Inactivation of ICa-L is the major determinant of use-dependent facilitation in rat cardiomyocytes
Open Access
- 1 March 2003
- journal article
- Published by Wiley in The Journal of Physiology
- Vol. 547 (3) , 797-805
- https://doi.org/10.1111/j.1469-7793.2003.00797.x
Abstract
No abstract availableThis publication has 50 references indexed in Scilit:
- Calmodulin kinase and a calmodulin‐binding ‘IQ’ domain facilitate L‐type Ca2+ current in rabbit ventricular myocytes by a common mechanismThe Journal of Physiology, 2001
- Molecular Basis of Calmodulin Tethering and Ca2+-dependent Inactivation of L-type Ca2+ ChannelsJournal of Biological Chemistry, 2001
- Determinants for Calmodulin Binding on Voltage-dependent Ca2+ ChannelsJournal of Biological Chemistry, 2000
- Facilitation of the L-type calcium current in rabbit sino-atrial cells: effect on cardiac automaticityCardiovascular Research, 2000
- Ca2+-sensitive Inactivation and Facilitation of L-type Ca2+ Channels Both Depend on Specific Amino Acid Residues in a Consensus Calmodulin-binding Motif in theα1C subunitJournal of Biological Chemistry, 2000
- Use-dependent facilitation and depression of ?-type Ca2+ current in guinea-pig ventricular myocytes: modulation by Ca2+ and isoprenalineCardiovascular Research, 1999
- Frequency-dependent Increase in Cardiac Ca2+Current is due to Reduced Ca2+Release by the Sarcoplasmic ReticulumJournal of Molecular and Cellular Cardiology, 1999
- Sarco/endoplasmic reticulum Ca2+(SERCA)-pumps: link to heart beats and calcium wavesCell Calcium, 1999
- Factors That Control Sarcoplasmic Reticulum Calcium Release in Intact Ventricular MyocytesaAnnals of the New York Academy of Sciences, 1998
- Sarcoplasmic reticulum Ca2+ content, L‐type Ca2+ current and the Ca2+ transient in rat myocytes during β‐adrenergic StimulationThe Journal of Physiology, 1997