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Heterodimer formation between c-Jun and Jun B proteins mediated by Epstein Barr virus encoded latent membrane protein 1

  1. Author:
    Song, X.
    Tao, Y. G.
    Tan, Y. N.
    Lee, L. M.
    Deng, X. Y.
    Wu, Q.
    Cao, Y.

  2. Author Address

    Cent S Univ, Xiangya Sch Med, Inst Canc Res, Changsha 410078, Peoples R China. Natl Canc Inst, SAIC Frederick, Lab Mol Technol, Ft Detrick, MD 21702 USA. Xiamen Univ, Sch Life Sci, Key Lab Minist Educ Cell Biol & Tumor Cell Engn, Xiamen 361005, Peoples R China Cao, Y, Cent S Univ, Xiangya Sch Med, Inst Canc Res, Changsha 410078, Peoples R China
    1. Year: 2005
    2. Date: FEB
  2. Journal: Science in China Series C-Life Sciences
    1. 48
    2. 1
    3. Pages: 70-80
  4. Type of Article: Article
  1. Abstract:

    Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) may trigger the transcription factor AP-1 including c-Jun and c-fos. In this report, using a Tet-on LMP1 HNE2 cell line which is a dual-stable LMP1 integrated nasopharyngeal carcinoma (NPC) cell line and the expression of LMP1 in which could be regulated by the Tet-on system, we show that Jun B can efficiently form a new heterodimeric complex with the c-Jun protein under the regulation of LMP1, phosphorylation of c-Jun (ser 63, ser 73) and Jun B is involved in the process of the new heterodimeric formation. We also find that this heterodimeric form can bind to the AP-1 consensus sequence. Transfection studies suggest that JNK interaction protein (JIP) could inhibit the heterodimer formation of c-Jun and Jun B through blocking the AP-1 signaling pathway triggered by LMP1. The interaction and function between c-Jun protein and Jun B protein increase the repertoire of possible regulatory complexes by LMP1 that could play an important role in the regulation of transcription of specific cellular genes in the process of genesis of nasopharyngeal carcinoma

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  1. View record in Web of Science®
  2. WOS: 000228190700009

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