ArticleProceedings of the National Academy of Sciences of the United States of America2005
Constitutively active L-type Ca2+ channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers.
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Who cites it
138 citing papers in PubMed, 199 citations in OpenAlex.
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- Milestone Papers on Signal Transduction Mechanisms of Hypertension and Its Complications.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Article
- A computational model predicts sex-specific responses to calcium channel blockers in mammalian mesenteric vascular smooth muscle.bioRxiv : the preprint server for biology · 2024Article
- The formation of KCommunications biology · 2023Article
- Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023Review
- NPC1-dependent alterations in KNature communications · 2023Article
- The formation of KResearch square · 2023Article
- αeLife · 2023Article
- Mechanisms of Vascular CaHandbook of experimental pharmacology · 2023Article
- Editorial: Molecular physiology of smooth muscle cells.Frontiers in physiology · 2023Article
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Peering into the Molecular Machinery for Regulation of Cav1.2 Channel Clusters.Circulation research · 2022Article
- Spatiotemporal Control of Vascular CaCirculation research · 2022Article
- Biological noise is a key determinant of the reproducibility and adaptability of cardiac pacemaking and EC coupling.The Journal of general physiology · 2022Review
78 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Ca(2+) influx through L-type Ca(2+) channels (LTCCs) influences numerous physiological processes ranging from contraction in muscle and memory in neurons to gene expression in many cell types. However, the spatiotemporal organization of functional LTCCs has been nearly impossible to investigate because of methodological limitations. Here, we examined LTCC function with high temporal and spatial resolution using evanescent field fluorescence microscopy. Surprisingly, we found that LTCCs operated in functionally organized clusters, not necessarily as individual proteins. Furthermore, LTCC function in these clusters does not appear to be controlled by simple stochastic gating but instead by a PKC-dependent switch mechanism. This work suggests that resting intracellular free calcium concentration in arterial myocytes is predominantly controlled by this process in combination with rare voltage-dependent openings of individual LTCCs. We propose that Ca(2+) influx via persistent LTCCs may be an important mechanism regulating steady-state local and global Ca(2+) signals.
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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.