ArticleThe Journal of general physiology2003
Pore structure influences gating properties of the T-type Ca2+ channel alpha1G.
Article in The Journal of general physiology, 2003. 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.
- Activation ofInternational journal of molecular sciences · 2021Article
- The Citrus Flavonoid Hesperetin Has an Inadequate Anti-Arrhythmic Profile in the ΔKPQ NaBiomolecules · 2020Article
- A compartmentalized mathematical model of mouse atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020Article
- Selectivity filters and cysteine-rich extracellular loops in voltage-gated sodium, calcium, and NALCN channels.Frontiers in physiology · 2015Review
- Cysteines in the loop between IS5 and the pore helix of Ca(V)3.1 are essential for channel gating.Pflugers Archiv : European journal of physiology · 2010Article
- Three-dimensional structure of CaV3.1: comparison with the cardiac L-type voltage-gated calcium channel monomer architecture.The Journal of biological chemistry · 2009Article
- I-II loop structural determinants in the gating and surface expression of low voltage-activated calcium channels.PloS one · 2008Article
- Permeation and gating in CaV3.1 (alpha1G) T-type calcium channels effects of Ca2+, Ba2+, Mg2+, and Na+.The Journal of general physiology · 2008Article
- Differential interactions of Na+ channel toxins with T-type Ca2+ channels.The Journal of general physiology · 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
- Molecular determinant for specific Ca/Ba selectivity profiles of low and high threshold Ca2+ channels.The Journal of general physiology · 2007Article
- Ca2+-dependent inactivation of CaV1.2 channels prevents Gd3+ block: does Ca2+ block the pore of inactivated channels?The Journal of general physiology · 2007Article
- Evidence for common structural determinants of activation and inactivation in T-type Ca2+ channels.Pflugers Archiv : European journal of physiology · 2006Article
- The ion channel inverse problem: neuroinformatics meets biophysics.PLoS computational biology · 2006Review
- Role of Domain IV/S4 outermost arginines in gating of T-type calcium channels.Pflugers Archiv : European journal of physiology · 2005Article
- Molecular regions underlying the activation of low- and high-voltage activating calcium channels.European biophysics journal : EBJ · 2005Article
- Ion trafficking through T-type Ca2+ channels: a way to look at channel gating position.The Journal of general physiology · 2004Article
- Mechanism of arachidonic acid modulation of the T-type Ca2+ channel alpha1G.The Journal of general physiology · 2004Article
- Block of tetrodotoxin-resistant Na+ channel pore by multivalent cations: gating modification and Na+ flow dependence.The Journal of general physiology · 2004Article
- Slow inactivation of the Ca(V)3.1 isotype of T-type calcium channels.The Journal of physiology · 2004Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The selectivity filter of all known T-type Ca2+ channels is built by an arrangement of two glutamate and two aspartate residues, each one located in the P-loops of domains I-IV of the alpha1 subunit (EEDD locus). The mutations of the aspartate residues to glutamate induce changes in the conduction properties, enhance Cd2+ and proton affinities, and modify the activation curve of the channel. Here we further analyze the role of the selectivity filter in the gating mechanisms of T-type channels by comparing the kinetic properties of the alpha1G subunit (CaV3.1) to those of pore mutants containing aspartate-to-glutamate substitution in domains III (EEED) or IV (EEDE). The change of the extracellular pH induced similar effects on the activation properties of alpha1G and both pore mutants, indicating that the larger affinity of the mutant channels for protons is not the cause of the gating modifications. Both mutants showed alterations in several gating properties with respect to alpha1G, i.e., faster macroscopic inactivation in the voltage range from -10 to 50 mV, positive voltage shift and decrease in the voltage sensitivity of the time constants of activation and deactivation, decrease of the voltage sensitivity of the steady-state inactivation, and faster recovery from inactivation for long repolarization periods. Kinetic modeling suggests that aspartate-to-glutamate mutations in the EEDD locus of alpha1G modify the movement of the gating charges and alter the rate of several gating transitions. These changes are independent of the alterations of the selectivity properties and channel protonation.
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