tetano
Editor, Senior Moderator
Eur J Immunol. 2012 Feb 13. doi: 10.1002/eji.201142125. [Epub ahead of print]
Ankrd17 positively regulates RIG-I-like receptor (RLR)-mediated immune signaling.
Wang Y, Tong X, Li G, Li J, Deng M, Ye X.
Source
Center for Molecular Immunology, CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences CAS, Beijing 100101, P. R. China; Graduate University of Chinese Academy of Sciences, Beijing 100101, China.
Abstract
RIG-I (retinoic acid-inducible gene-I)-like receptors (RLRs), such as RIG-I, MDA5 (melanoma differentiation-associated gene 5) and VISA (virus-induced signaling adaptor), are intracellular molecules that sense diverse viral RNAs and trigger immune responses. In this study, we demonstrate that the ankyrin repeat protein ankrd17 interacts with RIG-I, MDA5 and VISA and upregulates RLR-mediated immune signaling. Overexpression of ankrd17 enhances RLR-mediated activation of IRF-3 and NF-κB and upregulates the transcription of IFN-β. It also promotes RLR signaling in response to polyI:C, influenza virus RNA and Sandai virus (SeV). Consistently, knockdown of ankrd17 impairs RLR signaling. Furthermore, we demonstrate that ankrd17 enhances the interaction of RIG-I and MDA5 with VISA; the ankyrin repeat domain of ankrd17 is required for its interaction with RIG-I as well as for its function in regulating the RLR pathway. Taken together, our results indicate that ankrd17 is a positive regulator of the RLR signaling pathway.
? 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
PMID:
22328336
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22328336
Ankrd17 positively regulates RIG-I-like receptor (RLR)-mediated immune signaling.
Wang Y, Tong X, Li G, Li J, Deng M, Ye X.
Source
Center for Molecular Immunology, CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences CAS, Beijing 100101, P. R. China; Graduate University of Chinese Academy of Sciences, Beijing 100101, China.
Abstract
RIG-I (retinoic acid-inducible gene-I)-like receptors (RLRs), such as RIG-I, MDA5 (melanoma differentiation-associated gene 5) and VISA (virus-induced signaling adaptor), are intracellular molecules that sense diverse viral RNAs and trigger immune responses. In this study, we demonstrate that the ankyrin repeat protein ankrd17 interacts with RIG-I, MDA5 and VISA and upregulates RLR-mediated immune signaling. Overexpression of ankrd17 enhances RLR-mediated activation of IRF-3 and NF-κB and upregulates the transcription of IFN-β. It also promotes RLR signaling in response to polyI:C, influenza virus RNA and Sandai virus (SeV). Consistently, knockdown of ankrd17 impairs RLR signaling. Furthermore, we demonstrate that ankrd17 enhances the interaction of RIG-I and MDA5 with VISA; the ankyrin repeat domain of ankrd17 is required for its interaction with RIG-I as well as for its function in regulating the RLR pathway. Taken together, our results indicate that ankrd17 is a positive regulator of the RLR signaling pathway.
? 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
PMID:
22328336
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22328336