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. 2015 Dec 10;3(1):42–54. doi: 10.1002/acn3.271

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© 2015 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Oral administration (low‐dose, long‐term) of erythromycin improves splicing defects in Clcn1 and Atp2a1 in a DM1 mouse model. Analysis of Clcn1 (left) and Atp2a1 (right) alternative splicing by RT‐PCR in mice treated per oral with erythromycin (50 or 100 mg/kg for 21 days; n = 6 or more for experimental, control, and wild type). *P < 0.01. **P < 0.05. Error bars indicate SEM. DM1, myotonic dystrophy type 1; RT‐PCR, reverse transcription polymerase chain reaction; L; lactobionate, ES; ethylsuccinate.