ArticleThe Journal of biological chemistry2011
Functional properties of a newly identified C-terminal splice variant of Cav1.3 L-type Ca2+ channels.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed.
- Impact of CaInternational journal of molecular sciences · 2026Review
- Calmodulinopathy variants impair CaV1.3 and CaV2.1 regulation.The Journal of general physiology · 2026Article
- Sudden death-associated KCNH2 variants exert opposing effects on a nuclear subdomain of the cardiac potassium channel hERG1.The Journal of biological chemistry · 2026Article
- Sclareol and cinnarizine are non-selective inhibitors of voltage-gated Cav1.3 L-type CaChannels (Austin, Tex.) · 2025Article
- Exploring the potential for gene therapy in Cav1.4-related retinal channelopathies.Channels (Austin, Tex.) · 2025Review
- Role of the C-terminal domain in modifying pH-dependent regulation of CaChannels (Austin, Tex.) · 2025Article
- Sudden Death-AssociatedbioRxiv : the preprint server for biology · 2025Article
- Calcium channel-coupled transcription factors facilitate direct nuclear signaling.Research square · 2025Article
- L-Type Voltage-Gated CaBiochemistry · 2025Article
- Genetic Alterations in Atypical Cerebral Palsy Identified Through Chromosomal Microarray and Exome Sequencing.International journal of molecular sciences · 2025Article
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- CaBP1 and 2 enable sustained CaeLife · 2024Article
- Opto-chemogenetic inhibition of L-type CaCell reports methods · 2024Article
- Selective blockade of CaNature communications · 2024Article
- Clustering of CaJournal of neurochemistry · 2023Article
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- Germline de novo variant F747S extends the phenotypic spectrum of CACNA1D Ca2+ channelopathies.Human molecular genetics · 2023Article
- The Role of Voltage-Gated Calcium Channels in Basal Ganglia Neurodegenerative Disorders.Current neuropharmacology · 2023Review
- Regulation of Presynaptic Calcium Channels.Advances in neurobiology · 2023Article
- CACNA1D-Related Channelopathies: From Hypertension to Autism.Handbook of experimental pharmacology · 2023Review
38 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors.
Funding
Abstract
An intramolecular interaction between a distal (DCRD) and a proximal regulatory domain (PCRD) within the C terminus of long Ca(v)1.3 L-type Ca(2+) channels (Ca(v)1.3(L)) is a major determinant of their voltage- and Ca(2+)-dependent gating kinetics. Removal of these regulatory domains by alternative splicing generates Ca(v)1.3(42A) channels that activate at a more negative voltage range and exhibit more pronounced Ca(2+)-dependent inactivation. Here we describe the discovery of a novel short splice variant (Ca(v)1.3(43S)) that is expressed at high levels in the brain but not in the heart. It lacks the DCRD but, in contrast to Ca(v)1.3(42A), still contains PCRD. When expressed together with α2δ1 and β3 subunits in tsA-201 cells, Ca(v)1.3(43S) also activated at more negative voltages like Ca(v)1.3(42A) but Ca(2+)-dependent inactivation was less pronounced. Single channel recordings revealed much higher channel open probabilities for both short splice variants as compared with Ca(v)1.3(L). The presence of the proximal C terminus in Ca(v)1.3(43S) channels preserved their modulation by distal C terminus-containing Ca(v)1.3- and Ca(v)1.2-derived C-terminal peptides. Removal of the C-terminal modulation by alternative splicing also induced a faster decay of Ca(2+) influx during electrical activities mimicking trains of neuronal action potentials. Our findings extend the spectrum of functionally diverse Ca(v)1.3 L-type channels produced by tissue-specific alternative splicing. This diversity may help to fine tune Ca(2+) channel signaling and, in the case of short variants lacking a functional C-terminal modulation, prevent excessive Ca(2+) accumulation during burst firing in neurons. This may be especially important in neurons that are affected by Ca(2+)-induced neurodegenerative processes.
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