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IFNγ-inducible antiviral responses require ULK1-mediated activation of MLK3 and ERK5

Published Date:

November 20 2018

Source:

Sci Signal. 11(557)

Language:

English

[PDF-2.26 MB]

Details:

Alternative Title:

Sci Signal

Personal Author:

Saleiro, Diana ; Blyth, Gavin T. ; Kosciuczuk, Ewa M. ; Ozark, Patrick A. ; Majchrzak-Kita, Beata ; ... More ▼

Description:

It is well established that activation of the transcription factor signal transducer and activator of transcription 1 (STAT1) is required for the interferon-γ (IFN-γ)-mediated antiviral response. Here, we found that IFN-γ 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-γ-dependent antiviral effects. These findings define a previously unknown IFN-γ pathway that appears to be a key element of the antiviral response.

Subject:

[+]

Pubmed ID:

30459284

Pubmed Central ID:

PMC6684240

Document Type:

Journal Article

Funding:

R01 CA077816/NCI NIH HHS/National Cancer Institute/United States ; I01 CX000916/CSRD VA/Clinical Science Research & Development/United States ; S10 OD011996/ODCDC CDC HHS/Office of the Director/United States ; R01 CA161796/NCI NIH HHS/National Cancer Institute/United States ; P41 GM108569/NIGMS NIH HHS/National Institute of General Medical Sciences/United States ; ... More ▼

Collection(s):

CDC Public Access

Main Document Checksum:

[+]

Supporting Files:

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