ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
The [beta]2a subunit is a molecular groom for the Ca2+ channel inactivation gate.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed.
- Selective posttranslational inhibition of CaNature communications · 2022Article
- Mammalian Brain CaMembranes · 2022Article
- How CaThe Journal of general physiology · 2019Article
- Atomic Mechanisms of Timothy Syndrome-Associated Mutations in Calcium Channel Cav1.2.Frontiers in physiology · 2019Article
- The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection.The Biochemical journal · 2017Review
- Article
- Structural and functional plasticity in long-term cultures of adult ventricular myocytes.Journal of molecular and cellular cardiology · 2013Article
- Characterization of the first honeybee Ca²⁺ channel subunit reveals two novel species- and splicing-specific modes of regulation of channel inactivation.Pflugers Archiv : European journal of physiology · 2013Article
- Structure and function of the β subunit of voltage-gated Ca²⁺ channels.Biochimica et biophysica acta · 2013Review
- Bio-inspired voltage-dependent calcium channel blockers.Nature communications · 2013Article
- A quartet of leucine residues in the guanylate kinase domain of CaVβ determines the plasma membrane density of the CaV2.3 channel.The Journal of biological chemistry · 2012Article
- A short polybasic segment between the two conserved domains of the β2a-subunit modulates the rate of inactivation of R-type calcium channel.The Journal of biological chemistry · 2012Article
- How do T-type calcium channels control low-threshold exocytosis?Communicative & integrative biology · 2012Article
- Mechanism of auxiliary β-subunit-mediated membrane targeting of L-type (Ca(V)1.2) channels.The Journal of physiology · 2011Article
- The ß subunit of voltage-gated Ca2+ channels.Physiological reviews · 2010Review
- Ahnak1 modulates L-type Ca(2+) channel inactivation of rodent cardiomyocytes.Pflugers Archiv : European journal of physiology · 2010Article
- Functional dissection of the intramolecular Src homology 3-guanylate kinase domain coupling in voltage-gated Ca2+ channel beta-subunits.FEBS letters · 2009Article
- Regulation of voltage-gated Ca2+ channels by lipids.Cell calcium · 2009Review
- Arachidonic acid inhibition of L-type calcium (CaV1.3b) channels varies with accessory CaVbeta subunits.The Journal of general physiology · 2009Article
- Disruption of the IS6-AID linker affects voltage-gated calcium channel inactivation and facilitation.The Journal of general physiology · 2009Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca(2+) channel inactivation is a key element in controlling the level of Ca(2+) entry through voltage-gated Ca(2+) channels. Interaction between the pore-forming alpha(1) subunit and the auxiliary beta subunit is known to be a strong modulator of voltage-dependent inactivation. Here, we demonstrate that an N-terminal membrane anchoring site (MAS) of the beta(2a) subunit strongly reduces alpha(1A) (Ca(V)2.1) Ca(2+) channel inactivation. This effect can be mimicked by the addition of a transmembrane segment to the N terminus of the beta(2a) subunit. Inhibition of inactivation by beta(2a) also requires a link between MAS and another important molecular determinant, the beta interaction domain (BID). Our data suggest that mobility of the Ca(2+) channel I-II loop is necessary for channel inactivation. Interaction of this loop with other identified intracellular channel domains may constitute the basis of voltage-dependent inactivation. We thus propose a conceptually novel mechanism for slowing of inactivation by the beta(2a) subunit, in which the immobilization of the channel inactivation gate occurs by means of MAS and BID.
Indexed as
Identifiers
11124981PMC6773026What OpenQuestion holds
Registered trials
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.