ArticleHuman molecular genetics2009
Genetic isolation and characterization of a splicing mutant of zebrafish dystrophin.
Article in Human molecular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 76 citations in OpenAlex.
- Zebrafish as a Model Organism for Research in Rare Genetic Neuromuscular Diseases.International journal of molecular sciences · 2025Review
- Identifying kinematic biomarkers of the dystrophic phenotype in a zebrafish model of Duchenne muscular dystrophy.Skeletal muscle · 2025Article
- JAG1 overexpression partially rescues muscle function in a zebrafish model of duchenne muscular dystrophy.Journal of genetics · 2025Article
- Modeling Musculoskeletal Disorders in Zebrafish: Advancements in Muscle and Bone Research.Cells · 2024Review
- High resolution kinematic approach for quantifying impaired mobility of dystrophic zebrafish larvae.bioRxiv : the preprint server for biology · 2024Article
- Standardization of zebrafish drug testing parameters for muscle diseases.Disease models & mechanisms · 2024Article
- Modeling Human Muscular Dystrophies in Zebrafish: Mutant Lines, Transgenic Fluorescent Biosensors, and Phenotyping Assays.International journal of molecular sciences · 2023Review
- Transplantation-based screen identifies inducers of muscle progenitor cell engraftment across vertebrate species.Cell reports · 2023Article
- Development of a high-throughput tailored imaging method in zebrafish to understand and treat neuromuscular diseases.Frontiers in molecular neuroscience · 2022Article
- Animal models for researching approaches to therapy of Duchenne muscular dystrophy.Transgenic research · 2021Review
- PDE10A Inhibition Reduces the Manifestation of Pathology in DMD Zebrafish and Represses the Genetic Modifier PITPNA.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- A novel chemical-combination screen in zebrafish identifies epigenetic small molecule candidates for the treatment of Duchenne muscular dystrophy.Skeletal muscle · 2020Article
- Effect of serotonin modulation on dystrophin-deficient zebrafish.Biology open · 2020Article
- Duchenne muscular dystrophy animal models for high-throughput drug discovery and precision medicine.Expert opinion on drug discovery · 2020Review
- Zebrafish models of sarcopenia.Disease models & mechanisms · 2020Review
- Discovery of Novel Therapeutics for Muscular Dystrophies using Zebrafish Phenotypic Screens.Journal of neuromuscular diseases · 2019Review
- The psychoactive drug 25B-NBOMe recapitulates rhabdomyolysis in zebrafish larvae.Forensic toxicology · 2017Article
- Identification of novel MYO18A interaction partners required for myoblast adhesion and muscle integrity.Scientific reports · 2016Article
- Muscle dysfunction in a zebrafish model of Duchenne muscular dystrophy.Physiological genomics · 2016Article
- Dasatinib as a treatment for Duchenne muscular dystrophy.Human molecular genetics · 2016Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Sapje-like (sap(cl100)) was one of eight potential zebrafish muscle mutants isolated as part of an early-pressure screen of 500 families. This mutant shows a muscle tearing phenotype similar to sapje (dys-/-) and both mutants fail to genetically complement suggesting they have a mutation in the same gene. Protein analysis confirms a lack of dystrophin in developing sapje-like embryos. Sequence analysis of the sapje-like dystrophin mRNA shows that exon 62 is missing in the dystrophin transcript causing exon 63 to be translated out of frame terminating translation at a premature stop codon at the end of exon 63. Sequence analysis of sapje-like genomic DNA identified a mutation in the donor splice junction at the end of dystrophin exon 62. This mutation is similar to splicing mutations associated with human forms of Duchenne Muscular Dystrophy. Sapje-like is the first zebrafish dystrophin splicing mutant identified to date and represents a novel disease model which can be used in future studies to identify therapeutic compounds for treating diseases caused by splicing defects.
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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.