ArticleProceedings of the National Academy of Sciences of the United States of America1998
Ca2+-sensitive inactivation of L-type Ca2+ channels depends on multiple cytoplasmic amino acid sequences of the alpha1C subunit.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
68 citing papers in PubMed, 189 citations in OpenAlex.
- Calmodulin D133H Disrupts CaCells · 2025Article
- Calmodulin binding is required for calcium mediated TRPA1 desensitization.Nature communications · 2025Article
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated CaActa physiologica (Oxford, England) · 2025Article
- Structural biology and molecular pharmacology of voltage-gated ion channels.Nature reviews. Molecular cell biology · 2024Review
- Calmodulin Mutations in Human Disease.Channels (Austin, Tex.) · 2023Review
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- Calcium Channel Splice Variants and Their Effects in Brain and Cardiovascular Function.Advances in experimental medicine and biology · 2021Article
- Update on the Molecular Genetics of Timothy Syndrome.Frontiers in pediatrics · 2021Review
- Bilobal architecture is a requirement for calmodulin signaling to CaProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Direct visualization of interaction between calmodulin and connexin45.The Biochemical journal · 2017Article
- A rendezvous with the queen of ion channels: Three decades of ion channel research by David T Yue and his Calcium Signals Laboratory.Channels (Austin, Tex.) · 2016Article
- Polycystin-2 (TRPP2) Regulation by Ca(2+) Is Effected and Diversified by Actin-Binding Proteins.Biophysical journal · 2015Article
- Towards a Unified Theory of Calmodulin Regulation (Calmodulation) of Voltage-Gated Calcium and Sodium Channels.Current molecular pharmacology · 2015Review
- Article
- Calmodulin regulation (calmodulation) of voltage-gated calcium channels.The Journal of general physiology · 2014Review
- Gap junction regulation by calmodulin.FEBS letters · 2014Review
- Ca(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequences.Frontiers in pharmacology · 2014Review
- Structure-function of proteins interacting with the α1 pore-forming subunit of high-voltage-activated calcium channels.Frontiers in physiology · 2014Review
- Lobe-related concentration- and Ca(2+)-dependent interactions of calmodulin with C- and N-terminal tails of the CaV1.2 channel.The journal of physiological sciences : JPS · 2013Article
- Regulation of voltage-gated calcium channels by proteolysis.Sheng li xue bao : [Acta physiologica Sinica] · 2012Review
8 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca2+-dependent inactivation of Ca2+ currents is a physiological phenomenon widely associated with L-type Ca2+ channels. Although the pore-forming alpha1C subunit of the channel is the target for Ca2+ binding, the amino acid sequences involved in the binding and/or in the coordination of Ca2+-dependent inactivation are still unclear. Based on previous experiments, we have prepared truncation mutants of a human alpha1C subunit by systematically deleting an EF-hand motif and sequences in a segment of 80 amino acids in the carboxyl-terminal tail. We found that the rate as well as the Ca2+ dependence of inactivation of currents through these mutated channels were very different. We have identified three amino acid sequences, the presence of which is important for Ca2+-dependent inactivation: (i) a putative Ca2+-binding EF-hand motif, (ii) two hydrophilic residues (asparagine and glutamic acid) 77-78 amino acids downstream of the EF-hand motif, and (iii) a putative IQ calmodulin binding motif. We suggest that Ca2+-dependent inactivation is a cooperative process involving several amino acid sequences in cytoplasmic segments of the alpha1C subunit.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.