ArticleCell calcium2009
Alternative splicing of RyR1 alters the efficacy of skeletal EC coupling.
Article in Cell calcium, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- Elimination of myotonia improves myopathy in a muscleblind-like knockout model of myotonic dystrophy.Nature communications · 2026Article
- Disruptions of cell signaling pathways in myotonic dystrophy type 1 skeletal muscle, their pathogenic impact, and potential for combinatorial therapeutics.The Journal of biological chemistry · 2026Review
- Farnesyl diphosphate synthase promotes cell proliferation by regulating gene expression and alternative splicing profiles in HeLa cells.Oncology letters · 2023Article
- Alternative splicing diversifies the skeletal muscle transcriptome during prolonged spaceflight.Skeletal muscle · 2022Article
- A Comparative Perspective on Functionally-Related, Intracellular Calcium Channels: The Insect Ryanodine and Inositol 1,4,5-Trisphosphate Receptors.Biomolecules · 2021Review
- Targeted splice sequencing reveals RNA toxicity and therapeutic response in myotonic dystrophy.Nucleic acids research · 2021Article
- Article
- Pharmacological and physiological activation of AMPK improves the spliceopathy in DM1 mouse muscles.Human molecular genetics · 2018Article
- Diversification of the muscle proteome through alternative splicing.Skeletal muscle · 2018Review
- Review
- Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Electromechanical delays during a fatiguing exercise and recovery in patients with myotonic dystrophy type 1.European journal of applied physiology · 2017Article
- Targeting deregulated AMPK/mTORC1 pathways improves muscle function in myotonic dystrophy type I.The Journal of clinical investigation · 2017Article
- Unexpected dependence of RyR1 splice variant expression in human lower limb muscles on fiber-type composition.Pflugers Archiv : European journal of physiology · 2016Article
- Progressive impairment of CaV1.1 function in the skeletal muscle of mice expressing a mutant type 1 Cu/Zn superoxide dismutase (G93A) linked to amyotrophic lateral sclerosis.Skeletal muscle · 2016Article
- Characterization of the Ryanodine Receptor Gene With a Unique 3'-UTR and Alternative Splice Site From the Oriental Fruit Moth.Journal of insect science (Online) · 2016Article
- CUG-BP1 regulates RyR1 ASI alternative splicing in skeletal muscle atrophy.Scientific reports · 2015Article
- Molecular Characterization, mRNA Expression and Alternative Splicing of Ryanodine Receptor Gene in the Brown Citrus Aphid, Toxoptera citricida (Kirkaldy).International journal of molecular sciences · 2015Article
- Regions of ryanodine receptors that influence activation by the dihydropyridine receptor β1a subunit.Skeletal muscle · 2015Article
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Authors and funding
8 authors.
Funding
Abstract
Alternative splicing of ASI residues (Ala(3481)-Gln(3485)) in the skeletal muscle ryanodine receptor (RyR1) is developmentally regulated: the residues are present in adult ASI(+)RyR1, but absent in the juvenile ASI(-)RyR1 which is over-expressed in adult myotonic dystrophy type 1 (DM1). Although this splicing switch may influence RyR1 function in developing muscle and DM1, little is known about the properties of the splice variants. We examined excitation-contraction (EC) coupling and the structure and interactions of the ASI domain (Thr(3471)-Gly(3500)) in the splice variants. Depolarisation-dependent Ca(2+) release was enhanced by >50% in myotubes expressing ASI(-)RyR1 compared with ASI(+)RyR1, although DHPR L-type currents and SR Ca(2+) content were unaltered, while ASI(-)RyR1 channel function was actually depressed. The effect on EC coupling did not depend on changes in ASI domain secondary structure. Probing RyR1 function with peptides possessing the ASI domain sequence indicated that the domain contributes to an inhibitory module in RyR1. The action of the peptide depended on a sequence of basic residues and their alignment in an alpha-helix adjacent to the ASI splice site. This is the first evidence that the ASI residues contribute to an inhibitory module in RyR1 that influences EC coupling. Implications for development and DM1 are discussed.
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