ArticleThe Journal of general physiology2007
Ca2+-dependent inactivation of CaV1.2 channels prevents Gd3+ block: does Ca2+ block the pore of inactivated channels?
Article in The Journal of general physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 24 citations in OpenAlex.
- Advances in the Rational Design, Mechanisms, and Applications of Lanthanide Nanoparticles for the Regulation of Reactive Oxygen Species.International journal of nanomedicine · 2026Review
- Asymmetric contribution of a selectivity filter gate in triggering inactivation of CaV1.3 channels.The Journal of general physiology · 2024Article
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- A Selectivity Filter Gate Controls Voltage-Gated Calcium Channel Calcium-Dependent Inactivation.Neuron · 2019Article
- Lead poisoning: acute exposure of the heart to lead ions promotes changes in cardiac function and Cav1.2 ion channels.Biophysical reviews · 2017Review
- C-terminal splice variants of P/Q-type CaThe Journal of biological chemistry · 2017Article
- Role of protein dynamics in ion selectivity and allosteric coupling in the NaK channel.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Neuromodulatory changes in short-term synaptic dynamics may be mediated by two distinct mechanisms of presynaptic calcium entry.Journal of computational neuroscience · 2012Article
- The third transmembrane segment of orai1 protein modulates Ca2+ release-activated Ca2+ (CRAC) channel gating and permeation properties.The Journal of biological chemistry · 2011Article
- CaBP1 regulates voltage-dependent inactivation and activation of Ca(V)1.2 (L-type) calcium channels.The Journal of biological chemistry · 2011Article
- Structural modeling of calcium binding in the selectivity filter of the L-type calcium channel.European biophysics journal : EBJ · 2010Article
- The intracellular loop of Orai1 plays a central role in fast inactivation of Ca2+ release-activated Ca2+ channels.The Journal of biological chemistry · 2010Article
- A single amino acid change in Ca(v)1.2 channels eliminates the permeation and gating differences between Ca(2+) and Ba(2+).The Journal of membrane biology · 2010Article
- Pathways of abnormal stress-induced Ca2+ influx into dystrophic mdx cardiomyocytes.Cell calcium · 2009Article
- Disruption of the IS6-AID linker affects voltage-gated calcium channel inactivation and facilitation.The Journal of general physiology · 2009Article
- 2-Aminoethoxydiphenyl borate directly facilitates and indirectly inhibits STIM1-dependent gating of CRAC channels.The Journal of physiology · 2008Article
- Gadolinium limits myocardial infarction in the rat: dose-response, temporal relations and mechanisms.Journal of molecular and cellular cardiology · 2008Article
- Orai1 mutations alter ion permeation and Ca2+-dependent fast inactivation of CRAC channels: evidence for coupling of permeation and gating.The Journal of general physiology · 2007Article
- And yet it moves: conformational States of the Ca2+ channel pore.The Journal of general physiology · 2007Article
- Block of CaV1.2 channels by Gd3+ reveals preopening transitions in the selectivity filter.The Journal of general physiology · 2007Article
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4 authors at 2 institutions in 1 country.
Funding
Abstract
Lanthanide gadolinium (Gd(3+)) blocks Ca(V)1.2 channels at the selectivity filter. Here we investigated whether Gd(3+) block interferes with Ca(2+)-dependent inactivation, which requires Ca(2+) entry through the same site. Using brief pulses to 200 mV that relieve Gd(3+) block but not inactivation, we monitored how the proportions of open and open-blocked channels change during inactivation. We found that blocked channels inactivate much less. This is expected for Gd(3+) block of the Ca(2+) influx that enhances inactivation. However, we also found that the extent of Gd(3+) block did not change when inactivation was reduced by abolition of Ca(2+)/calmodulin interaction, showing that Gd(3+) does not block the inactivated channel. Thus, Gd(3+) block and inactivation are mutually exclusive, suggesting action at a common site. These observations suggest that inactivation causes a change at the selectivity filter that either hides the Gd(3+) site or reduces its affinity, or that Ca(2+) occupies the binding site at the selectivity filter in inactivated channels. The latter possibility is supported by previous findings that the EEQE mutation of the selectivity EEEE locus is void of Ca(2+)-dependent inactivation (Zong Z.Q., J.Y. Zhou, and T. Tanabe. 1994. Biochem. Biophys. Res. Commun. 201:1117-11123), and that Ca(2+)-inactivated channels conduct Na(+) when Ca(2+) is removed from the extracellular medium (Babich O., D. Isaev, and R. Shirokov. 2005. J. Physiol. 565:709-717). Based on these results, we propose that inactivation increases affinity of the selectivity filter for Ca(2+) so that Ca(2+) ion blocks the pore. A minimal model, in which the inactivation "gate" is an increase in affinity of the selectivity filter for permeating ions, successfully simulates the characteristic U-shaped voltage dependence of inactivation in Ca(2+).
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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.