ArticleDevelopment (Cambridge, England)2005
Normal myoblast fusion requires myoferlin.
Article in Development (Cambridge, England), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
What it found
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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
130 citing papers in PubMed, 209 citations in OpenAlex.
- Myoferlin at the crossroad of vesicle trafficking and mitochondrial function: implications for pancreatic cancer progression and stromal reprogramming.Biochemical Society transactions · 2026Review
- Differential Myopathic and Transcriptomic Changes in Soleus and Gastrocnemius Muscles in a Novel Chronic Hindlimb Ischemia Rat Model Induced by Endovascular Catheter Occlusion.Acta physiologica (Oxford, England) · 2026Article
- Site-specific glycosylation of Sec24D and myoferlin recruit ERGIC to ER exit sites for collagen trafficking.Nature communications · 2026Article
- PDGFRβ signaling restrains myocyte function to limit the regenerative capacity of skeletal muscle.The Journal of clinical investigation · 2026Article
- Myoferlin is a component of late-stage vRNP trafficking vesicles for enveloped RNA viruses.Nature communications · 2026Article
- Targeting myoferlin in ER/Golgi vesicle trafficking reprograms pancreatic cancer-associated fibroblasts.The EMBO journal · 2025Article
- Impaired myogenesis in limb girdle muscular dystrophy type 2B.Scientific reports · 2025Article
- Molecular Dynamics of Trogocytosis and Other Contact-Dependent Cell Trafficking Mechanisms in Tumor Pathogenesis.Cancers · 2025Review
- Structural insights into lipid membrane binding by human ferlins.The EMBO journal · 2025Article
- Lysosomal Repair in Health and Disease.Journal of cellular physiology · 2025Review
- Myotube Formation and Cellular Fusion Are Diminished Due to Low Birth Weight in Piglets.International journal of molecular sciences · 2025Article
- Suppressing PDGFRβ Signaling Enhances Myocyte Fusion to Promote Skeletal Muscle Regeneration.bioRxiv : the preprint server for biology · 2024Article
- The Dysferlinopathies Conundrum: Clinical Spectra, Disease Mechanism and Genetic Approaches for Treatments.Biomolecules · 2024Review
- Article
- p97/VCP Promotes the Recycling of Endocytic Cargo.Molecular biology of the cell · 2023Article
- Tetraspanin CD82 Associates with Trafficking Vesicle in Muscle Cells and Binds to Dysferlin and Myoferlin.Advanced biology · 2023Article
- Portrait of Dysferlinopathy: Diagnosis and Development of Therapy.Journal of clinical medicine · 2023Review
- Local IL-10 delivery modulates the immune response and enhances repair of volumetric muscle loss muscle injury.Scientific reports · 2023Article
- Chromosome-scale genomes reveal genomic consequences of inbreeding in the South China tiger: A comparative study with the Amur tiger.Molecular ecology resources · 2023Article
- Testis-enriched ferlin, FER1L5, is required for CaScience advances · 2023Article
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Muscle growth occurs during embryonic development and continues in adult life as regeneration. During embryonic muscle growth and regeneration in mature muscle, singly nucleated myoblasts fuse to each other to form myotubes. In muscle growth, singly nucleated myoblasts can also fuse to existing large, syncytial myofibers as a mechanism of increasing muscle mass without increasing myofiber number. Myoblast fusion requires the alignment and fusion of two apposed lipid bilayers. The repair of muscle plasma membrane disruptions also relies on the fusion of two apposed lipid bilayers. The protein dysferlin, the product of the Limb Girdle Muscular Dystrophy type 2 locus, has been shown to be necessary for efficient, calcium-sensitive, membrane resealing. We now show that the related protein myoferlin is highly expressed in myoblasts undergoing fusion, and is expressed at the site of myoblasts fusing to myotubes. Like dysferlin, we found that myoferlin binds phospholipids in a calcium-sensitive manner that requires the first C2A domain. We generated mice with a null allele of myoferlin. Myoferlin null myoblasts undergo initial fusion events, but they form large myotubes less efficiently in vitro, consistent with a defect in a later stage of myogenesis. In vivo, myoferlin null mice have smaller muscles than controls do, and myoferlin null muscle lacks large diameter myofibers. Additionally, myoferlin null muscle does not regenerate as well as wild-type muscle does, and instead displays a dystrophic phenotype. These data support a role for myoferlin in the maturation of myotubes and the formation of large myotubes that arise from the fusion of myoblasts to multinucleate myotubes.
Indexed as
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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.