Associated Papers
ANK2-MAVS signaling dysfunction triggers mitochondrial stress and enhances IL-8 mediated inflammatory responses in Takayasu arteritis.
Chen S et al.
Free Radical Biology & Medicine, 2026
Multiple Sclerosis patients carry an increased burden of exceedingly rare genetic variants in the inflammasome regulatory genes.
Vidmar L et al.
Scientific Reports, 2019
31235738 (PubMed )
Supplement: 41598_2019_45598_MOESM2_ESM.xlsx › Sheet1
Antiviral Adaptor MAVS Promotes Murine Lupus With a B Cell Autonomous Role.
Sun W et al.
Frontiers in Immunology, 2019
MAVS is not a Likely Susceptibility Locus for Addison's Disease and Type 1 Diabetes.
Zurawek M et al.
Archivum Immunologiae Et Therapiae Experimentalis, 2017
Alteration of Antiviral Signalling by Single Nucleotide Polymorphisms (SNPs) of Mitochondrial Antiviral Signalling Protein (MAVS).
Xing F et al.
Plos One, 2016
The role of the interactome in the maintenance of deleterious variability in human populations.
Garcia-Alonso L et al.
Molecular Systems Biology, 2014
Interferon alpha as a primary pathogenic factor in human lupus.
Niewold TB
Journal of Interferon & Cytokine Research : the Official Journal of the International Society for Interferon and Cytokine Research, 2011
A loss-of-function variant of the antiviral molecule MAVS is associated with a subset of systemic lupus patients.
Pothlichet J et al.
Embo Molecular Medicine, 2011
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