ArticleThe Journal of cell biology2009
Akt regulates L-type Ca2+ channel activity by modulating Cavalpha1 protein stability.
Article in The Journal of cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 65 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
65 citing papers in PubMed, 90 citations in OpenAlex.
- CaThe Journal of physiology · 2026Article
- Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease.Circulation research · 2026Article
- Degradation of voltage-gated calcium channels: mechanisms and applications in neurological and cardiovascular diseases.Cell communication and signaling : CCS · 2025Review
- Article
- Selective blockade of CaNature communications · 2024Article
- Natural compounds regulate the PI3K/Akt/GSK3β pathway in myocardial ischemia-reperfusion injury.Cell cycle (Georgetown, Tex.) · 2023Article
- β subunits of voltage-gated calcium channels in cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Article
- PI3K/Akt pathway mediates the positive inotropic effects of insulin in Langendorff-perfused rat hearts.Scientific reports · 2022Article
- Mechanisms and Regulation of Cardiac CaInternational journal of molecular sciences · 2021Review
- Insulin acutely increases agonist-induced airway smooth muscle contraction in humans and rats.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- The life cycle of voltage-gated CaNeuronal signaling · 2021Review
- Cardiac T-Tubule cBIN1-Microdomain, a Diagnostic Marker and Therapeutic Target of Heart Failure.International journal of molecular sciences · 2021Review
- Diabetes-induced changes in cardiac voltage-gated ion channels.World journal of diabetes · 2021Review
- Interaction of the Joining Region in Junctophilin-2 With the L-Type CaCirculation research · 2021Article
- Characterization and validation of a preventative therapy for hypertrophic cardiomyopathy in a murine model of the disease.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Regulation of cardiovascular calcium channel activity by post-translational modifications or interacting proteins.Pflugers Archiv : European journal of physiology · 2020Review
- Stimulation of TRPA1 attenuates ischemia-induced cardiomyocyte cell death through an eNOS-mediated mechanism.Channels (Austin, Tex.) · 2019Article
- Arsenite and its trivalent methylated metabolites inhibit glucose-stimulated calcium influx and insulin secretion in murine pancreatic islets.Archives of toxicology · 2019Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
Abstract
The insulin IGF-1-PI3K-Akt signaling pathway has been suggested to improve cardiac inotropism and increase Ca(2+) handling through the effects of the protein kinase Akt. However, the underlying molecular mechanisms remain largely unknown. In this study, we provide evidence for an unanticipated regulatory function of Akt controlling L-type Ca(2+) channel (LTCC) protein density. The pore-forming channel subunit Ca(v)alpha1 contains highly conserved PEST sequences (signals for rapid protein degradation), and in-frame deletion of these PEST sequences results in increased Ca(v)alpha1 protein levels. Our findings show that Akt-dependent phosphorylation of Ca(v)beta2, the LTCC chaperone for Ca(v)alpha1, antagonizes Ca(v)alpha1 protein degradation by preventing Ca(v)alpha1 PEST sequence recognition, leading to increased LTCC density and the consequent modulation of Ca(2+) channel function. This novel mechanism by which Akt modulates LTCC stability could profoundly influence cardiac myocyte Ca(2+) entry, Ca(2+) handling, and contractility.
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.