ArticleBiophysical journal2001
Ca(2+) channel inactivation heterogeneity reveals physiological unbinding of auxiliary beta subunits.
Article in Biophysical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Cacnb4 directly couples electrical activity to gene expression, a process defective in juvenile epilepsy.The EMBO journal · 2012Article
- Functional ion channels in human pulmonary artery smooth muscle cells: Voltage-dependent cation channels.Pulmonary circulation · 2011Article
- The Ca2+ channel beta subunit determines whether stimulation of Gq-coupled receptors enhances or inhibits N current.The Journal of general physiology · 2009Article
- Regulation of voltage-gated Ca2+ channels by lipids.Cell calcium · 2009Review
- Ablation of Ca2+ channel beta3 subunit leads to enhanced N-methyl-D-aspartate receptor-dependent long term potentiation and improved long term memory.The Journal of biological chemistry · 2008Article
- Alanine-scanning mutagenesis defines a conserved energetic hotspot in the CaValpha1 AID-CaVbeta interaction site that is critical for channel modulation.Structure (London, England : 1993) · 2008Article
- A novel Ca(V)1.2 N terminus expressed in smooth muscle cells of resistance size arteries modifies channel regulation by auxiliary subunits.The Journal of biological chemistry · 2007Article
- Modal gating of human CaV2.1 (P/Q-type) calcium channels: II. the b mode and reversible uncoupling of inactivation.The Journal of general physiology · 2004Article
- 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
- Physiological modulation of inactivation in L-type Ca2+ channels: one switch.The Journal of physiology · 2004Review
- Targeting mechanisms of high voltage-activated Ca2+ channels.Journal of bioenergetics and biomembranes · 2003Review
- Beta-adrenergic and muscarinic agonists modulate inactivation of L-type Ca2+ channel currents in guinea-pig ventricular myocytes.The Journal of physiology · 2002Article
- Calcium channels: when is a subunit not a subunit?The Journal of physiology · 2002Article
- Use of a purified and functional recombinant calcium-channel beta4 subunit in surface-plasmon resonance studies.The Biochemical journal · 2002Article
- Nuclear life of the voltage-gated Cacnb4 subunit and its role in gene transcription regulation.Channels (Austin, Tex.)Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage gated Ca(2+) channel (VGCC) auxiliary beta subunits increase membrane expression of the main pore-forming alpha(1) subunits and finely tune channel activation and inactivation properties. In expression studies, co-expression of beta subunits also reduced neuronal Ca(2+) channel regulation by heterotrimeric G protein. Biochemical studies suggest that VGCC beta subunits and G protein betagamma can compete for overlapping interaction sites on VGCC alpha(1) subunits, suggesting a dynamic association of these subunits with alpha(1). In this work we have analyzed the stability of the alpha(1)/beta association under physiological conditions. Regulation of the alpha(1A) Ca(2+) channel inactivation properties by beta(1b) and beta(2a) subunits had two major effects: a shift in voltage-dependent inactivation (E(in)), and an increase of the non-inactivating current (R(in)). Unexpectedly, large variations in magnitude of the effects were recorded on E(in), when beta(1b) was expressed, and R(in), when beta(2a) was expressed. These variations were not proportional to the current amplitude, and occurred at similar levels of beta subunit expression. beta(2a)-induced variations of R(in) were, however, inversely proportional to the magnitude of G protein block. These data underline the two different mechanisms used by beta(1b) and beta(2a) to regulate channel inactivation, and suggest that the VGCC beta subunit can unbind the alpha1 subunit in physiological situations.
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