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2014 Fiscal Year Final Research Report

Unc93B1 controls plasma membrane localization and signaling of TLR5

Research Project

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Project/Area Number 25860354
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Immunology
Research InstitutionThe University of Tokyo

Principal Investigator

SHIBATA Takuma  東京大学, 医科学研究所, 助教 (30554505)

Project Period (FY) 2013-04-01 – 2015-03-31
KeywordsUnc93B1 / TLR5
Outline of Final Research Achievements

The proper trafficking and localization of Toll-like receptors (TLRs) are important for specific ligand recognition and efficient signal transduction. The nucleotide-sensing TLRs are believed to localize inside cells and signal from the endolysosomes. Trafficking of the nucleotide-sensing TLRs from the ER to the endolysosomes strictly depends on UNC93B1. Although UNC93B1 was considered to have no role for the cell surface-localized TLRs,we unexpectedly discovered that TLR5, a cell surface receptor for bacterial protein flagellin, also requires UNC93B1 for plasma membrane localization and signaling. TLR5 physically interacts with UNC93B1, and the cells from the 3d(H412R) or UNC93B1-deficient mice not only lack TLR5 at the plasma membrane but also fail to secret cytokines upon flagellin stimulation, demonstrating the essential role of UNC93B1 in TLR5 signaling. Our study reveals that the role of UNC93B1 is not limited to the TLRs signaling from the endolysosomes.

Free Research Field

免疫学

URL: 

Published: 2016-06-03  

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