ArticleUpsala journal of medical sciences2009
Maintenance of muscle mass, fiber size, and contractile function in mice lacking the Z-disc protein myotilin.
Article in Upsala journal of medical sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Epidermal growth factor receptor-dependent maintenance of cardiac contractility.Cardiovascular research · 2022Article
- Molecular and cellular basis of genetically inherited skeletal muscle disorders.Nature reviews. Molecular cell biology · 2021Review
- Gene expression patterns in transgenic mouse models of hypertrophic cardiomyopathy caused by mutations in myosin regulatory light chain.Archives of biochemistry and biophysics · 2016Article
- RNAi-based gene therapy for dominant Limb Girdle Muscular Dystrophies.Current gene therapy · 2012Review
- Myotilin dynamics in cardiac and skeletal muscle cells.Cytoskeleton (Hoboken, N.J.) · 2011Article
- Inactivation of the mitochondrial carrier SLC25A25 (ATP-Mg2+/Pi transporter) reduces physical endurance and metabolic efficiency in mice.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyofibrillar myopathies constitute a rare group of congenital neuromuscular disorders, frequently associated with mutations in Z-disc proteins such as myotilin. Myotilin location and interactions with other Z-disc proteins are clearly defined, but its role in the regulation of muscle structure and function remains unknown. The present study aims at investigating this specific role of myotilin.
methodsSkeletal and cardiac muscles were collected from adult mice with a targeted deletion of myotilin (myo(-/-)) and wild-type animals (myo(+/+)). RESULTS AND
conclusionSimilar skeletal and cardiac muscle weights were observed in myo(-/-) and myo(+/+) mice. At the muscle cell level, the size and force production of single membrane permeabilized fibers were identical between myo(-/-) and myo(+/+) rodents. Thus, myotilin does not have a significant influence on muscle mass, muscle fiber size, or regulation of muscle contraction. Alternatively, compensatory over-expressions of other elements including proteins from the same subfamily, or Z-disc proteins such as telethonin, or intermediate filaments may compensate for the lack of myotilin.
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