ArticleThe Journal of biological chemistry2010
Interactions with M-band titin and calpain 3 link myospryn (CMYA5) to tibial and limb-girdle muscular dystrophies.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 73 citations in OpenAlex.
- The perijunctional zone is a molecularly distinct muscle subdomain altered in Duchenne muscular dystrophy.Nature communications · 2026Article
- Titin's P-zone domains A164-167 are essential for thick filament structural arrangement.The Journal of general physiology · 2026Article
- Novel Mutations in Titin Exon 363 With Different Phenotypes Including a Founder Mutation in Eastern Europe.European journal of neurology · 2025Article
- Transcriptional Signatures of Aerobic Exercise-Induced Muscle Adaptations in Humans.Journal of functional morphology and kinesiology · 2025Article
- Virally delivered CMYA5 enhances the assembly of cardiac dyads.Nature biomedical engineering · 2025Article
- An overview of insights and updates on TTN mutations in cardiomyopathies.Frontiers in pharmacology · 2025Review
- Distinct functional and molecular profiles between physiological and pathological atrial enlargement offer potential new therapeutic opportunities for atrial fibrillation.Clinical science (London, England : 1979) · 2024Article
- Article
- Speg interactions that regulate the stability of excitation-contraction coupling protein complexes in triads and dyads.Communications biology · 2023Article
- Pathogenesis of Cardiomyopathy Caused by Variants inCirculation · 2022Article
- Use of animal models to understand titin physiology and pathology.Journal of cellular and molecular medicine · 2022Review
- CMYA5 establishes cardiac dyad architecture and positioning.Nature communications · 2022Article
- Pairwise sequence similarity mapping with PaSiMap: Reclassification of immunoglobulin domains from titin as case study.Computational and structural biotechnology journal · 2022Article
- Article
- Calcineurin in the heart: New horizons for an old friend.Cellular signalling · 2021Review
- Titin M-line insertion sequence 7 is required for proper cardiac function in mice.Journal of cell science · 2021Article
- Myospryn deficiency leads to impaired cardiac structure and function and schizophrenia-associated symptoms.Cell and tissue research · 2021Article
- Muscle allele-specific expression QTLs may affect meat quality traits in Bos indicus.Scientific reports · 2021Article
- Panorama of the distal myopathies.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2020Review
- The M-band: The underestimated part of the sarcomere.Biochimica et biophysica acta. Molecular cell research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
Abstract
Mutations in the C terminus of titin, situated at the M-band of the striated muscle sarcomere, cause tibial muscular dystrophy (TMD) and limb-girdle muscular dystrophy (LGMD) type 2J. Mutations in the protease calpain 3 (CAPN3), in turn, lead to LGMD2A, and secondary CAPN3 deficiency in LGMD2J suggests that the pathomechanisms of the diseases are linked. Yeast two-hybrid screens carried out to elucidate the molecular pathways of TMD/LGMD2J and LGMD2A resulted in the identification of myospryn (CMYA5, cardiomyopathy-associated 5) as a binding partner for both M-band titin and CAPN3. Additional yeast two-hybrid and coimmunoprecipitation studies confirmed both interactions. The interaction of myospryn and M-band titin was supported by localization of endogenous and transfected myospryn at the M-band level. Coexpression studies showed that myospryn is a proteolytic substrate for CAPN3 and suggested that myospryn may protect CAPN3 from autolysis. Myospryn is a muscle-specific protein of the tripartite motif superfamily, reported to function in vesicular trafficking and protein kinase A signaling and implicated in the pathogenesis of Duchenne muscular dystrophy. The novel interactions indicate a role for myospryn in the sarcomeric M-band and may be relevant for the molecular pathomechanisms of TMD/LGMD2J and LGMD2A.
Indexed as
Identifiers
What OpenQuestion holds
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.