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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Mitochondrial antiviral signaling protein

VISA, IPS-1, MAVS, Cardif
This gene encodes an intermediary protein necessary in the virus-triggered beta interferon signaling pathways. It is required for activation of transcription factors which regulate expression of beta interferon and contributes to antiviral immunity. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Sep 2011] (from NCBI)
Top mentioned proteins: RIG-I, ACID, Interferon Regulatory Factor-3, MDA5, CAN
Papers on VISA
Structure determination of helical filaments by solid-state NMR spectroscopy.
Ritter et al., Braunschweig, Germany. In Proc Natl Acad Sci U S A, Feb 2016
The mitochondrial antiviral signaling protein (MAVS) is a central signal transduction hub in innate immunity that is activated by a receptor-induced conversion into helical superstructures (filaments) assembled from its globular caspase activation and recruitment domain.
Regulation of antiviral innate immune signaling by stress-induced RNA granules.
Onomoto et al., Chiba, Japan. In J Biochem, Feb 2016
Recent reports have clearly described the molecular machinery underlying the activation of RLRs and interactions with the downstream adaptor, mitochondrial antiviral signaling protein (MAVS).
Baculovirus vectors expressing F proteins in combination with virus-induced signaling adaptor (VISA) molecules confer protection against respiratory syncytial virus infection.
Pan et al., Wuhan, China. In Vaccine, Feb 2016
Bac-CF/tF64-VISA comprises Bac-CF/tF64 harboring the virus-induced signaling adaptor (VISA) gene.
Proton Pump Inhibitors and the Prescribing Cascade.
Dyer et al., In J Gerontol Nurs, Jan 2016
You will be asked to provide your name; contact information; and a VISA, MasterCard, or Discover card number for payment of the $20.00 fee.
ADAR1, inosine and the immune sensing system: distinguishing self from non-self.
Walkley et al., Australia. In Wiley Interdiscip Rev Rna, Jan 2016
Further analysis of this observation has lead to the conclusion that editing by ADAR1 is required to prevent activation of the cytosolic innate immune system, primarily focused on the dsRNA sensor MDA5 and leading to downstream signaling via MAVS.
Human ╬▓-D-3 Exacerbates MDA5 but Suppresses TLR3 Responses to the Viral Molecular Pattern Mimic Polyinosinic:Polycytidylic Acid.
Dorin et al., Edinburgh, United Kingdom. In Plos Genet, Dec 2015
Using bone marrow derived macrophages from knockout mice we demonstrate that hBD3 suppresses the polyI:C-induced TLR3 response mediated by TICAM1 (TRIF), while exacerbating the cytoplasmic response through MDA5 (IFIH1) and MAVS (IPS1/CARDIF).
Nucleic Acid-Sensing Receptors: Rheostats of Autoimmunity and Autoinflammation.
Marshak-Rothstein et al., Worcester, United States. In J Immunol, Nov 2015
These DNA and RNA sensors include endosomal TLRs and cytosolic sensors upstream of stimulator of type I IFN genes (STING) and MAVS.
Inhibiting DNA Methylation Causes an Interferon Response in Cancer via dsRNA Including Endogenous Retroviruses.
Strick et al., Baltimore, United States. In Cell, Sep 2015
Knocking down dsRNA sensors TLR3 and MAVS reduces this response 2-fold and blocking interferon beta or its receptor abrogates it.
DNA-Demethylating Agents Target Colorectal Cancer Cells by Inducing Viral Mimicry by Endogenous Transcripts.
De Carvalho et al., Toronto, Canada. In Cell, Sep 2015
This is associated with induction of dsRNAs derived at least in part from endogenous retroviral elements, activation of the MDA5/MAVS RNA recognition pathway, and downstream activation of IRF7.
Phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF induces IRF3 activation.
Chen et al., Dallas, United States. In Science, Apr 2015
During virus infection, the adaptor proteins MAVS and STING transduce signals from the cytosolic nucleic acid sensors RIG-I and cGAS, respectively, to induce type I interferons (IFNs) and other antiviral molecules.
MAVS, cGAS, and endogenous retroviruses in T-independent B cell responses.
Beutler et al., Dallas, United States. In Science, 2015
These RNAs are detected via a mitochondrial antiviral signaling protein (MAVS)-dependent RNA sensing pathway or reverse-transcribed and detected via the cGAS-cGAMP-STING pathway, triggering a second, sustained wave of signaling that promotes specific immunoglobulin M production.
Interferon (IFN) and Cellular Immune Response Evoked in RNA-Pattern Sensing During Infection with Hepatitis C Virus (HCV).
Sakamoto et al., Sapporo, Japan. In Sensors (basel), 2014
Using gene-disrupted mice and hydrodynamic injection strategy, we found the MAVS pathway to be crucial for induction of type III interferons (IFNs) in response to HCV in mouse.
Profile of oritavancin and its potential in the treatment of acute bacterial skin structure infections.
Stein et al., East Lansing, United States. In Infect Drug Resist, 2014
This novel second-generation semisynthetic lipoglycopeptide antibiotic has activity against a broad spectrum of Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-intermediate S. aureus (VISA), and vancomycin-resistant Enterococcus.
T cell responses are elicited against Respiratory Syncytial Virus in the absence of signalling through TLRs, RLRs and IL-1R/IL-18R.
Johansson et al., London, United Kingdom. In Sci Rep, 2014
To evaluate the collective contribution of PRRs and IL-1R signalling to RSV immunity, we generated Myd88/Trif/Mavs(-/-) mice that are deficient in signalling by all TLRs, RLRs and IL-1R, as well as other cytokine receptors such as IL-18 receptor.
Intracellular sensing of complement C3 activates cell autonomous immunity.
James et al., Cambridge, United Kingdom. In Science, 2014
Sensing of C3 in the cytosol activated mitochondrial antiviral signaling (MAVS)-dependent signaling cascades and induced proinflammatory cytokine secretion.
Human respiratory syncytial virus nucleoprotein and inclusion bodies antagonize the innate immune response mediated by MDA5 and MAVS.
Santangelo et al., Atlanta, United States. In J Virol, 2012
Human respiratory syncytial virus nucleoprotein and inclusion bodies antagonize the innate immune response mediated by MDA5 and MAVS.
Influenza virus protein PB1-F2 inhibits the induction of type I interferon by binding to MAVS and decreasing mitochondrial membrane potential.
Palese et al., New York City, United States. In J Virol, 2012
Using a flow cytometry-based assay, the authors demonstrate that the PB1-F2 protein inhibits MAVS-mediated IFN synthesis by decreasing the mitochondrial membrane potential (MMP).
Focal adhesion kinase is a component of antiviral RIG-I-like receptor signaling.
Coyne et al., Pittsburgh, United States. In Cell Host Microbe, 2012
The authors show that FAK interacts with MAVS at the mitochondrial membrane in a virus infection-dependent manner and potentiates MAVS-mediated signaling via a kinase-independent mechanism.
Respiratory syncytial virus NS1 protein colocalizes with mitochondrial antiviral signaling protein MAVS following infection.
Mohapatra et al., Tampa, United States. In Plos One, 2011
NS1 binds to MAVS and this binding inhibits the MAVS-RIG-I interaction required for IFN production
MAVS ubiquitination by the E3 ligase TRIM25 and degradation by the proteasome is involved in type I interferon production after activation of the antiviral RIG-I-like receptors.
Arnoult et al., Villejuif, France. In Bmc Biol, 2011
Study reports that RLR activation triggers MAVS ubiquitination on lysine 7 and 10 by the E3 ubiquitin ligase TRIM25 and marks it for proteasomal degradation concomitantly with downstream signaling.
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