PI3K signalling during influenza A virus infections

被引：31

作者：

Hale, B. G. ^{[1
]}

Randall, R. E. ^{[1
]}

机构：

[1] Univ St Andrews, Ctr Biomol Sci, St Andrews KY16 9ST, Fife, Scotland

来源：

BIOCHEMICAL SOCIETY TRANSACTIONS | 2007年 / 35卷

基金：

英国医学研究理事会;

关键词：

Akt; antiviral drug; influenza A virus; NS1; protein; phosphoinositide 3-kinase (PI3K); p85;

D O I：

10.1042/BST0350186

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：

Recent work has demonstrated that the PI3K (phosphoinositide 3-kinase) signalling pathway is important for efficient influenza A virus replication. Activation of PI3K in virus-infected cells is mediated by the viral NS1 protein, which binds directly to the p85 beta regulatory subunit of PI3K and causes the PI3K-dependent phosphorylation of Akt (protein kinase B). Given that recombinant influenza A viruses unable to activate PI3K signalling are attenuated in tissue culture, the PI3K pathway could be a novel target for the development of future anti-influenza drugs.

引用

页码：186 / 187

页数：2

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