ArticleChannels (Austin, Tex.)
Rem-GTPase regulates cardiac myocyte L-type calcium current.
Article in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Genetic architecture of basal heart rate and its modulation by dietary salt in Drosophila melanogaster.PLoS genetics · 2026Article
- The C-terminus of Rad is required for membrane localization and L-type calcium channel regulation.The Journal of general physiology · 2024Article
- Protective effects of 18β-Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting CaFood science & nutrition · 2021Article
- L-type channel inactivation balances the increased peak calcium current due to absence of Rad in cardiomyocytes.The Journal of general physiology · 2021Article
- Into the spotlight: RGK proteins in skeletal muscle.Cell calcium · 2021Review
- Increased Retention of Cardiac Cells to a Glass Substrate through Streptavidin-Biotin Affinity.ACS omega · 2021Article
- Regulation of cardiovascular calcium channel activity by post-translational modifications or interacting proteins.Pflugers Archiv : European journal of physiology · 2020Review
- Article
- Myocardial-restricted ablation of the GTPase RAD results in a pro-adaptive heart response in mice.The Journal of biological chemistry · 2019Article
- Optogenetic Control of Voltage-Gated Calcium Channels.Angewandte Chemie (International ed. in English) · 2018Article
- The small GTPase RSG1 controls a final step in primary cilia initiation.The Journal of cell biology · 2018Article
- Similar molecular determinants on Rem mediate two distinct modes of inhibition of CaChannels (Austin, Tex.) · 2016Article
- Rad and Rem are non-canonical G-proteins with respect to the regulatory role of guanine nucleotide binding in Ca(V)1.2 channel regulation.The Journal of physiology · 2015Article
- Loss of Rad-GTPase produces a novel adaptive cardiac phenotype resistant to systolic decline with aging.American journal of physiology. Heart and circulatory physiology · 2015Article
- RGK regulation of voltage-gated calcium channels.Science China. Life sciences · 2015Review
- Molecular mechanisms of activity-dependent changes in dendritic morphology: role of RGK proteins.Trends in neurosciences · 2014Review
- Arrhythmogenic calmodulin mutations disrupt intracellular cardiomyocyte Ca2+ regulation by distinct mechanisms.Journal of the American Heart Association · 2014Article
- Differential effects of RGK proteins on L-type channel function in adult mouse skeletal muscle.Biophysical journal · 2014Article
- Arterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.PloS one · 2014Article
- Rad GTPase deletion increases L-type calcium channel current leading to increased cardiac contraction.Journal of the American Heart Association · 2013Article
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
rationaleThe L-type calcium channels (LTCC) are critical for maintaining Ca(2+)-homeostasis. In heterologous expression studies, the RGK-class of Ras-related G-proteins regulates LTCC function; however, the physiological relevance of RGK-LTCC interactions is untested.
objectiveIn this report we test the hypothesis that the RGK protein, Rem, modulates native Ca(2+) current (I(Ca,L)) via LTCC in murine cardiomyocytes. METHODS AND
resultsRem knockout mice (Rem(-/-)) were engineered, and I(Ca,L) and Ca(2+) -handling properties were assessed. Rem(-/-) ventricular cardiomyocytes displayed increased I(Ca,L) density. I(Ca,L) activation was shifted positive on the voltage axis, and β-adrenergic stimulation normalized this shift compared with wild-type I(Ca,L). Current kinetics, steady-state inactivation, and facilitation was unaffected by Rem(-/-) . Cell shortening was not significantly different. Increased I(Ca,L) density in the absence of frank phenotypic differences motivated us to explore putative compensatory mechanisms. Despite the larger I(Ca,L) density, Rem(-/-) cardiomyocyte Ca(2+) twitch transient amplitude was significantly less than that compared with wild type. Computer simulations and immunoblot analysis suggests that relative dephosphorylation of Rem(-/-) LTCC can account for the paradoxical decrease of Ca(2+) transients.
conclusionsThis is the first demonstration that loss of an RGK protein influences I(Ca,L) in vivo in cardiac myocytes.
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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.