ArticleThe Journal of general physiology2006
Mechanisms underlying heterogeneous Ca2+ sparklet activity in arterial smooth muscle.
Article in The Journal of general physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
85 citing papers in PubMed, 121 citations in OpenAlex.
- CaThe Journal of physiology · 2026Article
- Aging Disrupts L-type CaCirculation research · 2026Article
- Aging reduces the number and function of L-type calcium channels in the membrane of cardiac pacemaker cells.bioRxiv : the preprint server for biology · 2025Article
- 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
- The formation of KResearch square · 2023Article
- Mechanisms of Vascular CaHandbook of experimental pharmacology · 2023Article
- Peering into the Molecular Machinery for Regulation of Cav1.2 Channel Clusters.Circulation research · 2022Article
- Ion channel molecular complexes in vascular smooth muscle.Frontiers in physiology · 2022Review
- Functional tuning of Vascular L-type CaFrontiers in physiology · 2022Review
- Regulation of neuronal excitation-transcription coupling by Kv2.1-induced clustering of somatic L-type CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Mechanisms and Regulation of Cardiac CaInternational journal of molecular sciences · 2021Review
- The Calcium Signaling Mechanisms in Arterial Smooth Muscle and Endothelial Cells.Comprehensive Physiology · 2021Article
- Transient receptor potential channel-dependent myogenic responsiveness in small-sized resistance arteries.Journal of exercise rehabilitation · 2021Review
- Cellular and molecular effects of hyperglycemia on ion channels in vascular smooth muscle.Cellular and molecular life sciences : CMLS · 2021Review
- AKAP5 complex facilitates purinergic modulation of vascular L-type CaNature communications · 2020Article
- Article
- Calcium signals that determine vascular resistance.Wiley interdisciplinary reviews. Systems biology and medicine · 2019Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In arterial smooth muscle, single or small clusters of Ca(2+) channels operate in a high probability mode, creating sites of nearly continual Ca(2+) influx (called "persistent Ca(2+) sparklet" sites). Persistent Ca(2+) sparklet activity varies regionally within any given cell. At present, the molecular identity of the Ca(2+) channels underlying Ca(2+) sparklets and the mechanisms that give rise to their spatial heterogeneity remain unclear. Here, we used total internal reflection fluorescence (TIRF) microscopy to directly investigate these issues. We found that tsA-201 cells expressing L-type Cavalpha1.2 channels recapitulated the general features of Ca(2+) sparklets in cerebral arterial myocytes, including amplitude of quantal event, voltage dependencies, gating modalities, and pharmacology. Furthermore, PKCalpha activity was required for basal persistent Ca(2+) sparklet activity in arterial myocytes and tsA-201 cells. In arterial myocytes, inhibition of protein phosphatase 2A (PP2A) and 2B (PP2B; calcineurin) increased Ca(2+) influx by evoking new persistent Ca(2+) sparklet sites and by increasing the activity of previously active sites. The actions of PP2A and PP2B inhibition on Ca(2+) sparklets required PKC activity, indicating that these phosphatases opposed PKC-mediated phosphorylation. Together, these data unequivocally demonstrate that persistent Ca(2+) sparklet activity is a fundamental property of L-type Ca(2+) channels when associated with PKC. Our findings support a novel model in which the gating modality of L-type Ca(2+) channels vary regionally within a cell depending on the relative activities of nearby PKCalpha, PP2A, and PP2B.
Indexed as
Identifiers
What OpenQuestion holds
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.