ArticleVision research2023
Expression of two major isoforms of MYO7A in the retina: Considerations for gene therapy of Usher syndrome type 1B.
Article in Vision research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Exploring extracellular vesicle MicroRNAs in Usher syndrome type 1B: Tear-Derived EVs as potential indicators of retinal health.Cellular and molecular life sciences : CMLS · 2026Article
- Multitarget protection by Chinese herbal medicines against sensorineural hearing loss: a focus on oxidative stress, apoptosis, and inflammation.Frontiers in medicine · 2026Review
- Deciphering the largest disease-associated transcript isoforms in the human neural retina with advanced long-read sequencing approaches.Genome research · 2025Article
- Detailed Clinical, Ophthalmic, and Genetic Characterization of MYO7A-Associated Usher Syndrome.Investigative ophthalmology & visual science · 2025Article
- Usher Syndrome: New Insights into Classification, Genotype-Phenotype Correlation, and Management.Genes · 2025Review
- The Role of Visual Electrophysiology in Systemic Hereditary Syndromes.International journal of molecular sciences · 2025Review
- Current approaches for Usher syndrome disease models and developing therapies.Frontiers in cell and developmental biology · 2025Review
- Identification of Unexpected Pathomechanisms Underlying the Human Usher Syndrome.Advances in experimental medicine and biology · 2025Review
- Gene therapy and therapeutic editing with outer or inner retina animal models.Vision research · 2023Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Usher syndrome type 1B (USH1B) is a deaf-blindness disorder, caused by mutations in the MYO7A gene, which encodes the heavy chain of an unconventional actin-based motor protein. Here, we examined the two retinal isoforms of MYO7A, IF1 and IF2. We compared 3D models of the two isoforms and noted that the 38-amino acid region that is present in IF1 but absent from IF2 affects the C lobe of the FERM1 domain and the opening of a cleft in this potentially important protein binding domain. Expression of each of the two isoforms of human MYO7A and pig and mouse Myo7a was detected in the RPE and neural retina. Quantification by qPCR showed that the expression of IF2 was typically ∼ 7-fold greater than that of IF1. We discuss the implications of these findings for any USH1B gene therapy strategy. Given the current incomplete knowledge of the functions of each isoform, both isoforms should be considered for targeting both the RPE and the neural retina in gene augmentation therapies.
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Registered trials
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