Deletion of Exon 51 in a Humanized Duchenne Muscular Dystrophy Mouse Model Abolishes Ventricular Arrhythmia Predisposition

Circ Genom Precis Med. 2025 Jun;18(3):e004867. doi: 10.1161/CIRCGEN.124.004867. Epub 2025 Apr 10.

Robin M Perelli¹, Madeleine J Sitton², Joel D Bohning², Adrian Pickar-Oliver², K Tyler McCullough², Mary E Moya-Mendez³, Scott Zheng³, Heather Daniels², Garth Devlin⁴, Aravind Asokan^{2

4

5

6}, Charles A Gersbach^{1

2

4

7

8

5}, Andrew P Landstrom^{1

3}

¹ Department of Cell Biology (R.M.P., C.A.G., A.P.L.), Duke University, Durham, NC.
² Department of Biomedical Engineering (M.J.S., J.D.B., A.P.-O., K.T.M.C., H.D., A.A., C.A.G.), Duke University, Durham, NC.
³ Department of Pediatrics, Division of Pediatric Cardiology (M.E.M.-M., S.Z., A.P.L.), Duke University, Durham, NC.
⁴ Department of Surgery (G.D., A.A., C.A.G.), Duke University, Durham, NC.
⁵ Center for Advanced Genomic Technologies (A.A., C.A.G.), Duke University, Durham, NC.
⁶ Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC (A.A.).
⁷ Department of Orthopedic Surgery (C.A.G.), Duke University, Durham, NC.
⁸ Duke Regeneration Center (C.A.G.), Duke University, Durham, NC.

No abstract available

Keywords: CRISPR; arrhythmias; dystrophin; gene therapy; sudden cardiac death.

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