Unknown

Dataset Information

0

COX5B regulates MAVS-mediated antiviral signaling through interaction with ATG5 and repressing ROS production.


ABSTRACT: Innate antiviral immunity is the first line of the host defense system that rapidly detects invading viruses. Mitochondria function as platforms for innate antiviral signal transduction in mammals through the adaptor protein, MAVS. Excessive activation of MAVS-mediated antiviral signaling leads to dysfunction of mitochondria and cell apoptosis that likely causes the pathogenesis of autoimmunity. However, the mechanism of how MAVS is regulated at mitochondria remains unknown. Here we show that the Cytochrome c Oxidase (CcO) complex subunit COX5B physically interacts with MAVS and negatively regulates the MAVS-mediated antiviral pathway. Mechanistically, we find that while activation of MAVS leads to increased ROS production and COX5B expression, COX5B down-regulated MAVS signaling by repressing ROS production. Importantly, our study reveals that COX5B coordinates with the autophagy pathway to control MAVS aggregation, thereby balancing the antiviral signaling activity. Thus, our study provides novel insights into the link between mitochondrial electron transport system and the autophagy pathway in regulating innate antiviral immunity.

SUBMITTER: Zhao Y 

PROVIDER: S-EPMC3534373 | biostudies-literature | 2012 Dec

REPOSITORIES: biostudies-literature

altmetric image

Publications

COX5B regulates MAVS-mediated antiviral signaling through interaction with ATG5 and repressing ROS production.

Zhao Yuanyuan Y   Sun Xiaofeng X   Nie Xuanli X   Sun Liwei L   Tang Tie-Shan TS   Chen Dahua D   Sun Qinmiao Q  

PLoS pathogens 20121220 12


Innate antiviral immunity is the first line of the host defense system that rapidly detects invading viruses. Mitochondria function as platforms for innate antiviral signal transduction in mammals through the adaptor protein, MAVS. Excessive activation of MAVS-mediated antiviral signaling leads to dysfunction of mitochondria and cell apoptosis that likely causes the pathogenesis of autoimmunity. However, the mechanism of how MAVS is regulated at mitochondria remains unknown. Here we show that th  ...[more]

Similar Datasets

| S-EPMC6613841 | biostudies-literature
| S-EPMC7239892 | biostudies-literature
2024-05-15 | GSE248667 | GEO
| S-EPMC5363539 | biostudies-literature
| S-EPMC2663242 | biostudies-literature
2024-05-15 | GSE248666 | GEO
2024-05-15 | GSE248665 | GEO
| S-EPMC10557580 | biostudies-literature
| S-EPMC5313200 | biostudies-literature
| S-EPMC4569712 | biostudies-literature