Divergent requirements for the MAPKERK signal transduction pathway during initial virus infection of quiescent primary B cells and disruption of Epstein-Barr virus latency by phorbol esters

被引：27

作者：

Fenton, M ^{[1
]}

Sinclair, AJ ^{[1
]}

机构：

[1] Univ Sussex, Sch Biol Sci, Brighton BN1 9QG, E Sussex, England

来源：

JOURNAL OF VIROLOGY | 1999年 / 73卷 / 10期

基金：

英国惠康基金;

关键词：

D O I：

10.1128/JVI.73.10.8913-8916.1999

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Quiescent primary B lymphocytes and Epstein-Barr virus (EBV)-immortalized lymphoblastoid cell lines express components of the extracellular response kinase arm of the mitogen-activated protein kinase (MAPK(ERK)) Signal transduction pathway and transmit signals through the pathway when exposed to appropriate stimuli. Although the MAPK(ERK) pathway is activated following infection with EBV, MAPK/ERK kinase (MEK1) activity is not required to drive the proliferation of infected cells. However, MEK1 contributes to EBV latency control.

引用

页码：8913 / 8916

页数：4

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