ArticleThe Journal of physiology2001
Inactivation determinants in segment IIIS6 of Ca(v)3.1.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- CaHandbook of experimental pharmacology · 2023Article
- Theoretical Study of the Structural Stability, Chemical Reactivity, and Protein Interaction for NMP Compounds as Modulators of the Endocannabinoid System.Molecules (Basel, Switzerland) · 2022Article
- Conceptual DFT, QTAIM, and Molecular Docking Approaches to Characterize the T-Type Calcium Channel Blocker Anandamide.Frontiers in chemistry · 2022Article
- Molecular Basis of Primary Aldosteronism and Adrenal Cushing Syndrome.Journal of the Endocrine Society · 2020Review
- Neuronal Cav3 channelopathies: recent progress and perspectives.Pflugers Archiv : European journal of physiology · 2020Review
- Molecular Mechanisms of Primary Aldosteronism.Endocrinology and metabolism (Seoul, Korea) · 2019Review
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- Ins and outs of T-channel structure function.Pflugers Archiv : European journal of physiology · 2014Review
- Cooperative activation of the T-type CaV3.2 channel: interaction between Domains II and III.The Journal of biological chemistry · 2013Article
- The voltage dependence of gating currents of the neuronal CA(v)3.3 channel is determined by the gating brake in the I-II loop.Pflugers Archiv : European journal of physiology · 2011Article
- Three-dimensional structure of CaV3.1: comparison with the cardiac L-type voltage-gated calcium channel monomer architecture.The Journal of biological chemistry · 2009Article
- Regulation of voltage-gated Ca2+ channels by lipids.Cell calcium · 2009Review
- I-II loop structural determinants in the gating and surface expression of low voltage-activated calcium channels.PloS one · 2008Article
- Characterization of the gating brake in the I-II loop of Ca(v)3.2 T-type Ca(2+) channels.The Journal of biological chemistry · 2008Article
- The I-II loop controls plasma membrane expression and gating of Ca(v)3.2 T-type Ca2+ channels: a paradigm for childhood absence epilepsy mutations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Evidence for common structural determinants of activation and inactivation in T-type Ca2+ channels.Pflugers Archiv : European journal of physiology · 2006Article
- Role of Domain IV/S4 outermost arginines in gating of T-type calcium channels.Pflugers Archiv : European journal of physiology · 2005Article
- Identification of R(-)-isomer of efonidipine as a selective blocker of T-type Ca2+ channels.British journal of pharmacology · 2004Article
- Mechanism of arachidonic acid modulation of the T-type Ca2+ channel alpha1G.The Journal of general physiology · 2004Article
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Authors and funding
6 authors.
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Abstract
1. Low threshold, T-type, Ca(2+) channels of the Ca(v)3 family display the fastest inactivation kinetics among all voltage-gated Ca(2+) channels. The molecular inactivation determinants of this channel family are largely unknown. Here we investigate whether segment IIIS6 plays a role in Ca(v)3.1 inactivation as observed previously in high voltage-activated Ca(2+) channels. 2. Amino acids that are identical in IIIS6 segments of all Ca(2+) channel subtypes were mutated to alanine (F1505A, F1506A, N1509A, F1511A, V1512A, F1519A, FV1511/1512AA). Additionally M1510 was mutated to isoleucine and alanine. 3. The kinetic properties of the mutants were analysed with the two-microelectrode voltage-clamp technique after expression in Xenopus oocytes. The time constant for the barium current (I(Ba)) inactivation, tau(inact), of wild-type channels at -20 mV was 9.5 +/- 0.4 ms; the corresponding time constants of the mutants ranged from 9.2 +/- 0.4 ms in V1512A to 45.7 +/- 5.2 ms (4.8-fold slowing) in M1510I. Recovery at -80 mV was most significantly slowed by V1512A and accelerated by F1511A. 4. We conclude that amino acids M1510, F1511 and V1512 corresponding to previously identified inactivation determinants in IIIS6 of Ca(v)2.1 (Hering et al. 1998) have a significant role in Ca(v)3.1 inactivation. These data suggest common elements in the molecular architecture of the inactivation mechanism in high and low threshold Ca(2+) channels.
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