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Additional molecular pathogenetic mechanisms in DM1. Results suggest an additional altered mechanism in DM1 nuclei, triggered by CUG-containing DMPK transcripts and mediated by the longer Ex5-MBNL142–43 protein isoforms: Tyr hyperphosphorylation of nuclear proteins may influence and mediate changes in gene expression and RNA processing, expanding the known mechanisms of RNA toxicity in DM1 cells
