ArticleScientific reports2020
Dystrophin Dp71ab is monoclonally expressed in human satellite cells and enhances proliferation of myoblast cells.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- The Multi-System Roles of Dp71 Dystrophin Isoforms in Duchenne Muscular Dystrophy.Muscles (Basel, Switzerland) · 2026Review
- Dystrophins DP71 and DP427 determine cell viability during proliferation and myofibre differentiation.Cell death & disease · 2026Article
- The molecular mechanism underlying the differential subcellular distribution of dystrophin Dp71 isoforms.Cell & bioscience · 2026Article
- Spatiotemporal analysis of dystrophin expression during muscle repair.Skeletal muscle · 2025Article
- Expression of Dystrophin Dp71 Splice Variants Is Temporally Regulated During Rodent Brain Development.Molecular neurobiology · 2024Article
- Dystrophin- and Utrophin-Based Therapeutic Approaches for Treatment of Duchenne Muscular Dystrophy: A Comparative Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024Review
- A novel splice variant of the human MSTN gene encodes a myostatin-specific myostatin inhibitor.Journal of cachexia, sarcopenia and muscle · 2023Article
- CRISPR-Cas9 correction in the DMD mouse model is accompanied by upregulation of Dp71f protein.Molecular therapy. Methods & clinical development · 2023Article
- Duchenne Muscular Dystrophy from Brain to Muscle: The Role of Brain Dystrophin Isoforms in Motor Functions.Journal of clinical medicine · 2023Article
- When SizeBiomedicines · 2023Article
- Development and Validation of a Western Blot Method to Quantify Mini-Dystrophin in Human Skeletal Muscle Biopsies.The AAPS journal · 2022Article
- Article
- Different responses of skeletal muscles to femoral artery ligation-induced ischemia identified in BABL/c and C57BL/6 mice.Frontiers in physiology · 2022Article
- The skeletal muscle phenotype of the DE50-MD dog model of Duchenne muscular dystrophy.Wellcome open research · 2022Article
- Human Dystrophin Dp71ab Enhances the Proliferation of Myoblasts Across Species But Not Human Nonmyoblast Cells.Frontiers in cell and developmental biology · 2022Article
- Dystrophin Dp71 Subisoforms Localize to the Mitochondria of Human Cells.Life (Basel, Switzerland) · 2021Article
- Optogenetic modeling of human neuromuscular circuits in Duchenne muscular dystrophy with CRISPR and pharmacological corrections.Science advances · 2021Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dystrophin Dp71 is the smallest isoform of the DMD gene, mutations in which cause Duchenne muscular dystrophy (DMD). Dp71 has also been shown to have roles in various cellular processes. Stem cell-based therapy may be effective in treating DMD, but the inability to generate a sufficient number of stem cells remains a significant obstacle. Although Dp71 is comprised of many variants, Dp71 in satellite cells has not yet been studied. Here, the full-length Dp71 consisting of 18 exons from exons G1 to 79 was amplified by reverse transcription-PCR from total RNA of human satellite cells. The amplified product showed deletion of both exons 71 and 78 in all sequenced clones, indicating monoclonal expression of Dp71ab. Western blotting of the satellite cell lysate showed a band corresponding to over-expressed Dp71ab. Transfection of a plasmid expressing Dp71ab into human myoblasts significantly enhanced cell proliferation when compared to the cells transfected with the mock plasmid. However, transfection of the Dp71 expression plasmid encoding all 18 exons did not enhance myoblast proliferation. These findings indicated that Dp71ab, but not Dp71, is a molecular enhancer of myoblast proliferation and that transfection with Dp71ab may generate a high yield of stem cells for DMD treatment.
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