ArticleThe Journal of clinical investigation2006
Molecular basis for the modulation of native T-type Ca2+ channels in vivo by Ca2+/calmodulin-dependent protein kinase II.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 62 citations in OpenAlex.
- Regulatory Action of Calcium and Calcium Channels in Pain Pathways.International journal of biological sciences · 2025Review
- Bioluminescence Imaging of Potassium Ion Using a Sensory Luciferin and an Engineered Luciferase.Journal of the American Chemical Society · 2024Article
- The T-type calcium channelosome.Pflugers Archiv : European journal of physiology · 2024Review
- Article
- Review
- Calcium/calmodulin-dependent protein kinase II associates with the KFrontiers in neuroanatomy · 2022Article
- Aldosterone-Regulated Sodium Transport and Blood Pressure.Frontiers in physiology · 2022Review
- Ion Channel Function and Electrical Excitability in the Zona Glomerulosa: A Network Perspective on Aldosterone Regulation.Annual review of physiology · 2021Review
- Cdk5-Dependent Phosphorylation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- A novel phospho-modulatory mechanism contributes to the calcium-dependent regulation of T-type CaScientific reports · 2019Article
- Activation of alpha-1 adrenergic receptors increases cytosolic calcium in neurones of the paraventricular nucleus of the hypothalamus.Journal of neuroendocrinology · 2019Article
- T-type Ca2+ channels are required for enhanced sympathetic axon growth by TNFα reverse signalling.Open biology · 2017Article
- Role of voltage-gated calcium channels in the regulation of aldosterone production from zona glomerulosa cells of the adrenal cortex.The Journal of physiology · 2016Review
- Phosphorylation of the Cav3.2 T-type calcium channel directly regulates its gating properties.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential.Pharmacological reviews · 2015Review
- Differential CaMKII regulation by voltage-gated calcium channels in the striatum.Molecular and cellular neurosciences · 2015Article
- CaV3.2 calcium channels control NMDA receptor-mediated transmission: a new mechanism for absence epilepsy.Genes & development · 2015Article
- Cav3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- CaMKII in sinoatrial node physiology and dysfunction.Frontiers in pharmacology · 2014Review
- The involvement of Nek2 and Notch in the proliferation of rat adrenal cortex triggered by POMC-derived peptides.PloS one · 2014Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Ang II receptor activation increases cytosolic Ca2+ levels to enhance the synthesis and secretion of aldosterone, a recently identified early pathogenic stimulus that adversely influences cardiovascular homeostasis. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a downstream effector of the Ang II-elicited signaling cascade that serves as a key intracellular Ca2+ sensor to feedback-regulate Ca2+ entry through voltage-gated Ca2+ channels. However, the molecular mechanism(s) by which CaMKII regulates these important physiological targets to increase Ca2+ entry remain unresolved. We show here that CaMKII forms a signaling complex with alpha1H T-type Ca2+ channels, directly interacting with the intracellular loop connecting domains II and III of the channel pore (II-III loop). Activation of the kinase mediated the phosphorylation of Ser1198 in the II-III loop and the positive feedback regulation of channel gating both in intact cells in situ and in cells of the native adrenal zona glomerulosa stimulated by Ang II in vivo. These data define the molecular basis for the in vivo modulation of native T-type Ca2+ channels by CaMKII and suggest that the disruption of this signaling complex in the zona glomerulosa may provide a new therapeutic approach to limit aldosterone production and cardiovascular disease progression.
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Registered trials
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.