ArticleBMC research notes2011
Myoblasts generated by lentiviral mediated MyoD transduction of myotonic dystrophy type 1 (DM1) fibroblasts can be used for assays of therapeutic molecules.
Article in BMC research notes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Generation of neural cells from DM1 induced pluripotent stem cells as cellular model for the study of central nervous system neuropathogenesis.Cellular reprogramming · 2013Trial
- Repeat length as a key determinant for disease severity and antisense oligonucleotide activity in myotonic dystrophy type 1.Molecular therapy. Methods & clinical development · 2025Article
- Characterization ofNAR molecular medicine · 2025Article
- Efficacy of Cystic Fibrosis Transmembrane Regulator Corrector C17 in Beta-Sarcoglycanopathy-Assessment of Patient's Primary Myotubes.International journal of molecular sciences · 2024Article
- Pluripotent Stem Cells in Disease Modeling and Drug Discovery for Myotonic Dystrophy Type 1.Cells · 2023Review
- Promising AAV.U7snRNAs vectors targetingFrontiers in cell and developmental biology · 2023Article
- Loss of the Nuclear Envelope Protein LAP1B Disrupts the Myogenic Differentiation of Patient-Derived Fibroblasts.International journal of molecular sciences · 2022Article
- Recent Progress and Challenges in the Development of Antisense Therapies for Myotonic Dystrophy Type 1.International journal of molecular sciences · 2022Review
- Brain Pathogenesis and Potential Therapeutic Strategies in Myotonic Dystrophy Type 1.Frontiers in aging neuroscience · 2021Review
- Intrinsic Myogenic Potential of Skeletal Muscle-Derived Pericytes from Patients with Myotonic Dystrophy Type 1.Molecular therapy. Methods & clinical development · 2019Article
- Recovery in the Myogenic Program of Congenital Myotonic Dystrophy Myoblasts after Excision of the Expanded (CTG)International journal of molecular sciences · 2019Article
- Distinct pathological signatures in human cellular models of myotonic dystrophy subtypes.JCI insight · 2019Article
- Cells of Matter-Frontiers in neurology · 2018Review
- CRISPR/Cas9-Mediated Deletion of CTG Expansions Recovers Normal Phenotype in Myogenic Cells Derived from Myotonic Dystrophy 1 Patients.Molecular therapy. Nucleic acids · 2017Article
- Immortalized human myotonic dystrophy muscle cell lines to assess therapeutic compounds.Disease models & mechanisms · 2017Article
- Reduction of Huntington's Disease RNA Foci by CAG Repeat-Targeting Reagents.Frontiers in cellular neuroscience · 2017Article
- Mutations in DNMT3B Modify Epigenetic Repression of the D4Z4 Repeat and the Penetrance of Facioscapulohumeral Dystrophy.American journal of human genetics · 2016Article
- A low absolute number of expanded transcripts is involved in myotonic dystrophy type 1 manifestation in muscle.Human molecular genetics · 2016Article
- Molecular mechanisms in DM1 - a focus on foci.Nucleic acids research · 2015Review
- DDX6 regulates sequestered nuclear CUG-expanded DMPK-mRNA in dystrophia myotonica type 1.Nucleic acids research · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyotonic dystrophy type 1 (DM1) is the most common muscle dystrophy in adults. The disease is caused by a triplet expansion in the 3'end of the myotonic dystrophy protein kinase (DMPK) gene. In order to develop a human cell model for investigation of possible effects of antisense and RNAi effector molecules we have used lentiviral mediated myoD-forced myogenesis of DM1 patient fibroblasts.
findingsTransduced fibroblasts show a multinuclear phenotype and express the differentiation marker myogenin. Furthermore, fluorescence in situ hybridization (FISH) analysis revealed a statistical significant increase in the amount of nuclear foci in DM1 patient fibroblasts after myogenesis. Finally, no nuclear foci were found after treatment with oligonucleotides targeting the repeat expansions.
conclusionsThe abundance of nuclear foci in DM1 patient fibroblasts increase following myogenesis, as visualized by FISH analysis. Foci were eradicated after treatment with antisense oligonucleotides. Thus, we propose that the current cell model is suitable for testing of novel treatment modalities.
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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.