ArticleScientific reports2016
Evidence for redox sensing by a human cardiac calcium channel.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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
20 citing papers in PubMed, 30 citations in OpenAlex.
- A Seven Amino Acid Long Region in the Cardiac CaCells · 2026Article
- Modulation of Redox-Sensitive Cardiac Ion Channels.Antioxidants (Basel, Switzerland) · 2025Review
- Hif1α-dependent mitochondrial acute ONature communications · 2024Article
- Ahf-Caltide, a Novel Polypeptide Derived from Calpastatin, Protects against Oxidative Stress Injury by Stabilizing the Expression of CaInternational journal of molecular sciences · 2023Article
- Flipping Off and On the Redox Switch in the Microcirculation.Annual review of physiology · 2023Review
- Acute oxygen sensing by vascular smooth muscle cells.Frontiers in physiology · 2023Review
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Extracellular Vesicles in Redox Signaling and Metabolic Regulation in Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Oxygen-dependent regulation of ion channels: acute responses, post-translational modification, and response to chronic hypoxia.Pflugers Archiv : European journal of physiology · 2021Review
- Thiol-Mediated Uptake.JACS Au · 2021Review
- Correcting QUEST Magnetic Resonance Imaging-Sensitive Free Radical Production in the Outer Retina In Vivo Does Not Correct Reduced Visual Performance in 24-Month-Old C57BL/6J Mice.Investigative ophthalmology & visual science · 2021Article
- Post-Translational Modification of Cav1.2 and its Role in Neurodegenerative Diseases.Frontiers in pharmacology · 2021Review
- Neuronal nitric oxide synthase regulation of calcium cycling in ventricular cardiomyocytes is independent of CaPflugers Archiv : European journal of physiology · 2020Article
- Redox-dependent thiol modifications: implications for the release of extracellular vesicles.Cellular and molecular life sciences : CMLS · 2018Review
- D-cis-Diltiazem Can Produce Oxidative Stress in Healthy Depolarized Rods In Vivo.Investigative ophthalmology & visual science · 2018Article
- Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium.Frontiers in physiology · 2018Review
- Identification of a novel cAMP dependent protein kinase A phosphorylation site on the human cardiac calcium channel.Scientific reports · 2017Article
- Oxidative toxicity in diabetes and Alzheimer's disease: mechanisms behind ROS/ RNS generation.Journal of biomedical science · 2017Review
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Altered Calcium Handling and Ventricular Arrhythmias in Acute Ischemia.Clinical Medicine Insights. Cardiology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ion channels are critical to life and respond rapidly to stimuli to evoke physiological responses. Calcium influx into heart muscle occurs through the ion conducting α1C subunit (Cav1.2) of the L-type Ca(2+) channel. Glutathionylation of Cav1.2 results in increased calcium influx and is evident in ischemic human heart. However controversy exists as to whether direct modification of Cav1.2 is responsible for altered function. We directly assessed the function of purified human Cav1.2 in proteoliposomes. Truncation of the C terminus and mutation of cysteines in the N terminal region and cytoplasmic loop III-IV linker did not alter the effects of thiol modifying agents on open probability of the channel. However mutation of cysteines in cytoplasmic loop I-II linker altered open probability and protein folding assessed by thermal shift assay. We find that C543 confers sensitivity of Cav1.2 to oxidative stress and is sufficient to modify channel function and posttranslational folding. Our data provide direct evidence for the calcium channel as a redox sensor that facilitates rapid physiological responses.
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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.