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ID 115053
Author
Takahama, Michihiro Tokushima University|Osaka University
Fukuda, Mitsunori Tohoku University
Ohbayashi, Norihiko Tohoku University|University of Tsukuba
Kozaki, Tatsuya Tokushima University|Osaka University
Misawa, Takuma Osaka University
Okamoto, Toru Osaka University
Matsuura, Yoshiharu Osaka University
Akira, Shizuo Osaka University
Saitoh, Tatsuya Tokushima University|Osaka University KAKEN Search Researchers
Content Type
Journal Article
Description
Cyclic GMP-AMP synthase (cGAS) is a cytosolic DNA sensor that induces the IFN antiviral response. However, the regulatory mechanisms that mediate cGAS-triggered signaling have not been fully explored. Here, we show the involvement of a small GTPase, RAB2B, and its effector protein, Golgi-associated RAB2B interactor-like 5 (GARIL5), in the cGAS-mediated IFN response. RAB2B-deficiency affects the IFN response induced by cytosolic DNA. Consistent with this, RAB2B deficiency enhances replication of vaccinia virus, a DNA virus. After DNA stimulation, RAB2B colocalizes with stimulator of interferon genes (STING), the downstream signal mediator of cGAS, on the Golgi apparatus. The GTP-binding activity of RAB2B is required for its localization on the Golgi apparatus and for recruitment of GARIL5. GARIL5 deficiency also affects the IFN response induced by cytosolic DNA and enhances replication of vaccinia virus. These findings indicate that the RAB2B-GARIL5 complex promotes IFN responses against DNA viruses by regulating the cGAS-STING signaling axis.
Journal Title
Cell Reports
ISSN
22111247
Publisher
Elsevier
Volume
20
Issue
12
Start Page
2944
End Page
2954
Published Date
2017-09-19
Rights
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Institute of Advanced Medical Sciences