ArticleThe Journal of physiology2000
Modulation of slow inactivation in class A Ca2+ channels by beta-subunits.
Article 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 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Calcium Channel Splice Variants and Their Effects in Brain and Cardiovascular Function.Advances in experimental medicine and biology · 2021Article
- 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
- Measuring Ca2+-Dependent Modulation of Voltage-Gated Ca2+ Channels in HEK-293T Cells.Cold Spring Harbor protocols · 2016Article
- Article
- Selective modulation of cellular voltage-dependent calcium channels by hyperbaric pressure-a suggested HPNS partial mechanism.Frontiers in cellular neuroscience · 2014Article
- 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
- Compensatory regulation of Cav2.1 Ca2+ channels in cerebellar Purkinje neurons lacking parvalbumin and calbindin D-28k.Journal of neurophysiology · 2010Article
- Introduction into Ca(v)2.1 of the homologous mutation of Ca(v)1.2 causing the Timothy syndrome questions the role of V421 in the phenotypic definition of P-type Ca(2+) channel.Pflugers Archiv : European journal of physiology · 2008Article
- Localization and targeting of voltage-dependent ion channels in mammalian central neurons.Physiological reviews · 2008Review
- The guanylate kinase domain of the beta-subunit of voltage-gated calcium channels suffices to modulate gating.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Mutations of nonconserved residues within the calcium channel alpha1-interaction domain inhibit beta-subunit potentiation.The Journal of general physiology · 2008Article
- Orientation of the calcium channel beta relative to the alpha(1)2.2 subunit is critical for its regulation of channel activity.PloS one · 2008Article
- Modal gating of human CaV2.1 (P/Q-type) calcium channels: I. The slow and the fast gating modes and their modulation by beta subunits.The Journal of general physiology · 2004Article
- Voltage-gated rearrangements associated with differential beta-subunit modulation of the L-type Ca(2+) channel inactivation.Biophysical journal · 2004Article
- Modulation of the voltage sensor of L-type Ca2+ channels by intracellular Ca2+.The Journal of general physiology · 2004Article
- Overexpressed Ca(v)beta3 inhibits N-type (Cav2.2) calcium channel currents through a hyperpolarizing shift of ultra-slow and closed-state inactivation.The Journal of general physiology · 2004Article
- Functional roles of cytoplasmic loops and pore lining transmembrane helices in the voltage-dependent inactivation of HVA calcium channels.The Journal of physiology · 2004Review
- Distinctive modulatory effects of five human auxiliary beta2 subunit splice variants on L-type calcium channel gating.Biophysical journal · 2003Article
- Inactivation determinants in segment IIIS6 of Ca(v)3.1.The Journal of physiology · 2001Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
beta-subunit modulation of slow inactivation of class A calcium (Ca2+) channels was studied with two-microlectrode voltage clamp after expression of the alpha1A- (BI-2) together with beta1a-, beta2a-, beta3- or beta4-subunits in Xenopus oocytes. On- and off-rates of slow inactivation were estimated from the kinetics of recovery from slow inactivation. Ca2+ channels with an alpha1A/beta-subunit composition inducing the slower rate of fast inactivation displayed the faster rate of slow inactivation. The corresponding order of slow inactivation time constants (tau[onset]) was: alpha1A/beta2a, 33 +/- 3 s; alpha1A/beta4, 42 +/- 4 s; alpha1A/beta1a, 59 +/- 4 s; alpha1A/beta3, 67 +/- 5 s (n >= 7). Recovery of class A Ca2+ channels from slow inactivation was voltage dependent and accelerated at hyperpolarized voltages. At a given holding potential recovery kinetics were not significantly modulated by different beta-subunits. Two mutations in segment IIIS6 (IF1612/1613AA) slowed fast inactivation and accelerated the onset of slow inactivation in the resulting mutant (alpha1A/IF-AA/beta3) in a similar manner as coexpression of the beta2a-subunit. Recovery from slow inactivation was slightly slowed in the double mutant. Our data suggest that class A Ca2+ channels enter the 'slow inactivated' state more willingly from the open than from the 'fast inactivated' state. The rate of slow inactivation is, therefore, indirectly modulated by different beta-subunits. Fast and slow inactivation in class A Ca2+ channels appears to represent structurally independent conformational changes. Fast inactivation is not a prerequisite for slow inactivation.
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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.