Review
Version 1
Preserved in Portico This version is not peer-reviewed
Extracellular Signal-Regulated Kinases: One Pathway, Multiple Fates
Version 1
: Received: 24 November 2023 / Approved: 27 November 2023 / Online: 28 November 2023 (08:10:31 CET)
A peer-reviewed article of this Preprint also exists.
Deschênes-Simard, X.; Malleshaiah, M.; Ferbeyre, G. Extracellular Signal-Regulated Kinases: One Pathway, Multiple Fates. Cancers 2024, 16, 95. Deschênes-Simard, X.; Malleshaiah, M.; Ferbeyre, G. Extracellular Signal-Regulated Kinases: One Pathway, Multiple Fates. Cancers 2024, 16, 95.
Abstract
This comprehensive review delves into the multifaceted aspects of ERK signaling and the intricate mechanisms underlying distinct cellular fates. ERK1 and ERK2 (ERK) govern proliferation, transformation, epithelial-mesenchymal transition, differentiation, senescence, or cell death, con-tingent upon activation strength, duration, and context. The biochemical mechanisms underlying these outcomes are inadequately understood, shaped by signaling feedback and the spatial localization of ERK activation. Generally, ERK activation aligns with the Goldilocks principle in cell fate determination. Excessive or insufficient ERK activity inhibits growth, whereas moderated activation supports proliferation and survival. Unraveling the intricacies of how the degree of ERK activation dictates cell fate requires deciphering mechanisms encompassing protein stability, transcription factors downstream of ERK, and the chromatin landscape.
Keywords
cell proliferation; cell fate; ERK; senescence; cell signaling; EMT; apoptosis; pluripotency
Subject
Medicine and Pharmacology, Oncology and Oncogenics
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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