Cited by 112Ion channel regulation and functionCardiac electrophysiology and arrhythmiasIon Channels and Receptors

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Ca2+-dependent modulation of voltage-gated Ca2+ channels

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Christel, Carl, Lee, Amy·2012·Biochimica et Biophysica Acta (BBA) - General Subjects

DOI 10.1016/j.bbagen.2011.12.012PMC PMC3345169

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Abstract

Background Voltage-gated (Cav) Ca2+ channels are multi-subunit complexes that play diverse roles in a wide variety of tissues. A fundamental mechanism controlling Cav channel function involves the Ca2+ ions that permeate the channel pore. Ca2+ influx through Cav channels mediates feedback regulation to the channel that is both negative (Ca2+-dependent inactivation, CDI) and positive (Ca2+-dependent facilitation, CDF).Scope of review This review highlights general mechanisms of CDI and CDF with an emphasis on how these processes have been studied electrophysiologically in native and heterologous expression systems.Major conclusions Electrophysiological analyses have led to detailed insights into the mechanisms and prevalence of CDI and CDF as Cav channel regulatory mechanisms. All Cav channel family members undergo some form of Ca2+-dependent feedback that relies on CaM or a related Ca2+ binding protein. Tremendous progress has been made in characterizing the role of CaM in CDI and CDF. Yet, what contributes to the heterogeneity of CDI/CDF in various cell-types and how Ca2+-dependent regulation of Cav channels controls Ca2+ signaling remain largely unexplored.General significance Ca2+ influx through Cav channels regulates diverse physiological events including excitation-contraction coupling in muscle, neurotransmitter and hormone release, and Ca2+-dependent gene transcription. Therefore, the mechanisms that regulate channels, such as CDI and CDF, can have a large impact on the signaling potential of excitable cells in various physiological contexts. This article is part of a Special Issue entitled Biochemical, biophysical and genetic approaches to intracellular calcium signaling.

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Authors: Christel, C., & Lee, A.
Affiliations: University of Iowa (US)
Corresponding author: Lee, Amy
ORCID: Lee, Amy
Venue: Biochimica et Biophysica Acta (BBA) - General Subjects
Publisher: Elsevier BV
Published: 2012-08
Volume: 1820
Issue: 8
Pages: 1243-1252
ISSN: 0304-4165 (ISSN-L)
DOI: 10.1016/j.bbagen.2011.12.012
PMC: PMC3345169
OpenAlex: W2124030990
Cited by: 112
References: 182
Citations by year: 2026: 2 · 2025: 3 · 2024: 6 · 2023: 4 · 2022: 7 · 2021: 2 · 2020: 5 · 2019: 8 · 2018: 8 · 2017: 8 · 2016: 7 · 2015: 12 · 2014: 21 · 2013: 10 · 2012: 6
FWCI: 1.10
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Biochimica et Biophysica Acta (BBA) - General Subjects (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: U.S. Public Health Service (T32007121)
National Heart, Lung, and Blood Institute (R01HL087120, HL087120)
National Institute on Deafness and Other Communication Disorders (R55DC009433, DC009433, R01DC009433)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords: voltage-gated calcium channels, calcium-dependent inactivation, calcium feedback regulation, calmodulin, calcium signaling, excitation-contraction coupling, neurotransmitter release, heterologous expression systems
MeSH terms: Animals, Calcium, Calcium-Binding Proteins, Humans, Membrane Potentials, Neurons, Organ Specificity, Calcium Channels, Calcium Signaling, Protein Isoforms, Protein Subunits, Feedback, Physiological

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Ca2+-dependent modulation of voltage-gated Ca2+ channels

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