Priming Phosphorylation of TANK-Binding Kinase 1 by IκB Kinase β Is Essential in Toll-Like Receptor 3/4 Signaling

Author:

Abe Hiroto12,Satoh Junko3,Shirasaka Yutaro12,Kogure Amane1,Kato Hiroki14,Ito Shinji3,Fujita Takashi12

Affiliation:

1. Laboratory of Molecular Genetics, Institute for Frontier Life and Medical Science, Kyoto University, Kyoto, Japan

2. Laboratory of Molecular and Cellular Immunology, Graduate School of Biostudies, Kyoto University, Kyoto, Japan

3. Medical Research Support Center, Graduate School of Medicine, Kyoto University, Kyoto, Japan

4. Institute of Cardiovascular Immunology, University Hospital Bonn, University of Bonn, Bonn, Germany

Abstract

TRIF is an essential adaptor for Toll-like receptor 3/4 (TLR3/4) signaling to activate transcription factor interferon regulatory factor 3 (IRF-3). We examined the molecular mechanism of TLR3 signaling and found that TLR3 stimulation by double-stranded RNA (dsRNA) induces phosphorylation of TRIF at Ser210 and is required for IRF-3 recruitment. TANK-binding kinase 1 (TBK1) is known to be responsible for IRF-3 phosphorylation and activation.

Funder

Japan Agency for Medical Research and Development

Ministry of Education, Culture, Sports, Science and Technology

MEXT | Japan Society for the Promotion of Science

Publisher

American Society for Microbiology

Subject

Cell Biology,Molecular Biology

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