Activation of a novel ULK1-MLK3-ERK5 pathway by the IFNg receptor is required for IFNg-inducible antiviral responses

ABSTRACT: Although well established that signal transducer and activator of transcription 1 (STAT1) activation is required for an interferon (IFN)-mediated antiviral response, the potential roles of other IFNg-activated cellular pathways in the process are unknown. We provide evidence that Unc-51-like kinase 1 (ULK1) is activated during engagement of the Type II IFN receptor and is required for IFNg-mediated transcription of key interferon stimulated genes involved in anti-viral and innate immune responses.

ORGANISM(S): Mus musculus

PROVIDER: GSE118766 | GEO | 2018/11/20

REPOSITORIES: GEO