Eur J Immunol. 2012 May;42(5):1304-15. doi: 10.1002/eji.201142125.

Ankrd17 positively regulates RIG-I-like receptor (RLR)-mediated immune signaling.External

Wang, Y., Tong, X., Li, G., Li, J., Deng, M., Ye, X.,
--- - Center for Molecular Immunology, CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, P R China.
Retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), such as RIG-I, melanoma differentiation-associated gene 5 (MDA5), and virus-induced signaling adaptor (VISA), 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-kappaB and upregulates the transcription of IFN-beta. It also promotes RLR signaling in response to poly (I:C), influenza virus RNA, and Sendai virus. 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.
PMID: 22328336External
Arrow2 In vitro interaction Arrow2 In vivo interaction Arrow2 Characterization Arrow2 Functional role Arrow2 top
In vivo interaction
Overexpression DD1 DD2 Reference
Family DD1 DD2 Method Species Region Species Region
CARD MDA5 Link RIG-1 Co-immunoprecipitation HEK293 Not specified Not specified Not specified Not specified 22328336
(Link: click this icon to show interactions only between the two corresponding DDs)