ArticlePflugers Archiv : European journal of physiology2015
Contrasting the roles of the I-II loop gating brake in CaV3.1 and CaV3.3 calcium channels.
Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Analysing an allelic series of rare missense variants of CACNA1I in a Swedish schizophrenia cohort.Brain : a journal of neurology · 2022Pooled it
- The four voltage-sensing domains of T-type calcium channels activate near the resting membrane potential.Nature communications · 2026Article
- Selective inhibition of neuronal CaMolecular brain · 2020Article
- Identification of a molecular gating determinant within the carboxy terminal region of CaMolecular brain · 2019Article
- Calcium channel gating.Pflugers Archiv : European journal of physiology · 2018Review
- Role of individual S4 segments in gating of CaChannels (Austin, Tex.) · 2018Article
- A CaChannels (Austin, Tex.) · 2016Article
- T-type channels: release a brake, engage a gear.Channels (Austin, Tex.) · 2016Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Low-voltage-activated CaV3 channels are distinguished among other voltage-activated calcium channels by the most negative voltage activation threshold. The voltage dependence of current activation is virtually identical in all three CaV3 channels while the current kinetics of the CaV3.3 current is one order slower than that of the CaV3.1 and CaV3.2 channels. We have analyzed the voltage dependence and kinetics of charge (Q) movement in human recombinant CaV3.3 and CaV3.1 channels. The voltage dependence of voltage sensor activation (Qon-V) of the CaV3.3 channel was significantly shifted with respect to that of the CaV3.1 channel by +18.6 mV and the kinetic of Qon activation in the CaV3.3 channel was significantly slower than that of the CaV3.1 channel. Removal of the gating brake in the intracellular loop connecting repeats I and II in the CaV3.3 channel in the ID12 mutant channel shifted the Qon-V relation to a value even more negative than that for the CaV3.1 channel. The kinetic of Qon activation was not significantly different between ID12 and CaV3.1 channels. Deletion of the gating brake in the CaV3.1 channel resulted in a GD12 channel with the voltage dependence of the gating current activation significantly shifted toward more negative potentials. The Qon kinetic was not significantly altered. ID12 and GD12 mutants did not differ significantly in voltage dependence nor in the kinetic of voltage sensor activation. In conclusion, the putative gating brake in the intracellular loop connecting repeats I and II controls the gating current of the CaV3 channels. We suggest that activation of the voltage sensor in domain I is limiting both the voltage dependence and the kinetics of CaV3 channel activation.
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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.