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Regulation of Ca(2+) transient by PP2A in normal and failing heart

Calcium transient in cardiomyocytes is regulated by multiple protein kinases and phosphatases. PP2A is a major protein phosphatase in the heart modulating Ca(2+) handling through an array of ion channels, antiporters and pumps, etc. The assembly, localization/translocation, and substrate specificity...

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Detalles Bibliográficos
Autores principales: Lei, Ming, Wang, Xin, Ke, Yunbo, Solaro, R. John
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4310266/
https://www.ncbi.nlm.nih.gov/pubmed/25688213
http://dx.doi.org/10.3389/fphys.2015.00013
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author Lei, Ming
Wang, Xin
Ke, Yunbo
Solaro, R. John
author_facet Lei, Ming
Wang, Xin
Ke, Yunbo
Solaro, R. John
author_sort Lei, Ming
collection PubMed
description Calcium transient in cardiomyocytes is regulated by multiple protein kinases and phosphatases. PP2A is a major protein phosphatase in the heart modulating Ca(2+) handling through an array of ion channels, antiporters and pumps, etc. The assembly, localization/translocation, and substrate specificity of PP2A are controlled by different post-translational mechanisms, which in turn are linked to the activities of upstream signaling molecules. Abnormal PP2A expression and activities are associated with defective response to β-adrenergic stimulation and are indication and causal factors in arrhythmia and heart failure.
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spelling pubmed-43102662015-02-16 Regulation of Ca(2+) transient by PP2A in normal and failing heart Lei, Ming Wang, Xin Ke, Yunbo Solaro, R. John Front Physiol Physiology Calcium transient in cardiomyocytes is regulated by multiple protein kinases and phosphatases. PP2A is a major protein phosphatase in the heart modulating Ca(2+) handling through an array of ion channels, antiporters and pumps, etc. The assembly, localization/translocation, and substrate specificity of PP2A are controlled by different post-translational mechanisms, which in turn are linked to the activities of upstream signaling molecules. Abnormal PP2A expression and activities are associated with defective response to β-adrenergic stimulation and are indication and causal factors in arrhythmia and heart failure. Frontiers Media S.A. 2015-01-29 /pmc/articles/PMC4310266/ /pubmed/25688213 http://dx.doi.org/10.3389/fphys.2015.00013 Text en Copyright © 2015 Lei, Wang, Ke and Solaro. 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 Physiology
Lei, Ming
Wang, Xin
Ke, Yunbo
Solaro, R. John
Regulation of Ca(2+) transient by PP2A in normal and failing heart
title Regulation of Ca(2+) transient by PP2A in normal and failing heart
title_full Regulation of Ca(2+) transient by PP2A in normal and failing heart
title_fullStr Regulation of Ca(2+) transient by PP2A in normal and failing heart
title_full_unstemmed Regulation of Ca(2+) transient by PP2A in normal and failing heart
title_short Regulation of Ca(2+) transient by PP2A in normal and failing heart
title_sort regulation of ca(2+) transient by pp2a in normal and failing heart
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4310266/
https://www.ncbi.nlm.nih.gov/pubmed/25688213
http://dx.doi.org/10.3389/fphys.2015.00013
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