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A Ca2+-dependent signalling circuit regulates influenza A virus internalization and infection

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/55820

Title: A Ca2+-dependent signalling circuit regulates influenza A virus internalization and infection
Authors: Fujioka, Yoichiro Browse this author
Tsuda, Masumi Browse this author →KAKEN DB
Nanbo, Asuka Browse this author →KAKEN DB
Hattori, Tomoe Browse this author
Sasaki, Junko Browse this author
Sasaki, Takehiko Browse this author
Miyazaki, Tadaaki Browse this author →KAKEN DB
Ohba, Yusuke Browse this author →KAKEN DB
Issue Date: 14-Nov-2013
Publisher: Nature publishing group
Journal Title: Nature communications
Volume: 4
Start Page: 2763
Publisher DOI: 10.1038/ncomms3763
PMID: 24434940
Abstract: Various viruses enter host cells via endocytosis, but the molecular mechanisms underlying the specific internalization pathways remain unclear. Here we show that influenza A viruses (IAVs) enter cells via redundant pathways of clathrin-mediated and clathrin-independent endocytosis, with intracellular Ca2+ having a central role in regulation of both pathways by activating a signalling axis comprising RhoA, Rho-kinase, phosphatidylinositol 4-phosphate 5-kinase (PIP5K) and phospholipase C (PLC). IAV infection induces oscillations in the cytosolic Ca2+ concentration of host cells, the prevention of which markedly attenuates virus internalization and infection. The small GTPase RhoA is found both to function downstream of the virus-induced Ca2+ response and itself to induce Ca2+ oscillations in a manner dependent on Rho-kinase and subsequent PIP5K-PLC signalling. This signalling circuit regulates both clathrin-mediated and clathrin-independent endocytosis during virus infection and seems to constitute a key mechanism for regulation of IAV internalization and infection.
Type: article (author version)
URI: http://hdl.handle.net/2115/55820
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 大場 雄介

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