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• W2133846320 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." @default.
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• W2133846320 date "2009-03-06" @default.
• W2133846320 modified "2023-10-08" @default.
• W2133846320 title "ISG15 modification of filamin B negatively regulates the type I interferon‐induced JNK signalling pathway" @default.
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• W2133846320 doi "https://doi.org/10.1038/embor.2009.23" @default.
• W2133846320 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2672892" @default.
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