Journal article
The road to ERK activation: Do neurons take alternate routes?
Cellular signalling, Vol.68, pp.109541-109541
04/01/2020
DOI: 10.1016/j.cellsig.2020.109541
PMCID: 7127974
PMID: 31945453
Abstract
The ERK cascade is a central signaling pathway that regulates a wide variety of cellular processes including proliferation, differentiation, learning and memory, development, and synaptic plasticity. A wide range of inputs travel from the membrane through different signaling pathway routes to reach activation of one set of output kinases, ERK1&2. The classical ERK activation pathway beings with growth factor activation of receptor tyrosine kinases. Numerous G-protein coupled receptors and ionotropic receptors also lead to ERK through increases in the second messengers calcium and cAMP. Though both types of pathways are present in diverse cell types, a key difference is that most stimuli to neurons, e.g. synaptic inputs, are transient, on the order of milliseconds to seconds, whereas many stimuli acting on non-neural tissue, e.g. growth factors, are longer duration. The ability to consolidate these inputs to regulate the activation of ERK in response to diverse signals raises the question of which factors influence the difference in ERK activation pathways. This review presents both experimental studies and computational models aimed at understanding the control of ERK activation and whether there are fundamental differences between neurons and other cells. Our main conclusion is that differences between cell types are quite subtle, often related to differences in expression pattern and quantity of some molecules such as Raf isoforms. In addition, the spatial location of ERK is critical, with regulation by scaffolding proteins producing differences due to colocalization of upstream molecules that may differ between neurons and other cells.
Details
- Title: Subtitle
- The road to ERK activation: Do neurons take alternate routes?
- Creators
- Nadiatou Miningou - George Mason UniversityKim T. Blackwell - George Mason University
- Resource Type
- Journal article
- Publication Details
- Cellular signalling, Vol.68, pp.109541-109541
- DOI
- 10.1016/j.cellsig.2020.109541
- PMID
- 31945453
- PMCID
- 7127974
- NLM abbreviation
- Cell Signal
- ISSN
- 0898-6568
- eISSN
- 1873-3913
- Publisher
- Elsevier
- Number of pages
- 13
- Grant note
- R01 AA016022 / NIAAA; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute on Alcohol Abuse & Alcoholism (NIAAA) 1515686 / joint NIH-NSF CRCNS program through NSF
- Language
- English
- Date published
- 04/01/2020
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Iowa Neuroscience Institute
- Record Identifier
- 9984446268802771
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