ArticleThe Journal of general physiology2006
Regulation of CRAC channel activity by recruitment of silent channels to a high open-probability gating mode.
Article in The Journal of general physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed.
- Mechanistic insights into Orai dynamics during pore opening.Channels (Austin, Tex.) · 2026Review
- Optical single-channel recording of CRAC channels with HaloTag and a CabioRxiv : the preprint server for biology · 2026Article
- Plasma membrane-endoplasmic reticulum coupling probed with genetically-encoded voltage sensors.bioRxiv : the preprint server for biology · 2025Article
- The Molecular Biology of Placental Transport of Calcium to the Human Foetus.International journal of molecular sciences · 2025Review
- Synthetic Biology Meets CaCells · 2024Review
- Photocrosslinking-induced CRAC channel-like Orai1 activation independent of STIM1.Nature communications · 2023Article
- A pathogenic human Orai1 mutation unmasks STIM1-independent rapid inactivation of Orai1 channels.eLife · 2023Article
- Regulatory mechanisms controlling store-operated calcium entry.Frontiers in physiology · 2023Review
- Mechanisms of ion selectivity and throughput in the mitochondrial calcium uniporter.Science advances · 2022Article
- Orai1 Boosts SK3 Channel Activation.Cancers · 2021Article
- Structural Insights into CaCells · 2021Review
- Isoform-Specific Properties of Orai Homologues in Activation, Downstream Signaling, Physiology and Pathophysiology.International journal of molecular sciences · 2021Review
- Improper Remodeling of Organelles Deputed to CaInternational journal of molecular sciences · 2021Review
- The Orai Pore Opening Mechanism.International journal of molecular sciences · 2021Review
- The Impact of Mutation L138F/L210F on the Orai Channel: A Molecular Dynamics Simulation Study.Frontiers in molecular biosciences · 2021Article
- Interrogating permeation and gating of Orai channels using chemical modification of cysteine residues.Methods in enzymology · 2021Article
- Transmembrane Domain 3 (TM3) Governs Orai1 and Orai3 Pore Opening in an Isoform-Specific Manner.Frontiers in cell and developmental biology · 2021Article
- Molecular Choreography and Structure of CaMembranes · 2020Review
- Cryo-EM structure of the calcium release-activated calcium channel Orai in an open conformation.eLife · 2020Article
- Article
19 more citing papers are in PubMed but not listed here.
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2 authors.
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Abstract
CRAC (calcium release-activated Ca(2+)) channels attain an extremely high selectivity for Ca(2+) from the blockade of monovalent cation permeation by Ca(2+) within the pore. In this study we have exploited the blockade by Ca(2+) to examine the size of the CRAC channel pore, its unitary conductance for monovalent cations, and channel gating properties. The permeation of a series of methylammonium compounds under divalent cation-free conditions indicates a minimum pore diameter of 3.9 A. Extracellular Ca(2+) blocks monovalent flux in a manner consistent with a single intrapore site having an effective K(i) of 20 microM at -110 mV. Block increases with hyperpolarization, but declines below -100 mV, most likely due to permeation of Ca(2+). Analysis of monovalent current noise induced by increasing levels of block by extracellular Ca(2+) indicates an open probability (P(o)) of approximately 0.8. By extrapolating the variance/mean current ratio to the condition of full blockade (P(o) = 0), we estimate a unitary conductance of approximately 0.7 pS for Na(+), or three to fourfold higher than previous estimates. Removal of extracellular Ca(2+) causes the monovalent current to decline over tens of seconds, a process termed depotentiation. The declining current appears to result from a reduction in the number of active channels without a change in their high open probability. Similarly, low concentrations of 2-APB that enhance I(CRAC) increase the number of active channels while open probability remains constant. We conclude that the slow regulation of whole-cell CRAC current by store depletion, extracellular Ca(2+), and 2-APB involves the stepwise recruitment of silent channels to a high open-probability gating mode.
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