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Type I Interferon (IFN)-Regulated Activation of Canonical and Non-Canonical Signaling Pathways Open Access (recommended)

Descriptions

Resource type(s)

Review

Keyword

interferon
signaling
MAP kinase signaling
signal transducer and activator of transcription
mammalian target of rapamycin
mRNA translation
SARS-CoV-2
COVID-19

Rights

Attribution 4.0 International

Creator

Mazewski, Candice Elise
Perez, Ricardo Ernesto
Fish, Eleanor N
Platanias, Leonidas C

Abstract

For several decades there has been accumulating evidence implicating type I interferons (IFNs) as key elements of the immune response. Therapeutic approaches incorporating different recombinant type I IFN proteins have been successfully employed to treat a diverse group of diseases with significant and positive outcomes. The biological activities of type I IFNs are consequences of signaling events occurring in the cytoplasm and nucleus of cells. Biochemical events involving JAK/STAT proteins that control transcriptional activation of IFN-stimulated genes (ISGs) were the first to be identified and are referred to as canonical signaling. Subsequent identification of JAK/STAT-independent signaling pathways, critical for ISG transcription and/or mRNA translation, are denoted as non-canonical or non-classical pathways. In this review, we summarize these signaling cascades and discuss recent developments in the field, specifically as they relate to the biological and clinical implications of engagement of both canonical and non-canonical pathways.

Original Bibliographic Citation

Mazewski C, Perez RE, Fish EN, Platanias LC. Type I Interferon (IFN)-Regulated Activation of Canonical and Non-Canonical Signaling Pathways. Frontiers in Immunology. 2020;11:13.

Related URL

 https://www.frontiersin.org/articles/10.3389/fimmu.2020.606456/full

Publisher

FRONTIERS MEDIA SA

Date Created

2020-11-23

Original Identifier

(PMID) 33329603

Language

English

Subject: MESH

Receptor, Interferon alpha-beta
Signal Transduction
MAP Kinase Signaling System
Sirolimus
Protein Biosynthesis
COVID-19
SARS-CoV-2

Grants and funding

NIH United States Department of Health & Human Services National Institutes of Health (NIH) - USA [CA77816, CA121192]; NIH/NCI United States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Cancer Institute (NCI) [T32 CA070085]

DOI

10.3389/fimmu.2020.606456

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