jun B heterodimer, a transcription factor, but little is known about the target gene regulated by it. In this paper, results indicated that a c-Jun/Jun B heterodimer induced by LMP1 upregulated cyclin D1 promoters activity and expression, on the contrary, downregulated p16, and maladjustment of cyclin D1 and p16 expression accelerated progression of cell cycle. Firstly, we found a c-Jun/Jun B heterodimer regulated synchronously and directly cyclin D1 and p16 in the Tet-on-LMP1-HNE2 cell line, in which LMP1 expression is regulated by Tet-on system. This paper investigated in depth function of the newly forming active c-Jun/Jun B heterodimer, and built new connection between environmental pathogenic factor, signal transduction and cell cycle. (c) 2005 Elsevier B.V. All rights reserved

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External Sources

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  2. DOI: 10.1016/j.virusres.2005.04.019
  3. View record in Web of Science®
  4. WOS: 000232500300003

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