Abstract
Virus-induced signaling adaptor (VISA) functions as a critical adaptor in the regulation of both the production of type I IFNs and the subsequent control of the innate antiviral response. In this study, we demonstrate that tripartite motif (Trim)44 interacts with VISA and promotes VISA-mediated antiviral responses. The overexpression of Trim44 enhances the cellular response to viral infection, whereas Trim44 knockdown yields the opposite effect. Trim44 stabilizes VISA by preventing VISA ubiquitination and degradation. These findings suggest that Trim44 functions as a positive regulator of the virus-triggered immune response by enhancing the stability of VISA.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics
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Adaptor Proteins, Signal Transducing / metabolism*
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Carrier Proteins / genetics
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Carrier Proteins / metabolism*
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Cell Line
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Gene Knockdown Techniques
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Humans
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Interferon Type I / metabolism
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Intracellular Signaling Peptides and Proteins
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NF-kappa B / metabolism
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Protein Binding
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Protein Stability
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Receptors, Retinoic Acid / metabolism
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Signal Transduction
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Tripartite Motif Proteins
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Ubiquitination
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Virus Diseases / genetics
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Virus Diseases / immunology*
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Viruses / immunology*
Substances
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Adaptor Proteins, Signal Transducing
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Carrier Proteins
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Interferon Type I
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Intracellular Signaling Peptides and Proteins
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MAVS protein, human
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NF-kappa B
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PLAAT4 protein, human
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Receptors, Retinoic Acid
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TRIM44 protein, human
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Tripartite Motif Proteins