TRIM56 Is an Essential Component of the TLR3 Antiviral Signaling Pathway.
In: Journal of Biological Chemistry, Jg. 287 (2012-10-19), Heft 43, S. 36404-36413
academicJournal
Zugriff:
Members of the tripartite motif (TRIM) proteins are being recognized as important regulators of host innate immunity. However, specific TRIMs that contribute to TLR3-mediated antiviral defense have not been identified. We show here that TRIM56 is a positive regulator of TLR3 signaling. Overexpression of TRIM56 substantially potentiated extracellular dsRNAinduced expression of interferon (IFN)-β and interferon-stimulated genes (ISGs), while knockdown of TRIM56 greatly impaired activation of IRF3, induction of IFN-β and ISGs, and establishment of an antiviral state by TLR3 ligand and severely compromised TLR3-mediated chemokine induction following infection by hepatitis C virus. The ability to promote TLR3 signaling was independent of the E3 ubiquitin ligase activity of TRIM56. Rather, it correlated with a physical interaction between TRIM56 and TRIF. Deletion of the C-terminal portion of TRIM56 abrogated the TRIM56-TRIF interaction as well as the augmentation of TLR3-mediated IFN response. Together, our data demonstrate TRIM56 is an essential component of the TLR3 antiviral signaling pathway and reveal a novel role for TRIM56 in innate antiviral immunity. [ABSTRACT FROM AUTHOR]
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TRIM56 Is an Essential Component of the TLR3 Antiviral Signaling Pathway.
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Autor/in / Beteiligte Person: | Shen, Yang ; Li, Nan L. ; Wang, Jie ; Liu, Baoming ; Lester, Sandra ; Li, Kui |
Zeitschrift: | Journal of Biological Chemistry, Jg. 287 (2012-10-19), Heft 43, S. 36404-36413 |
Veröffentlichung: | 2012 |
Medientyp: | academicJournal |
ISSN: | 0021-9258 (print) |
DOI: | 10.1074/jbc.M112.397075 |
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