ArticleThe Journal of biological chemistry2011
Deletion of the distal C terminus of CaV1.2 channels leads to loss of beta-adrenergic regulation and heart failure in vivo.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 81 citations in OpenAlex.
- Testosterone acts through the membrane protein GPRC6A to cause cardiac edema in zebrafish embryos.Development (Cambridge, England) · 2024Article
- Role of the CaChannels (Austin, Tex.) · 2024Article
- A-Kinase Anchoring Proteins in Cardiac Myocytes and Their Roles in Regulating Calcium Cycling.Cells · 2023Review
- Impairment of β-adrenergic regulation and exacerbation of pressure-induced heart failure in mice with mutations in phosphoregulatory sites in the cardiac CaFrontiers in physiology · 2023Article
- Sympathetic Nervous System Regulation of Cardiac Calcium Channels.Handbook of experimental pharmacology · 2023Article
- Convergent regulation of CaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Adrenergic Regulation of Calcium Channels in the Heart.Annual review of physiology · 2022Review
- The Interface of Nuclear and Membrane Steroid Signaling.Endocrinology · 2021Review
- Use of Proximity Labeling in Cardiovascular Research.JACC. Basic to translational science · 2021Review
- A Meta-Analysis of Bioelectric Data in Cancer, Embryogenesis, and Regeneration.Bioelectricity · 2021Article
- The CaMKII phosphorylation site Thr1604 in the CaChannels (Austin, Tex.) · 2020Article
- Nanoscale regulation of L-type calcium channels differentiates between ischemic and dilated cardiomyopathies.EBioMedicine · 2020Article
- Cardiac function modulation depends on the A-kinase anchoring protein complex.Journal of cellular and molecular medicine · 2019Review
- Cardiac CaV1.2 channels require β subunits for β-adrenergic-mediated modulation but not trafficking.The Journal of clinical investigation · 2019Article
- The Role of 17β-Estradiol and Estrogen Receptors in Regulation of CaFrontiers in endocrinology · 2019Review
- An African loss-of-function CACNA1C variant p.T1787M associated with a risk of ventricular fibrillation.Scientific reports · 2018Article
- Voltage-Dependent Calcium Channels, Calcium Binding Proteins, and Their Interaction in the Pathological Process of Epilepsy.International journal of molecular sciences · 2018Review
- The AKAP Cypher/Zasp contributes to β-adrenergic/PKA stimulation of cardiac CaThe Journal of general physiology · 2018Article
- PDGF-induced migration of synthetic vascular smooth muscle cells through c-Src-activated L-type CaPflugers Archiv : European journal of physiology · 2018Article
- Identification of a novel cAMP dependent protein kinase A phosphorylation site on the human cardiac calcium channel.Scientific reports · 2017Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
L-type calcium currents conducted by CaV1.2 channels initiate excitation-contraction coupling in cardiac and vascular smooth muscle. In the heart, the distal portion of the C terminus (DCT) is proteolytically processed in vivo and serves as a noncovalently associated autoinhibitor of CaV1.2 channel activity. This autoinhibitory complex, with A-kinase anchoring protein-15 (AKAP15) bound to the DCT, is hypothesized to serve as the substrate for β-adrenergic regulation in the fight-or-flight response. Mice expressing CaV1.2 channels with the distal C terminus deleted (DCT-/-) develop cardiac hypertrophy and die prematurely after E15. Cardiac hypertrophy and survival rate were improved by drug treatments that reduce peripheral vascular resistance and hypertension, consistent with the hypothesis that CaV1.2 hyperactivity in vascular smooth muscle causes hypertension, hypertrophy, and premature death. However, in contrast to expectation, L-type Ca2+ currents in cardiac myocytes from DCT-/- mice were dramatically reduced due to decreased cell-surface expression of CaV1.2 protein, and the voltage dependence of activation and the kinetics of inactivation were altered. CaV1.2 channels in DCT-/- myocytes fail to respond to activation of adenylyl cyclase by forskolin, and the localized expression of AKAP15 is reduced. Therefore, we conclude that the DCT of CaV1.2 channels is required in vivo for normal vascular regulation, cell-surface expression of CaV1.2 channels in cardiac myocytes, and β-adrenergic stimulation of L-type Ca2+ currents in the heart.
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