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• W2095342509 abstract "Successful gene therapy for Duchenne muscular dystrophy (DMD) requires the restoration of dystrophin protein in skeletal muscles. To achieve this goal, appropriate regulatory elements that impart tissue-specific transgene expression need to be identified. Currently, most muscle-directed gene therapy studies utilize the muscle creatine kinase promoter. We have previously described a muscle enhancer element (mDME-1) derived from the mouse dystrophin gene that increases transcription from the mouse dystrophin muscle promoter. Here, we explore the use of this native mouse dystrophin muscle promoter/enhancer to drive expression of a human dystrophin minigene in transgenic mice. We show that the dystrophin promoter can provide tissue-specific transgene expression and that the mini-dystrophin protein is expressed at the sarcolemma of skeletal muscles from mdx mice, where it restores the dystrophin-associated glycoprotein complex. The level of transgene expression obtained is sufficient to protect mdx muscles from the morphological and physiological symptoms of muscular dystrophy, as well as from exercise-induced damage. Therefore, the dystrophin muscle promoter/enhancer sequence represents an alternative for use in gene therapy vectors for the treatment of DMD." @default.
• W2095342509 created "2016-06-24" @default.
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• W2095342509 date "2006-11-01" @default.
• W2095342509 modified "2023-10-11" @default.
• W2095342509 title "The Mouse Dystrophin Muscle Promoter/Enhancer Drives Expression of Mini-dystrophin in Transgenic mdx Mice and Rescues the Dystrophy in These Mice" @default.
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• W2095342509 doi "https://doi.org/10.1016/j.ymthe.2006.04.013" @default.
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