ArticleThe Journal of physiology2007
Loss of caveolin-3 induced by the dystrophy-associated P104L mutation impairs L-type calcium channel function in mouse skeletal muscle cells.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Pannexin-1 and CaV1.1 show reciprocal interaction during excitation-contraction and excitation-transcription coupling in skeletal muscle.The Journal of general physiology · 2021Article
- Membrane Cholesterol in Skeletal Muscle: A Novel Player in Excitation-Contraction Coupling and Insulin Resistance.Journal of diabetes research · 2017Review
- Anaesthetic tricaine acts preferentially on neural voltage-gated sodium channels and fails to block directly evoked muscle contraction.PloS one · 2014Article
- The interaction of caveolin 3 protein with the potassium inward rectifier channel Kir2.1: physiology and pathology related to long qt syndrome 9 (LQT9).The Journal of biological chemistry · 2013Article
- A family with discordance between malignant hyperthermia susceptibility and rippling muscle disease.Journal of anesthesia · 2013Article
- Characterization of the molecular architecture of human caveolin-3 and interaction with the skeletal muscle ryanodine receptor.The Journal of biological chemistry · 2012Article
- Magnetically enhanced nucleic acid delivery. Ten years of magnetofection-progress and prospects.Advanced drug delivery reviews · 2011Review
- Alterations of excitation-contraction coupling and excitation coupled Ca(2+) entry in human myotubes carrying CAV3 mutations linked to rippling muscle.Human mutation · 2011Article
- Caveolin regulation of neuronal intracellular signaling.Cellular and molecular life sciences : CMLS · 2010Review
- In vivo expression of G-protein beta1gamma2 dimer in adult mouse skeletal muscle alters L-type calcium current and excitation-contraction coupling.The Journal of physiology · 2010Article
- Caveolin 3 is associated with the calcium release complex and is modified via in vivo triadin modification.Biochemistry · 2010Article
- Caveolin-3 associates with and affects the function of hyperpolarization-activated cyclic nucleotide-gated channel 4.Biochemistry · 2008Article
- Expression of the muscular dystrophy-associated caveolin-3(P104L) mutant in adult mouse skeletal muscle specifically alters the Ca(2+) channel function of the dihydropyridine receptor.Pflugers Archiv : European journal of physiology · 2008Article
- Caveolin proteins and estrogen signaling in the brain.Molecular and cellular endocrinology · 2008Review
- Caveolin proteins are essential for distinct effects of membrane estrogen receptors in neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caveolins are membrane scaffolding proteins that associate with and regulate a variety of signalling proteins, including ion channels. A deficiency in caveolin-3 (Cav-3), the major striated muscle isoform, is responsible for skeletal muscle disorders, such as limb-girdle muscular dystrophy 1C (LGMD 1C). The molecular mechanisms leading to the muscle wasting that characterizes this pathology are poorly understood. Here we show that a loss of Cav-3 induced by the expression of the LGMD 1C-associated mutant P104L (Cav-3(P104L)) provokes a reduction by half of the maximal conductance of the voltage-dependent L-type Ca(2+) channel in mouse primary cultured myotubes and fetal skeletal muscle fibres. Confocal immunomiscrocopy indicated a colocalization of Cav-3 and Ca(v)1.1, the pore-forming subunit of the L-type Ca(2+) channel, at the surface membrane and in the developing T-tubule network in control myotubes and fetal fibres. In myotubes expressing Cav-3(P104L), the loss of Cav-3 was accompanied by a 66% reduction in Ca(v)1.1 mean labelling intensity. Our results suggest that Cav-3 is involved in L-type Ca(2+) channel membrane function and localization in skeletal muscle cells and that an alteration of L-type Ca(2+) channels could be involved in the physiopathological mechanisms of caveolinopathies.
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