ArticleThe Journal of physiology2004
Mini-dystrophin restores L-type calcium currents in skeletal muscle of transgenic mdx mice.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- Validation of an in vitro muscle platform to evaluate myogenesis and calcium handling in control and dystrophic human myotubes.Scientific reports · 2025Article
- Disrupted Calcium Homeostasis in Duchenne Muscular Dystrophy: A Common Mechanism behind Diverse Consequences.International journal of molecular sciences · 2021Review
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Biochemical and Functional Interplay Between Ion Channels and the Components of the Dystrophin-Associated Glycoprotein Complex.The Journal of membrane biology · 2018Review
- P2RX7 purinoceptor: a therapeutic target for ameliorating the symptoms of duchenne muscular dystrophy.PLoS medicine · 2015Article
- Phosphorylation within the cysteine-rich region of dystrophin enhances its association with β-dystroglycan and identifies a potential novel therapeutic target for skeletal muscle wasting.Human molecular genetics · 2014Article
- Dysferlin stabilizes stress-induced Ca2+ signaling in the transverse tubule membrane.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Acute failure of action potential conduction in mdx muscle reveals new mechanism of contraction-induced force loss.The Journal of physiology · 2013Article
- P2X7 purinoceptor alterations in dystrophic mdx mouse muscles: relationship to pathology and potential target for treatment.Journal of cellular and molecular medicine · 2012Article
- Quadriceps myopathy caused by skeletal muscle-specific ablation of β(cyto)-actin.Journal of cell science · 2011Article
- Functional expression of transgenic 1sDHPR channels in adult mammalian skeletal muscle fibres.The Journal of physiology · 2011Article
- The inotropic peptide βARKct improves βAR responsiveness in normal and failing cardiomyocytes through G(βγ)-mediated L-type calcium current disinhibition.Circulation research · 2011Article
- Nitrosative stress elicited by nNOSµ delocalization inhibits muscle force in dystrophin-null mice.The Journal of pathology · 2011Article
- Genetic inhibition of PKA phosphorylation of RyR2 prevents dystrophic cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Enhanced muscle shortening and impaired Ca2+ channel function in an acute septic myopathy model.Journal of neurology · 2010Article
- Microarchitecture is severely compromised but motor protein function is preserved in dystrophic mdx skeletal muscle.Biophysical journal · 2010Article
- Regulation of TRPC1 and TRPC4 cation channels requires an alpha1-syntrophin-dependent complex in skeletal mouse myotubes.The Journal of biological chemistry · 2009Article
- Rapid Ca2+ flux through the transverse tubular membrane, activated by individual action potentials in mammalian skeletal muscle.The Journal of physiology · 2009Article
- Unloaded speed of shortening in voltage-clamped intact skeletal muscle fibers from wt, mdx, and transgenic minidystrophin mice using a novel high-speed acquisition system.Biophysical journal · 2008Article
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Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
L-type calcium currents (iCa) were recorded using the two-microelectrode voltage-clamp technique in single short toe muscle fibres of three different mouse strains: (i) C57/SV129 wild-type mice (wt); (ii) mdx mice (an animal model for Duchenne muscular dystrophy; and (iii) transgenically engineered mini-dystrophin (MinD)-expressing mdx mice. The activation and inactivation properties of iCa were examined in 2- to 18-month-old animals. Ca2+ current densities at 0 mV in mdx fibres increased with age, but were always significantly smaller compared to age-matched wild-type fibres. Time-to-peak (TTP) of iCa was prolonged in mdx fibres compared to wt fibres. MinD fibres always showed similar TTP and current amplitudes compared to age-matched wt fibres. In all three genotypes, the voltage-dependent inactivation and deactivation of iCa were similar. Intracellular resting calcium concentration ([Ca2+]i) and the distribution of dihydropyridine binding sites were also not different in young animals of all three genotypes, whereas iCa was markedly reduced in mdx fibres. We conclude, that dystrophin influences L-type Ca2+ channels via a direct or indirect linkage which may be disrupted in mdx mice and may be crucial for proper excitation-contraction coupling initiating Ca2+ release from the sarcoplasmic reticulum. This linkage seems to be fully restored in the presence of mini-dystrophin.
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