INDUCTION OF BCL-2 EXPRESSION BY EPSTEIN-BARR-VIRUS LATENT MEMBRANE PROTEIN-1 PROTECTS INFECTED B-CELLS FROM PROGRAMMED CELL-DEATH

被引：1121

作者：

HENDERSON, S ^{[1
]}

ROWE, M ^{[1
]}

GREGORY, C ^{[1
]}

CROOMCARTER, D ^{[1
]}

WANG, F ^{[1
]}

LONGNECKER, R ^{[1
]}

KIEFF, E ^{[1
]}

RICKINSON, A ^{[1
]}

机构：

[1] BRIGHAM & WOMENS HOSP,BOSTON,MA 02115

来源：

CELL | 1991年 / 65卷 / 07期

基金：

英国惠康基金;

关键词：

D O I：

10.1016/0092-8674(91)90007-L

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：

Epstein-Barr virus (EBV) not only induces growth transformation in human B lymphocytes, but has more recently been shown to enhance B cell survival under suboptimal conditions where growth is inhibited; both effects are mediated through the coordinate action of eight virus-coded latent proteins. The effect upon cell survival is best recognized in EBV-positive Burkitt's lymphoma cell lines where activation of full virus latent gene expression protects the cells from programmed cell death (apoptosis). Here we show by DNA transfection into human B cells that protection from apoptosis is conferred through expression of a single EBV latent protein, the latent membrane protein LMP 1. Furthermore, we demonstrate that LMP 1 mediates this effect by up-regulating expression of the cellular oncogene bcl-2. The interplay between EBV infection and expression of this cellular oncogene has important implications for virus persistence and for the pathogenesis of virus-associated malignant disease.

引用

页码：1107 / 1115

页数：9

共 50 条

[11] DOWN-REGULATION OF CELL-ADHESION MOLECULES LFA-3 AND ICAM-1 IN EPSTEIN-BARR VIRUS-POSITIVE BURKITTS-LYMPHOMA UNDERLIES TUMOR-CELL ESCAPE FROM VIRUS-SPECIFIC T-CELL SURVEILLANCE
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