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Molecular Determinants of Ca(v)1.2 Calcium Channel Inactivation

Voltage-gated L-type Ca(v)1.2 calcium channels couple membrane depolarization to transient increase in cytoplasmic free Ca(2+) concentration that initiates a number of essential cellular functions including cardiac and vascular muscle contraction, gene expression, neuronal plasticity, and exocytosis...

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Detalles Bibliográficos
Autor principal: Soldatov, Nikolai M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scholarly Research Network 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4890872/
https://www.ncbi.nlm.nih.gov/pubmed/27335667
http://dx.doi.org/10.5402/2012/691341
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author Soldatov, Nikolai M.
author_facet Soldatov, Nikolai M.
author_sort Soldatov, Nikolai M.
collection PubMed
description Voltage-gated L-type Ca(v)1.2 calcium channels couple membrane depolarization to transient increase in cytoplasmic free Ca(2+) concentration that initiates a number of essential cellular functions including cardiac and vascular muscle contraction, gene expression, neuronal plasticity, and exocytosis. Inactivation or spontaneous termination of the calcium current through Ca(v)1.2 is a critical step in regulation of these processes. The pathophysiological significance of this process is manifested in hypertension, heart failure, arrhythmia, and a number of other diseases where acceleration of the calcium current decay should present a benefit function. The central issue of this paper is the inactivation of the Ca(v)1.2 calcium channel mediated by multiple determinants.
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spelling pubmed-48908722016-06-22 Molecular Determinants of Ca(v)1.2 Calcium Channel Inactivation Soldatov, Nikolai M. ISRN Mol Biol Review Article Voltage-gated L-type Ca(v)1.2 calcium channels couple membrane depolarization to transient increase in cytoplasmic free Ca(2+) concentration that initiates a number of essential cellular functions including cardiac and vascular muscle contraction, gene expression, neuronal plasticity, and exocytosis. Inactivation or spontaneous termination of the calcium current through Ca(v)1.2 is a critical step in regulation of these processes. The pathophysiological significance of this process is manifested in hypertension, heart failure, arrhythmia, and a number of other diseases where acceleration of the calcium current decay should present a benefit function. The central issue of this paper is the inactivation of the Ca(v)1.2 calcium channel mediated by multiple determinants. International Scholarly Research Network 2012-10-17 /pmc/articles/PMC4890872/ /pubmed/27335667 http://dx.doi.org/10.5402/2012/691341 Text en Copyright © 2012 Nikolai M. Soldatov. https://creativecommons.org/licenses/by/3.0/ 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.
spellingShingle Review Article
Soldatov, Nikolai M.
Molecular Determinants of Ca(v)1.2 Calcium Channel Inactivation
title Molecular Determinants of Ca(v)1.2 Calcium Channel Inactivation
title_full Molecular Determinants of Ca(v)1.2 Calcium Channel Inactivation
title_fullStr Molecular Determinants of Ca(v)1.2 Calcium Channel Inactivation
title_full_unstemmed Molecular Determinants of Ca(v)1.2 Calcium Channel Inactivation
title_short Molecular Determinants of Ca(v)1.2 Calcium Channel Inactivation
title_sort molecular determinants of ca(v)1.2 calcium channel inactivation
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4890872/
https://www.ncbi.nlm.nih.gov/pubmed/27335667
http://dx.doi.org/10.5402/2012/691341
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