期刊
JOURNAL OF VIROLOGY
卷 84, 期 2, 页码 1169-1175出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01372-09
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类别
资金
- NIH [U54 AI057158]
- National Institutes of Health [AI059536]
- INSERM
- French Ministere de la Recherche [04G537]
- Agence Nationale de la Recherche (ANR)
- Deutsche Forschungsgemeinschaft [SFB 593]
- ADR Region Rhone-Alpes Cluster 10
- FRM [FDT20090916821]
The Ebolavirus VP24 protein counteracts alpha/beta interferon (IFN-alpha/beta) and IFN-gamma signaling by blocking the nuclear accumulation of tyrosine-phosphorylated STAT1 (PY-STAT1). According to the proposed model, VP24 binding to members of the NPI-1 subfamily of karyopherin alpha (KPN alpha) nuclear localization signal receptors prevents their binding to PY-STAT1, thereby preventing PY-STAT1 nuclear accumulation. This study now identifies two domains of VP24 required for inhibition of IFN-beta-induced gene expression and PY-STAT1 nuclear accumulation. We demonstrate that loss of function correlates with loss of binding to KPN alpha proteins. Thus, the VP24 IFN antagonist function requires the ability of VP24 to interact with KPN alpha.
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