E. Frair
Biochemistry, Genetics and Molecular Biology · The Ohio State University
Publications
38
Citations
336
Est. group size
~7
Recurring co-author estimate
Active years
11
Publishing since 2016
E. Frair's research focuses on Duchenne muscular dystrophy (DMD), a genetic muscle-wasting disease, with an emphasis on developing and testing gene therapy approaches such as exon skipping, CRISPR/Cas9 gene editing, and AAV-based gene delivery to restore dystrophin protein production. Work spans mouse models, patient-derived cell lines, and early-phase clinical trials, alongside detailed characterization of DMD gene mutations and their molecular consequences.
Publication output grew from essentially none in 2017-2018 to a peak of 8 in 2021, with continued steady activity averaging under 5 papers per year over the last five years.
Generated by claude-sonnet-5 from public bibliographic data · Jul 20, 2026
- Generation of an induced pluripotent stem cell line (NCHi026-A) from a patient with a partial deletion of exon 55 in the DMD gene
Stem Cell Research · 2026
- U7snRNA-mediated skipping of intron-derived pseudoexons restores full-length DMD expression in patient-derived cell lines
Molecular Therapy Advances · 2026
- Correction of Duchenne Muscular Dystrophy Mutations by CRISPR/Cas9 Gene Editing Using Homology-Independent Targeted Integration (P7-6.006)
Neurology · 2025
- Preparation, Sectioning, and Histochemical Staining of Muscle Tissue
Methods in molecular biology · 2025
- 283PGenomic rearrangements in Duchenne muscular dystrophy diagnosed by RNA and long-read genome sequencing
Neuromuscular Disorders · 2025
- 294PNovel dystrophic mouse models with duplication and/or large deletion mutations: an invaluable tool for targeted exon skipping and dystrophin restoration in DMD patients
Neuromuscular Disorders · 2025
- 277PDefining the relationship between DMD mutation type and location within the exons 1-5 window to IRES activity
Neuromuscular Disorders · 2025
- 264PCharacterization of dystrophin expression in muscle biopsies from patients with in-frame deletions in the DMD gene
Neuromuscular Disorders · 2025
- Increase in Full-Length Dystrophin by Exon Skipping in Duchenne Muscular Dystrophy Patients with Single Exon Duplications: An Open-label Study
Journal of Neuromuscular Diseases · 2024
- 679P Clinical and molecular characterization of DMD pseudo-3’-terminal exons
Neuromuscular Disorders · 2024
- 684P Complex duplications containing terminal exon duplications in the DMD gene
Neuromuscular Disorders · 2024
- CRISPR-Cas9 homology-independent targeted integration of exons 1–19 restores full-length dystrophin in mice
Molecular Therapy — Methods & Clinical Development · 2023
- Persistence of exon 2 skipping and dystrophin expression at 18 months after U7snRNA-mediated therapy in the Dup2 mouse model
Molecular Therapy — Methods & Clinical Development · 2023
- P13 Comparison of U7snRNA-induced dystrophin expression following systemic delivery with AAV9, MyoAAV 2A, and MyoAAV 3A capsids in the Dup2 mouse
Neuromuscular Disorders · 2023
- P12 Comparison of U7snRNA-induced dystrophin expression following systemic delivery with AAV9 and AAVrh74 capsids
Neuromuscular Disorders · 2023
- Neuromuscular Disorders×21
- Molecular Therapy — Methods & Clinical Development×4
- Human Gene Therapy×2
- Journal of Visualized Experiments×2
- Oncogene×1
- Tatyana A. Vetter
Biochemistry, Genetics and Molecular Biology · The Ohio State University
- Scott Q. Harper
Biochemistry, Genetics and Molecular Biology · The Ohio State University
- K. Flanigan
Biochemistry, Genetics and Molecular Biology · The Ohio State University
- Liubov V. Gushchina
Biochemistry, Genetics and Molecular Biology · The Ohio State University
- Nicolas Wein
Biochemistry, Genetics and Molecular Biology · The Ohio State University
This profile was generated automatically from public scholarly data (OpenAlex). Group size and activity levels are estimates derived from co-authorship patterns.
Last updated Jul 19, 2026.
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