ArticleProceedings of the National Academy of Sciences of the United States of America2012
Ca2+ signaling amplification by oligomerization of L-type Cav1.2 channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed.
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- A precision medicine approach to interpret a GATA4 genetic variant in a paediatric patient with congenital heart disease.Human genomics · 2026Article
- Piezo1 in intestinal smooth muscle cells: Emerging perspectives.The Journal of physiology · 2026Review
- CaMKII clusters neuronal LTCCs in biomolecular condensates to gate excitation-transcription coupling.bioRxiv : the preprint server for biology · 2025Article
- Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025Review
- 14-3-3 promotes sarcolemmal expression of cardiac CaProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Ion channel traffic jams: the significance of trafficking deficiency in long QT syndrome.Cell discovery · 2025Review
- BIN1 knockdown rescues systolic dysfunction in aging male mouse hearts.Nature communications · 2024Article
- Unraveling the Connection: Cholesterol, Calcium Signaling, and Neurodegeneration.Neuroscience insights · 2024Article
- Gene editing and cardiac disease modelling for the interpretation of genetic variants of uncertain significance in congenital heart disease.Stem cell research & therapy · 2023Article
- Cardiac optogenetics: shining light on signaling pathways.Pflugers Archiv : European journal of physiology · 2023Review
- The formation of KCommunications biology · 2023Article
- Excitation-transcription coupling, neuronal gene expression and synaptic plasticity.Nature reviews. Neuroscience · 2023Review
- Pairwise biosynthesis of ion channels stabilizes excitability and mitigates arrhythmias.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Clustering of CaJournal of neurochemistry · 2023Article
- NPC1-dependent alterations in KNature communications · 2023Article
- The formation of KResearch square · 2023Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Ca(2+) influx via L-type Ca(v)1.2 channels is essential for multiple physiological processes, including gene expression, excitability, and contraction. Amplification of the Ca(2+) signals produced by the opening of these channels is a hallmark of many intracellular signaling cascades, including excitation-contraction coupling in heart. Using optogenetic approaches, we discovered that Ca(v)1.2 channels form clusters of varied sizes in ventricular myocytes. Physical interaction between these channels via their C-tails renders them capable of coordinating their gating, thereby amplifying Ca(2+) influx and excitation-contraction coupling. Light-induced fusion of WT Ca(v)1.2 channels with Ca(v)1.2 channels carrying a gain-of-function mutation that causes arrhythmias and autism in humans with Timothy syndrome (Ca(v)1.2-TS) increased Ca(2+) currents, diastolic and systolic Ca(2+) levels, contractility and the frequency of arrhythmogenic Ca(2+) fluctuations in ventricular myocytes. Our data indicate that these changes in Ca(2+) signaling resulted from Ca(v)1.2-TS increasing the activity of adjoining WT Ca(v)1.2 channels. Collectively, these data support the concept that oligomerization of Ca(v)1.2 channels via their C termini can result in the amplification of Ca(2+) influx into excitable cells.
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