Mitochondrial antiviral signaling protein
From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history
Mitochondrial antiviral-signaling protein (MAVS) is a protein encoded by the MAVS gene. It mediates the activation of NFκB and IRFs and the induction of interferons in response to viral infection.
MAVS is also a pro-apoptosis molecule that triggers disruption of the mitochondrial membrane potential and activation of caspases.[1]
Many viruses evade the host innate immune response by cleaving MAVS from mitochondria. Coxsackievirus B3 cleaves MAVS protein to inhibit type I interferon induction.[2]
MAVS plays a role in maintaining intestinal homeostasis. MAVS knockout mice developed more severe mortality and morbidity than wild type mice in an experimental model of colitis.[3]
References[edit | edit source]
- ↑ Yu, Chia-Yi (December 2009). "The Interferon Stimulator Mitochondrial Antiviral Signaling Protein Facilitates Cell Death by Disrupting the Mitochondrial Membrane Potential and by Activating Caspases". Journal of Virology.
- ↑ Mukherjee, A (March 2011). "The coxsackievirus B 3C protease cleaves MAVS and TRIF to attenuate host type I interferon and apoptotic signaling". PLoS Pathology. 7.
- ↑ Li, Xiao-Dong (October 8, 2011). "Mitochondrial antiviral signaling protein (MAVS) monitors commensal bacteria and induces an immune response that prevents experimental colitis". Proceedings of the National Academy of Sciences. 108: 17390–17395.
