ReviewThe Journal of physiology2000
Molecular determinants of inactivation in voltage-gated Ca2+ channels.
Review in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 136 citations in OpenAlex.
- Characterization of Three Distinct Loss-of-Function Cav2.3 Variants.International journal of molecular sciences · 2026Article
- Developmental mechanisms underlying pediatric epilepsy.Frontiers in neurology · 2025Review
- Role of the CaChannels (Austin, Tex.) · 2024Article
- Beta-Cell Ion Channels and Their Role in Regulating Insulin Secretion.Comprehensive Physiology · 2021Review
- Calcium channel gating.Pflugers Archiv : European journal of physiology · 2018Review
- Key role of segment IS4 in Cav1.2 inactivation: link between activation and inactivation.Pflugers Archiv : European journal of physiology · 2017Article
- Lead poisoning: acute exposure of the heart to lead ions promotes changes in cardiac function and Cav1.2 ion channels.Biophysical reviews · 2017Review
- C-terminal splice variants of P/Q-type CaThe Journal of biological chemistry · 2017Article
- Selective pressure modulation of synaptic voltage-dependent calcium channels-involvement in HPNS mechanism.Journal of cellular and molecular medicine · 2016Article
- Article
- Selective modulation of cellular voltage-dependent calcium channels by hyperbaric pressure-a suggested HPNS partial mechanism.Frontiers in cellular neuroscience · 2014Article
- Structure and function of the β subunit of voltage-gated Ca²⁺ channels.Biochimica et biophysica acta · 2013Review
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- 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
- Molecular Determinants of Cav1.2 Calcium Channel Inactivation.ISRN molecular biology · 2012Review
- Timothy mutation disrupts the link between activation and inactivation in Ca(V)1.2 protein.The Journal of biological chemistry · 2011Article
- Functional coupling of Rab3-interacting molecule 1 (RIM1) and L-type Ca2+ channels in insulin release.The Journal of biological chemistry · 2011Article
- CaBP1 regulates voltage-dependent inactivation and activation of Ca(V)1.2 (L-type) calcium channels.The Journal of biological chemistry · 2011Article
- The ß subunit of voltage-gated Ca2+ channels.Physiological reviews · 2010Review
- Regulation of voltage-gated Ca2+ channels by lipids.Cell calcium · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evolution has created a large family of different classes of voltage-gated Ca2+ channels and a variety of additional splice variants with different inactivation properties. Inactivation controls the amount of Ca2+ entry during an action potential and is, therefore, believed to play an important role in tissue-specific Ca2+ signalling. Furthermore, mutations in a neuronal Ca2+ channel (Ca(v)2.1) that are associated with the aetiology of neurological disorders such as familial hemiplegic migraine and ataxia cause significant changes in the process of channel inactivation. Ca2+ channels of a given subtype may inactivate by three different conformational changes: a fast and a slow voltage-dependent inactivation process and in some channel types by an additional Ca2+-dependent inactivation mechanism. Inactivation kinetics of Ca2+ channels are determined by the intrinsic properties of their pore-forming alpha1-subunits and by interactions with other channel subunits. This review focuses on structural determinants of Ca2+ channel inactivation in different parts of Ca2+ channel alpha1-subunits, including pore-forming transmembrane segments and loops, intracellular domain linkers and the carboxyl terminus. Inactivation is also affected by the interaction of the alpha1-subunits with auxiliary beta-subunits and intracellular regulator proteins. The evidence shows that pore-forming S6 segments and conformational changes in extra- (pore loop) and intracellular linkers connected to pore-forming segments may play a principal role in the modulation of Ca2+ channel inactivation. Structural concepts of Ca2+ channel inactivation are discussed.
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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.