Epstein-Barr virus-derived EBNA2 regulates STAT3 activation

被引：32
|
作者：
Muromoto, Ryuta [1 ]
Ikeda, Osamu [1 ]
Okabe, Kanako [1 ]
Togi, Sumihito [1 ]
Kamitani, Shinya [1 ]
Fujimuro, Masahiro [2 ]
Harada, Shizuko [3 ]
Oritani, Kenji [4 ]
Matsud, Tadashi [1 ]
机构：
[1] Hokkaido Univ, Grad Sch Pharmaceut Sci, Dept Immunol, Kita Ku, Kira 12 Nishi 6, Sapporo, Hokkaido 0600812, Japan
[2] Univ Yamanashi, Interdisciplinary Grad Sch Med & Engn, Dept Mol Cell Biol, Chuo 4093898, Japan
[3] Natl Inst Infect Dis, Dept Virol 1, Shinjuku Ku, Tokyo 1628640, Japan
[4] Osaka Univ, Grad Sch Med, Dept Hematol & Oncol, Suita, Osaka 5650871, Japan
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 378卷 / 03期
关键词：
STAT3; EBV; EBNA2; LMP1; LIF; Transcription; FUNCTIONAL INTERACTIONS; TRANSCRIPTION FACTORS; BINDING-PROTEIN; LEUKEMIA-CELLS; J-KAPPA; GROWTH; DIFFERENTIATION; EXPRESSION; FAMILY; DNA;
D O I：
10.1016/j.bbrc.2008.11.053
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The Epstein-Barr virus (EBV)-encoded latency protein EBNA2 is a nuclear transcriptional activator that is essential for EBV-induced cellular transformation. Here, we show that EBNA2 interacts with STAT3, a signal transducer for an interleukin-6 family cytokine, and enhances the transcriptional activity of STAT3 by influencing its DNA-binding activity. Furthermore, EBNA2 cooperatively acts on STAT3 activation with LMP1, These data demonstrate that EBNA2 acts as a transcriptional coactivator of STAT3. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码：439 / 443
页数：5
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