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We identified candidate pools of epigenetic compounds that improve skeletal muscle structure in dmd mutant zebrafish.
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Results: We performed a novel chemical-combination screen of a library of epigenetic compounds using the zebrafish dmd model.
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A commercially available library of epigenetic small molecules was used to treat embryonic-larval stages of dmd mutant zebrafish.
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Methods: Eight families at risk for DMD were recruited for this study.
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DMD segment supplies newspaper and magazines to airlines and provides inflight services.
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Analysis of dystrophin now allows confirmation of the existence of this disorder.
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Recent studies suggest that the site specific anchoring depends on the dystrophin complex.
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In dogs with DMD, you can see the absence of the dystrophin protein.
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Analysis of DNA revealed a deletion in the 1st third of the dystrophin gene.
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No dystrophin gene defects were found in our patients, whose average age was 50 years.
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Dp71 has also been shown to have roles in various cellular processes.
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Western blotting of the satellite cell lysate showed a band corresponding to over-expressed Dp71ab.
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Although Dp71 is comprised of many variants, Dp71 in satellite cells has not yet been studied.
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The amplified product showed deletion of both exons 71 and 78 in all sequenced clones, indicating monoclonal expression of Dp71ab.
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Here, the full-length Dp71 consisting of 18 exons from exons G1 to 79 was amplified by reverse transcription-PCR from total RNA of human satellite cells.