ArticleProceedings of the National Academy of Sciences of the United States of America2010
Facilitation of murine cardiac L-type Ca(v)1.2 channel is modulated by calmodulin kinase II-dependent phosphorylation of S1512 and S1570.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed.
- A Seven Amino Acid Long Region in the Cardiac CaCells · 2026Article
- Nuclear CaMKII Isoforms as Regulators of Transcription: From Developmental to Pathological Persistence.Medical sciences (Basel, Switzerland) · 2025Review
- CaCells · 2024Review
- Reduced O-GlcNAcylation diminishes cardiomyocyte CaJournal of molecular and cellular cardiology · 2023Article
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- L-type CaPhysiological reports · 2022Article
- Transcriptional profiles of genes related to electrophysiological function in Scn5aPhysiological reports · 2021Article
- Post-Translational Modification of Cav1.2 and its Role in Neurodegenerative Diseases.Frontiers in pharmacology · 2021Review
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- The CaMKII phosphorylation site Thr1604 in the CaChannels (Austin, Tex.) · 2020Article
- Regulation of cardiovascular calcium channel activity by post-translational modifications or interacting proteins.Pflugers Archiv : European journal of physiology · 2020Review
- Trimethylamine-American journal of physiology. Heart and circulatory physiology · 2020Article
- Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?Cardiovascular diabetology · 2020Article
- Control of cardiac contraction by sodium: Promises, reckonings, and new beginnings.Cell calcium · 2020Review
- The Protective Effect of Qishen Granule on Heart Failure after Myocardial Infarction through Regulation of Calcium Homeostasis.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Role of Oxidation-Dependent CaMKII Activation in the Genesis of Abnormal Action Potentials in Atrial Cardiomyocytes: A Simulation Study.BioMed research international · 2020Article
- Article
- Roles and Regulation of Voltage-gated Calcium Channels in Arrhythmias.The Journal of innovations in cardiac rhythm management · 2019Review
- Mitochondrial-Mediated Oxidative CaJournal of the American Heart Association · 2018Article
- Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus.Frontiers in physiology · 2018Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activity-dependent means of altering calcium (Ca(2)(+)) influx are assumed to be of great physiological consequence, although definitive tests of this assumption have only begun to emerge. Facilitation and inactivation offer two opposing, activity-dependent means of altering Ca(2+) influx via cardiac Ca(v)1.2 calcium channels. Voltage- and frequency-dependent facilitation of Ca(v)1.2 has been reported to depend on Calmodulin (CaM) and/or the activity of Calmodulin kinase II (CaMKII). Several sites within the cardiac L-type calcium channel complex have been proposed as the targets of CaMKII. Here, we generated mice with knockin mutations of alpha(1)1.2 S1512 and S1570 phosphorylation sites [sine facilitation (SF) mice]. Homocygote SF mice were viable and reproduced in a Mendelian ratio. Voltage-dependent facilitation in ventricular cardiomyocytes carrying the SF mutation was decreased from 1.58- to 1.18-fold. The CaMKII inhibitor KN-93 reduced facilitation to 1.28 in control cardiomyocytes. SF mutation negatively shifted the voltage-dependent inactivation and slowed recovery from inactivation, thereby making fewer channels available for activation. Telemetric ECG recordings at different heart rates showed that QT time decreased significantly more in SF than in control mice at higher rates. Our results strongly support the notion that CaMKII-dependent phosphorylation of Cav1.2 at S1512 and S1570 mediates Ca(2+) current facilitation in the murine heart.
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