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2014 Fiscal Year Final Research Report

Analysis of structure and function of viral proteins that suppress innate immunity

Research Project

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Project/Area Number 24590554
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Virology
Research InstitutionHiroshima University

Principal Investigator

SAKAGUCHI Takemasa  広島大学, 医歯薬保健学研究院(医), 教授 (70196070)

Co-Investigator(Kenkyū-buntansha) ODA Kosuke  広島大学, 大学院医歯薬保健学研究院, 助教 (60571255)
IRIE Takashi  広島大学, 大学院医歯薬保健学研究院, 准教授 (70419498)
Project Period (FY) 2012-04-01 – 2015-03-31
Keywordsウイルス / アクセサリー蛋白質 / 自然免疫 / インターフェロン / 蛋白質結晶化 / 蛋白質構造解析 / 共結晶化 / STAT1
Outline of Final Research Achievements

We investigated the mechanism by which an accessory protein of Sendai virus, the C protein, inhibits the STAT1 function. We determined the crystal structure of STAT1ND associated with the C-terminal half of the C protein (Y3). Molecular modeling suggested that a parallel form of the STAT1 dimer can bind two Y3 molecules. Kinetic analysis demonstrated anti-cooperative binding of two Y3 molecules with the STAT1 dimer, thereby implying that the second Y3 molecule can only target the STAT1 dimer in a parallel form. STAT1 with excess amounts of Y3 was prone to be phosphorylated at Tyr705 as shown by an in vitro dephosphorylation assay. Since it is reported that the full-length C protein induces a high molecular weight complex of pY-STAT1, the results of this study suggest that the C protein induces complex formation of the parallel form of pY-STAT1, leading to inhibition of transcription.

Free Research Field

ウイルス学

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Published: 2016-06-03  

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