ArticleProceedings of the National Academy of Sciences of the United States of America2005
Convergent regulation of skeletal muscle Ca2+ channels by dystrophin, the actin cytoskeleton, and cAMP-dependent protein kinase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
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- Skeletal Muscle Transcriptome Analysis of Hanzhong Ma Duck at Different Growth Stages Using RNA-Seq.Biomolecules · 2021Article
- Comprehensive analysis of the expression profile of circRNAs and their predicted protein-coding ability in the muscle of mdx mice.Functional & integrative genomics · 2020Article
- Syntrophins entangled in cytoskeletal meshwork: Helping to hold it all together.Cell proliferation · 2019Review
- Biochemical and Functional Interplay Between Ion Channels and the Components of the Dystrophin-Associated Glycoprotein Complex.The Journal of membrane biology · 2018Review
- Dynamin-2 mutations linked to Centronuclear Myopathy impair actin-dependent trafficking in muscle cells.Scientific reports · 2017Article
- Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Physiological reviews · 2016Review
- β-Adrenergic modulation of skeletal muscle contraction: key role of excitation-contraction coupling.The Journal of physiology · 2015Review
- Forskolin Regulates L-Type Calcium Channel through Interaction between Actinin 4 and β3 Subunit in Osteoblasts.PloS one · 2015Article
- Enhanced currents through L-type calcium channels in cardiomyocytes disturb the electrophysiology of the dystrophic heart.American journal of physiology. Heart and circulatory physiology · 2014Article
- Community Structure Analysis of Gene Interaction Networks in Duchenne Muscular Dystrophy.PloS one · 2013Article
- Article
- L-type calcium channel activity in osteoblast cells is regulated by the actin cytoskeleton independent of protein trafficking.Journal of bone and mineral metabolism · 2011Article
- Drug screening in a zebrafish model of Duchenne muscular dystrophy.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- HSPB1, HSPB6, HSPB7 and HSPB8 protect against RhoA GTPase-induced remodeling in tachypaced atrial myocytes.PloS one · 2011Article
- Multiple kinase pathways regulate voltage-dependent Ca2+ influx and migration in oligodendrocyte precursor cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Automated drug screening with contractile muscle tissue engineered from dystrophic myoblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Rapid Ca2+ flux through the transverse tubular membrane, activated by individual action potentials in mammalian skeletal muscle.The Journal of physiology · 2009Article
- Sodium current properties of primary skeletal myocytes and cardiomyocytes derived from different mouse strains.Pflugers Archiv : European journal of physiology · 2009Article
- Diverse roles of the actin cytoskeleton in striated muscle.Journal of muscle research and cell motility · 2009Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The skeletal muscle L-type Ca2+ channel (Ca(V)1.1), which is responsible for initiating muscle contraction, is regulated by phosphorylation by cAMP-dependent protein kinase (PKA) in a voltage-dependent manner that requires direct physical association between the channel and the kinase mediated through A-kinase anchoring proteins (AKAPs). The role of the actin cytoskeleton in channel regulation was investigated in skeletal myocytes cultured from wild-type mice, mdx mice that lack the cytoskeletal linkage protein dystrophin, and a skeletal muscle cell line, 129 CB3. Voltage dependence of channel activation was shifted positively, and potentiation was greatly diminished in mdx myocytes and in 129 CB3 cells treated with the microfilament stabilizer phalloidin. Voltage-dependent potentiation by strong depolarizing prepulses was reduced in mdx myocytes but could be restored by positively shifting the stimulus potentials to compensate for the positive shift in the voltage dependence of gating. Inclusion of PKA in the pipette caused a negative shift in the voltage dependence of activation and restored voltage-dependent potentiation in mdx myocytes. These results show that skeletal muscle Ca2+ channel activity and voltage-dependent potentiation are controlled by PKA and microfilaments in a convergent manner. Regulation of Ca2+ channel activity by hormones and neurotransmitters that use the PKA signal transduction pathway may interact in a critical way with the cytoskeleton and may be impaired by deletion of dystrophin, contributing to abnormal regulation of intracellular calcium concentrations in dystrophic muscle.
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