ArticleMolecular genetics & genomic medicine2021
CRISPR/Cas9 in zebrafish: An attractive model for FBN1 genetic defects in humans.
Article in Molecular genetics & genomic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Advances in Fish Gene Editing.Animals : an open access journal from MDPI · 2026Review
- Systematic Disruption of Zebrafish Fibrillin Genes Identifies a Translational Zebrafish Model for Marfan Syndrome.JACC. Basic to translational science · 2026Article
- Identification and functional validation of a novel FBN1 variant in a Marfan syndrome family using a zebrafish model.BMC genomics · 2025Article
- Therapeutic Opportunities of Marfan Syndrome: Current Perspectives.Drug design, development and therapy · 2025Review
- Review
- Navigating toward gene therapy in Marfan syndrome: A hope for halting aortic aneurysm.Molecular therapy. Methods & clinical development · 2024Article
- Genetic models of fibrillinopathies.Genetics · 2024Review
- Human stem cell models for Marfan syndrome: aFrontiers in cell and developmental biology · 2024Review
- Marfan syndrome: insights from animal models.Frontiers in genetics · 2024Review
- Zebrafish as a Model to Study Vascular Elastic Fibers and Associated Pathologies.International journal of molecular sciences · 2022Review
- Zebrafish Is a Powerful Tool for Precision Medicine Approaches to Neurological Disorders.Frontiers in molecular neuroscience · 2022Review
- CRISPR/Cas9 in zebrafish: An attractive model for FBN1 genetic defects in humans.Molecular genetics & genomic medicine · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMutations in the fibrillin-1 gene (FBN1) are associated with various heritable connective tissue disorders (HCTD). The most studied HCTD is Marfan syndrome. Ninety percent of Marfan syndrome is caused by mutations in the FBN1 gene. The zebrafish share high genetic similarity to humans, representing an ideal model for genetic research of human diseases. This study aimed to generate and characterize fbn1
methodsCRISPR/Cas9 was applied to generate an fbn1 frameshift mutation (fbn1
resultsWe successfully generated a transgenic line of fbn1
conclusionWe generated the first fbn1
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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 Socratic graph.