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PTEN: A master regulator of neuronal structure, function, and plasticity

PTEN (phosphatase and tensin homolog on chromosome ten) is a dual protein/lipid phosphatase that dephosphorylates PIP3, thereby inhibiting the AKT/mTOR pathway. This inhibition ultimately decreases protein translation, cell proliferation and cell growth. In the central nervous system, inhibition of...

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Detalles Bibliográficos
Autores principales: Garcia-Junco-Clemente, Pablo, Golshani, Peyman
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3995733/
https://www.ncbi.nlm.nih.gov/pubmed/24778766
http://dx.doi.org/10.4161/cib.28358
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author Garcia-Junco-Clemente, Pablo
Golshani, Peyman
author_facet Garcia-Junco-Clemente, Pablo
Golshani, Peyman
author_sort Garcia-Junco-Clemente, Pablo
collection PubMed
description PTEN (phosphatase and tensin homolog on chromosome ten) is a dual protein/lipid phosphatase that dephosphorylates PIP3, thereby inhibiting the AKT/mTOR pathway. This inhibition ultimately decreases protein translation, cell proliferation and cell growth. In the central nervous system, inhibition of PTEN leads to increased stem cell proliferation, somatic, dendritic and axonal growth, accelerated spine maturation, diminished synaptic plasticity, and altered intrinsic excitability. In agreement with these findings, patients carrying single-copy inactivating mutations of PTEN suffer from autism, macrocephaly, mental retardation, and epilepsy.(1)(-)(9) Understanding the mechanisms through which PTEN modulates the structure, function, and plasticity of cortical networks is a major focus of study. Preventing and reversing the changes induced by loss of Pten in model animals will pave the way for treatments in humans.
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spelling pubmed-39957332014-04-28 PTEN: A master regulator of neuronal structure, function, and plasticity Garcia-Junco-Clemente, Pablo Golshani, Peyman Commun Integr Biol Mini Review PTEN (phosphatase and tensin homolog on chromosome ten) is a dual protein/lipid phosphatase that dephosphorylates PIP3, thereby inhibiting the AKT/mTOR pathway. This inhibition ultimately decreases protein translation, cell proliferation and cell growth. In the central nervous system, inhibition of PTEN leads to increased stem cell proliferation, somatic, dendritic and axonal growth, accelerated spine maturation, diminished synaptic plasticity, and altered intrinsic excitability. In agreement with these findings, patients carrying single-copy inactivating mutations of PTEN suffer from autism, macrocephaly, mental retardation, and epilepsy.(1)(-)(9) Understanding the mechanisms through which PTEN modulates the structure, function, and plasticity of cortical networks is a major focus of study. Preventing and reversing the changes induced by loss of Pten in model animals will pave the way for treatments in humans. Landes Bioscience 2014-03-05 /pmc/articles/PMC3995733/ /pubmed/24778766 http://dx.doi.org/10.4161/cib.28358 Text en Copyright © 2014 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Mini Review
Garcia-Junco-Clemente, Pablo
Golshani, Peyman
PTEN: A master regulator of neuronal structure, function, and plasticity
title PTEN: A master regulator of neuronal structure, function, and plasticity
title_full PTEN: A master regulator of neuronal structure, function, and plasticity
title_fullStr PTEN: A master regulator of neuronal structure, function, and plasticity
title_full_unstemmed PTEN: A master regulator of neuronal structure, function, and plasticity
title_short PTEN: A master regulator of neuronal structure, function, and plasticity
title_sort pten: a master regulator of neuronal structure, function, and plasticity
topic Mini Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3995733/
https://www.ncbi.nlm.nih.gov/pubmed/24778766
http://dx.doi.org/10.4161/cib.28358
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