期刊
BIOCHEMICAL SOCIETY TRANSACTIONS
卷 35, 期 -, 页码 186-187出版社
PORTLAND PRESS LTD
DOI: 10.1042/BST0350186
关键词
Akt; antiviral drug; influenza A virus; NS1 protein; phosphoinositide 3-kinase (PI3K); p85
资金
- Medical Research Council [G0601126] Funding Source: Medline
- MRC [G0601126] Funding Source: UKRI
- Medical Research Council [G0601126] Funding Source: researchfish
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.
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