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ISG15 modification of filamin B negatively regulates the type I interferon-induced JNK signalling pathway

Authors
Jeon, Young JooChoi, Joon SeokLee, Jung YunYu, Kyung RyunKim, Sangman MichaelKa, Seung HyeunOh, Kyu HeeKim, Keun IlZhang, Dong-ErBang, Ok SunChung, Chin Ha
Issue Date
Apr-2009
Publisher
WILEY
Keywords
apoptosis; filamin B scaffold; ISG15; JNK signalling pathway; type I interferon
Citation
EMBO REPORTS, v.10, no.4, pp.374 - 380
Journal Title
EMBO REPORTS
Volume
10
Number
4
Start Page
374
End Page
380
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13790
DOI
10.1038/embor.2009.23
ISSN
1469-221X
Abstract
Interferon (IFN)-induced signalling pathways have essential functions in innate immune responses. In response to type I IFNs, filamin B tethers RAC1 and a Jun N-terminal kinase (JNK)-specific mitogen-activated protein kinase ( MAPK) module-MEKK1, MKK4 and JNK-and thereby promotes the activation of JNK and JNK-mediated apoptosis. Here, we show that type I IFNs induce the conjugation of filamin B by interferon-stimulated gene 15 (ISG15). ISGylation of filamin B led to the release of RAC1, MEKK1 and MKK4 from the scaffold protein and thus to the prevention of sequential activation of the JNK cascade. By contrast, blockade of filamin B ISGylation by substitution of Lys 2467 with arginine or by knockdown of ubiquitin-activating enzyme E1-like (UBEL1) prevented the release of the signalling molecules from filamin B, resulting in persistent promotion of JNK activation and JNK-mediated apoptosis. These results indicate that filamin B ISGylation acts as a negative feedback regulatory gate for the desensitization of type I IFN-induced JNK signalling.
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