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Redundancy in the World of MAP Kinases: All for One

The protein kinases ERK1 and ERK2 are the effector components of the prototypical ERK1/2 mitogen-activated protein (MAP) kinase pathway. This signaling pathway regulates cell proliferation, differentiation and survival, and is essential for embryonic development and cellular homeostasis. ERK1 and ER...

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Autores principales: Saba-El-Leil, Marc K., Frémin, Christophe, Meloche, Sylvain
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4921452/
https://www.ncbi.nlm.nih.gov/pubmed/27446918
http://dx.doi.org/10.3389/fcell.2016.00067
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author Saba-El-Leil, Marc K.
Frémin, Christophe
Meloche, Sylvain
author_facet Saba-El-Leil, Marc K.
Frémin, Christophe
Meloche, Sylvain
author_sort Saba-El-Leil, Marc K.
collection PubMed
description The protein kinases ERK1 and ERK2 are the effector components of the prototypical ERK1/2 mitogen-activated protein (MAP) kinase pathway. This signaling pathway regulates cell proliferation, differentiation and survival, and is essential for embryonic development and cellular homeostasis. ERK1 and ERK2 homologs share similar biochemical properties but whether they exert specific physiological functions or act redundantly has been a matter of controversy. However, recent studies now provide compelling evidence in support of functionally redundant roles of ERK1 and ERK2 in embryonic development and physiology. In this review, we present a critical assessment of the evidence for the functional specificity or redundancy of MAP kinase isoforms. We focus on the ERK1/ERK2 pathway but also discuss the case of JNK and p38 isoforms.
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spelling pubmed-49214522016-07-21 Redundancy in the World of MAP Kinases: All for One Saba-El-Leil, Marc K. Frémin, Christophe Meloche, Sylvain Front Cell Dev Biol Cell and Developmental Biology The protein kinases ERK1 and ERK2 are the effector components of the prototypical ERK1/2 mitogen-activated protein (MAP) kinase pathway. This signaling pathway regulates cell proliferation, differentiation and survival, and is essential for embryonic development and cellular homeostasis. ERK1 and ERK2 homologs share similar biochemical properties but whether they exert specific physiological functions or act redundantly has been a matter of controversy. However, recent studies now provide compelling evidence in support of functionally redundant roles of ERK1 and ERK2 in embryonic development and physiology. In this review, we present a critical assessment of the evidence for the functional specificity or redundancy of MAP kinase isoforms. We focus on the ERK1/ERK2 pathway but also discuss the case of JNK and p38 isoforms. Frontiers Media S.A. 2016-06-27 /pmc/articles/PMC4921452/ /pubmed/27446918 http://dx.doi.org/10.3389/fcell.2016.00067 Text en Copyright © 2016 Saba-El-Leil, Frémin and Meloche. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cell and Developmental Biology
Saba-El-Leil, Marc K.
Frémin, Christophe
Meloche, Sylvain
Redundancy in the World of MAP Kinases: All for One
title Redundancy in the World of MAP Kinases: All for One
title_full Redundancy in the World of MAP Kinases: All for One
title_fullStr Redundancy in the World of MAP Kinases: All for One
title_full_unstemmed Redundancy in the World of MAP Kinases: All for One
title_short Redundancy in the World of MAP Kinases: All for One
title_sort redundancy in the world of map kinases: all for one
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4921452/
https://www.ncbi.nlm.nih.gov/pubmed/27446918
http://dx.doi.org/10.3389/fcell.2016.00067
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