ArticleThe Journal of general physiology1998
Effect of bay K 8644 (-) and the beta2a subunit on Ca2+-dependent inactivation in alpha1C Ca2+ channels.
Article in The Journal of general physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- A Selectivity Filter Gate Controls Voltage-Gated Calcium Channel Calcium-Dependent Inactivation.Neuron · 2019Article
- Complex modulation of L-type Ca(2+) current inactivation by sorcin in isolated rabbit cardiomyocytes.Pflugers Archiv : European journal of physiology · 2009Article
- Ca2+-dependent inactivation of CaV1.2 channels prevents Gd3+ block: does Ca2+ block the pore of inactivated channels?The Journal of general physiology · 2007Article
- Effects of the enantiomers of BayK 8644 on the charge movement of L-type Ca channels in guinea-pig ventricular myocytes.The Journal of membrane biology · 2003Article
- Slow deactivation and U-shaped inactivation properties in cloned Cav1.2b channels in Chinese hamster ovary cells.Biophysical journal · 2003Article
- Potentiation and inhibition of Ca(2+) release-activated Ca(2+) channels by 2-aminoethyldiphenyl borate (2-APB) occurs independently of IP(3) receptors.The Journal of physiology · 2001Article
- The alpha 1-subunit of smooth muscle Ca(2+) channel preserves multiple open states induced by depolarization.The Journal of physiology · 2000Article
- Critical determinants of Ca(2+)-dependent inactivation within an EF-hand motif of L-type Ca(2+) channels.Biophysical journal · 2000Article
- Ca2+-induced inhibition of the cardiac Ca2+ channel depends on calmodulin.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Mutations in the EF-hand motif impair the inactivation of barium currents of the cardiac alpha1C channel.Biophysical journal · 1998Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Ca2+ currents recorded from Xenopus oocytes expressing only the alpha1C pore-forming subunit of the cardiac Ca2+ channel show Ca2+-dependent inactivation with a single exponential decay. This current-dependent inactivation is not detected for inward Ba2+ currents in external Ba2+. Facilitation of pore opening speeds up the Ca2+-dependent inactivation process and makes evident an initial fast rate of decay. Facilitation can be achieved by (a) coexpression of the beta2a subunit with the alpha1C subunit, or (b) addition of saturating Bay K 8644 (-) concentration to alpha1C channels. The addition of Bay K 8644 (-) to alpha1Cbeta2a channels makes both rates of inactivation faster. All these maneuvers do not induce inactivation in Ba2+ currents in our expression system. These results support the hypothesis of a mechanism for the Ca2+-dependent inactivation process that is sensitive to both Ca2+ flux (single channel amplitude) and open probability. We conclude that the Ca2+ site for inactivation is in the alpha1C pore-forming subunit and we propose a kinetic model to account for the main features of alpha1Cbeta2a Ca2+ currents.
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