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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
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.
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页码:439 / 443
页数:5
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