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Published November 23, 2020 | Version v1.0.0
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Type I Interferon (IFN)-Regulated Activation of Canonical and Non-Canonical Signaling Pathways

Creators

  • 1. ROR icon Northwestern University
  • 2. ROR icon University of Toronto

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.

Other

original_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.

Files

fimmu-11-606456.pdf

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Additional details

Identifiers

PMID
33329603

Related works

Is related to
https://www.frontiersin.org/articles/10.3389/fimmu.2020.606456/full (URL)

Funding

National Cancer Institute
Targeting Novel Protein Complexes for the Treatment of Acute Myeloid Leukemia 5R01CA121192
National Cancer Institute
Signal Transduction of Type 1 Interferons in Malignant Cells 5R01CA077816
National Cancer Institute
Training Program in Signal Transduction and Cancer 5T32CA070085

Dates

Created
2020-11-23
When the item was originally created.