The DOI matches its Crossref record; 177 of the 182 references it cites were found in a registry or an index.
Ca2+-dependent modulation of voltage-gated Ca2+ channels
Open accessAbstract
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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“Voltage-gated calcium channels are essential in regulating extracellular Ca2+ influx in a wide variety of tissues [40].”
From G-protein-coupled receptor participates in 20-hydroxyecdysone signaling on the plasma membrane (2014) · cites this paper as [40]
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Calmodulin kinase determines calcium-dependent facilitation of L-type calcium channels
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RetractedRETRACTED: L-Type Ca2+ Channel Facilitation Mediated by Phosphorylation of the β Subunit by CaMKII
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RetractedStructure and Regulation of Voltage-Gated Ca 2+ Channels
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- Halling, 2006, Regulation of voltage-gated Ca2+ channels by calmodulin, Sci. STKE, er1
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Items 101–111 of 111
Rose, R. A. (2013) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.717959842.793473203
Neuromodulation of Calcium Channels☆
Lee, A. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.04685-7
Self-citationThe calcium transient coupled to the L-type calcium current attenuates cardiac alternans
Warren, M. D., & Poelzing, S. (2024) · Frontiers in Physiology · doi:10.3389/fphys.2024.1404886
Thomas, J. R., Sun, J., Vázquez, J. D. L. R., & Lee, A. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.11.19.624430
Self-citationComplex regulation of Cav2.2 N-type Ca2+ channels by Ca2+ and G-proteins
Thomas, J. R., Sun, J., Vázquez, J. D. L. R., & Lee, A. (2025) · PLoS ONE · doi:10.1371/journal.pone.0314839
Self-citationStructural Insights into L-Type Voltage-Gated Ca 2+ Channel (Ca V 1.2) Activation by CaBP1
Salveson, I., Anderson, D. E., Bej, A., Nieves‐Cintrón, M., Navedo, M. F., Hell, J. W., & Ames, J. B. (2026) · Biochemistry · doi:10.1021/acs.biochem.6c00032
Cardioprotection contre les lésions d’ischémie-reperfusion par réduction de la fréquence cardiaque
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Presynaptic CaV2.1 calcium-dependent facilitation enables reliable auditory information transfer
Al-Yaari, M., Li, J., Keine, C., Hunger, B., Hansen, M. R., & Young, S. (2026) · Cell Reports · doi:10.1016/j.celrep.2026.117874
Metadata
- 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)
- 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
- 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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