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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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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scholarly Research Network
2012
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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 |
Sumario: | 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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