ArticleThe Journal of biological chemistry2009
Triadin deletion induces impaired skeletal muscle function.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 86 citations in OpenAlex.
- Trdn-as directs m6A-dependent transcriptional termination for accurate triadin isoform switching, preventing aberrant dyads and cardiomyopathy.Nature communications · 2026Article
- Benfotiamine promotes diabetic wound healing by modulating Trisk95 and reducing oxidative stress.Diabetology & metabolic syndrome · 2026Article
- Impact of polymorphisms on gene expression and splicing in response to exercise and diet-induced weight loss in human skeletal muscle tissues.Cell genomics · 2025Article
- Review
- RyR1 Is Involved in the Control of Myogenesis.Cells · 2025Article
- Architecture and molecular machinery of skeletal myofibers: a systematic review of the structure-function relationships.Frontiers in cell and developmental biology · 2025Review
- Molecular determinants of skeletal muscle force loss in response to 5 days of dry immersion in human.Journal of cachexia, sarcopenia and muscle · 2024Article
- Functional benefit of CRISPR-Cas9-induced allele deletion forMolecular therapy. Nucleic acids · 2024Article
- Speg interactions that regulate the stability of excitation-contraction coupling protein complexes in triads and dyads.Communications biology · 2023Article
- Cellular and electrophysiological characterization of triadin knockout syndrome using induced pluripotent stem cell-derived cardiomyocytes.Stem cell reports · 2023Article
- Huntingtin regulates calcium fluxes in skeletal muscle.The Journal of general physiology · 2023Article
- Belayer: Modeling discrete and continuous spatial variation in gene expression from spatially resolved transcriptomics.Cell systems · 2022Article
- The Sarcoplasmic Reticulum of Skeletal Muscle Cells: A Labyrinth of Membrane Contact Sites.Biomolecules · 2022Review
- Article
- Integrated proteomic, phosphoproteomic, and N-glycoproteomic analyses of theCurrent research in food science · 2022Article
- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Association of decreased triadin expression level with apoptosis of dopaminergic cells in Parkinson's disease mouse model.BMC neuroscience · 2021Article
- Generation of a Triadin KnockOut Syndrome Zebrafish Model.International journal of molecular sciences · 2021Article
- Calsequestrin, a key protein in striated muscle health and disease.Journal of muscle research and cell motility · 2021Review
- Exome sequencing in patient-parent trios suggests new candidate genes for early-onset primary sclerosing cholangitis.Liver international : official journal of the International Association for the Study of the Liver · 2021Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triadin is a multiple proteins family, some isoforms being involved in muscle excitation-contraction coupling, and some having still unknown functions. To obtain clues on triadin functions, we engineered a triadin knock-out mouse line and characterized the physiological effect of triadin ablation on skeletal muscle function. These mice presented a reduced muscle strength, which seemed not to alter their survival and has been characterized in the present work. We first checked in these mice the expression level of the different proteins involved in calcium homeostasis and observed in fast muscles an increase in expression of dihydropyridine receptor, with a large reduction in calsequestrin expression. Electron microscopy analysis of KO muscles morphology demonstrated the presence of triads in abnormal orientation and a reduction in the sarcoplasmic reticulum terminal cisternae volume. Using calcium imaging on cultured myotubes, we observed a reduction in the total amount of calcium stored in the sarcoplasmic reticulum. Physiological studies have been performed to evaluate the influence of triadin deletion on skeletal muscle function. Muscle strength has been measured both on the whole animal model, using hang test or electrical stimulation combined with NMR analysis and strength measurement, or on isolated muscle using electrical stimulation. All the results obtained demonstrate an important reduction in muscle strength, indicating that triadin plays an essential role in skeletal muscle function and in skeletal muscle structure. These results indicate that triadin alteration leads to the development of a myopathy, which could be studied using this new animal model.
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Registered trials
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.