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ERK1/2 in immune signalling

Extracellular signal-related kinases 1 and 2 (ERK1/2) are the final components of the mitogen-activated protein kinase (MAPK) phosphorylation cascade, an integral module in a diverse array of signalling pathways for shaping cell behaviour and fate. More recently, studies have shown that ERK1/2 plays...

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Detalles Bibliográficos
Autores principales: Lucas, Richard M., Luo, Lin, Stow, Jennifer L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9704528/
https://www.ncbi.nlm.nih.gov/pubmed/36281999
http://dx.doi.org/10.1042/BST20220271
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author Lucas, Richard M.
Luo, Lin
Stow, Jennifer L.
author_facet Lucas, Richard M.
Luo, Lin
Stow, Jennifer L.
author_sort Lucas, Richard M.
collection PubMed
description Extracellular signal-related kinases 1 and 2 (ERK1/2) are the final components of the mitogen-activated protein kinase (MAPK) phosphorylation cascade, an integral module in a diverse array of signalling pathways for shaping cell behaviour and fate. More recently, studies have shown that ERK1/2 plays an essential role downstream of immune receptors to elicit inflammatory gene expression in response to infection and cell or tissue damage. Much of this work has studied ERK1/2 activation in Toll-like receptor (TLR) pathways, providing mechanistic insights into its recruitment, compartmentalisation and activation in cells of the innate immune system. In this review, we summarise the typical activation of ERK1/2 in growth factor receptor pathways before discussing its known roles in immune cell signalling with a focus downstream of TLRs. We examine emerging research uncovering evidence of dysfunctional ERK1/2 signalling in inflammatory diseases and discuss the potential therapeutic benefit of targeting ERK1/2 pathways in inflammation.
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spelling pubmed-97045282022-12-06 ERK1/2 in immune signalling Lucas, Richard M. Luo, Lin Stow, Jennifer L. Biochem Soc Trans Review Articles Extracellular signal-related kinases 1 and 2 (ERK1/2) are the final components of the mitogen-activated protein kinase (MAPK) phosphorylation cascade, an integral module in a diverse array of signalling pathways for shaping cell behaviour and fate. More recently, studies have shown that ERK1/2 plays an essential role downstream of immune receptors to elicit inflammatory gene expression in response to infection and cell or tissue damage. Much of this work has studied ERK1/2 activation in Toll-like receptor (TLR) pathways, providing mechanistic insights into its recruitment, compartmentalisation and activation in cells of the innate immune system. In this review, we summarise the typical activation of ERK1/2 in growth factor receptor pathways before discussing its known roles in immune cell signalling with a focus downstream of TLRs. We examine emerging research uncovering evidence of dysfunctional ERK1/2 signalling in inflammatory diseases and discuss the potential therapeutic benefit of targeting ERK1/2 pathways in inflammation. Portland Press Ltd. 2022-10-31 2022-10-25 /pmc/articles/PMC9704528/ /pubmed/36281999 http://dx.doi.org/10.1042/BST20220271 Text en © 2022 The Author(s) https://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) . Open access for this article was enabled by the participation of the University of Queensland in an all-inclusive Read & Publish agreement with Portland Press and the Biochemical Society under a transformative agreement with CAUL.
spellingShingle Review Articles
Lucas, Richard M.
Luo, Lin
Stow, Jennifer L.
ERK1/2 in immune signalling
title ERK1/2 in immune signalling
title_full ERK1/2 in immune signalling
title_fullStr ERK1/2 in immune signalling
title_full_unstemmed ERK1/2 in immune signalling
title_short ERK1/2 in immune signalling
title_sort erk1/2 in immune signalling
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9704528/
https://www.ncbi.nlm.nih.gov/pubmed/36281999
http://dx.doi.org/10.1042/BST20220271
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