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PI3K Signaling in Neurons: A Central Node for the Control of Multiple Functions

Phosphoinositide 3-kinase (PI3K) signaling contributes to a variety of processes, mediating many aspects of cellular function, including nutrient uptake, anabolic reactions, cell growth, proliferation, and survival. Less is known regarding its critical role in neuronal physiology, neuronal metabolis...

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Detalles Bibliográficos
Autores principales: Sánchez-Alegría, Karina, Flores-León, Manuel, Avila-Muñoz, Evangelina, Rodríguez-Corona, Nelly, Arias, Clorinda
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6321294/
https://www.ncbi.nlm.nih.gov/pubmed/30477115
http://dx.doi.org/10.3390/ijms19123725
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author Sánchez-Alegría, Karina
Flores-León, Manuel
Avila-Muñoz, Evangelina
Rodríguez-Corona, Nelly
Arias, Clorinda
author_facet Sánchez-Alegría, Karina
Flores-León, Manuel
Avila-Muñoz, Evangelina
Rodríguez-Corona, Nelly
Arias, Clorinda
author_sort Sánchez-Alegría, Karina
collection PubMed
description Phosphoinositide 3-kinase (PI3K) signaling contributes to a variety of processes, mediating many aspects of cellular function, including nutrient uptake, anabolic reactions, cell growth, proliferation, and survival. Less is known regarding its critical role in neuronal physiology, neuronal metabolism, tissue homeostasis, and the control of gene expression in the central nervous system in healthy and diseased states. The aim of the present work is to review cumulative evidence regarding the participation of PI3K pathways in neuronal function, focusing on their role in neuronal metabolism and transcriptional regulation of genes involved in neuronal maintenance and plasticity or on the expression of pathological hallmarks associated with neurodegeneration.
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spelling pubmed-63212942019-01-07 PI3K Signaling in Neurons: A Central Node for the Control of Multiple Functions Sánchez-Alegría, Karina Flores-León, Manuel Avila-Muñoz, Evangelina Rodríguez-Corona, Nelly Arias, Clorinda Int J Mol Sci Review Phosphoinositide 3-kinase (PI3K) signaling contributes to a variety of processes, mediating many aspects of cellular function, including nutrient uptake, anabolic reactions, cell growth, proliferation, and survival. Less is known regarding its critical role in neuronal physiology, neuronal metabolism, tissue homeostasis, and the control of gene expression in the central nervous system in healthy and diseased states. The aim of the present work is to review cumulative evidence regarding the participation of PI3K pathways in neuronal function, focusing on their role in neuronal metabolism and transcriptional regulation of genes involved in neuronal maintenance and plasticity or on the expression of pathological hallmarks associated with neurodegeneration. MDPI 2018-11-23 /pmc/articles/PMC6321294/ /pubmed/30477115 http://dx.doi.org/10.3390/ijms19123725 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Sánchez-Alegría, Karina
Flores-León, Manuel
Avila-Muñoz, Evangelina
Rodríguez-Corona, Nelly
Arias, Clorinda
PI3K Signaling in Neurons: A Central Node for the Control of Multiple Functions
title PI3K Signaling in Neurons: A Central Node for the Control of Multiple Functions
title_full PI3K Signaling in Neurons: A Central Node for the Control of Multiple Functions
title_fullStr PI3K Signaling in Neurons: A Central Node for the Control of Multiple Functions
title_full_unstemmed PI3K Signaling in Neurons: A Central Node for the Control of Multiple Functions
title_short PI3K Signaling in Neurons: A Central Node for the Control of Multiple Functions
title_sort pi3k signaling in neurons: a central node for the control of multiple functions
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6321294/
https://www.ncbi.nlm.nih.gov/pubmed/30477115
http://dx.doi.org/10.3390/ijms19123725
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