Publication Date:
2018
Description:
〈p〉It is well established that activation of the transcription factor signal transducer and activator of transcription 1 (STAT1) is required for the interferon- (IFN-)–mediated antiviral response. Here, we found that IFN- receptor stimulation also activated Unc-51–like kinase 1 (ULK1), an initiator of Beclin-1–mediated autophagy. Furthermore, the interaction between ULK1 and the mitogen-activated protein kinase kinase kinase MLK3 (mixed lineage kinase 3) was necessary for MLK3 phosphorylation and downstream activation of the kinase ERK5. This autophagy-independent activity of ULK1 promoted the transcription of key antiviral IFN-stimulated genes (ISGs) and was essential for IFN-–dependent antiviral effects. These findings define a previously unknown IFN- pathway that appears to be a key element of the antiviral response.〈/p〉
Print ISSN:
1945-0877
Electronic ISSN:
1937-9145
Topics:
Biology
,
Medicine
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