Vaccine and Infectious Disease Organization, University of Saskatchewan, Saskatoon, Saskatchewan, S7N 5E3, Canada.
J Gen Virol. 2013 May;94(Pt 5):977-984. doi: 10.1099/vir.0.049395-0. Epub 2013 Jan 9.
Influenza A virus vRNP nuclear export is CRM1-dependent. Ran-binding protein 3 (RanBP3) is a Ran-interacting protein that is best known for its role as a cofactor of CRM1-mediated cargo nuclear export. In this study, we investigated the role of RanBP3 during the influenza A virus life cycle. We found that RanBP3 was phosphorylated at Ser58 in the early and late phases of infection. Knockdown of RanBP3 expression led to vRNP nuclear retention, suggesting that RanBP3 is involved in vRNP nuclear export. Moreover, we demonstrated that the function of RanBP3 during vRNP nuclear export is regulated by phosphorylation at Ser58, and that RanBP3 phosphorylation is modulated by both PI3K/Akt and Ras/ERK/RSK pathways in the late phase of viral infection.
甲型流感病毒 vRNP 的核输出依赖于 CRM1。Ran 结合蛋白 3(RanBP3)是一种 Ran 相互作用蛋白,其作为 CRM1 介导的货物核输出辅助因子的作用最为人所知。在这项研究中,我们研究了 RanBP3 在甲型流感病毒生命周期中的作用。我们发现,RanBP3 在感染的早期和晚期被磷酸化 Ser58。RanBP3 表达的敲低导致 vRNP 核滞留,表明 RanBP3 参与 vRNP 核输出。此外,我们证明了 RanBP3 在 vRNP 核输出中的功能受 Ser58 磷酸化调节,并且 RanBP3 磷酸化在病毒感染的晚期受 PI3K/Akt 和 Ras/ERK/RSK 途径调节。