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. 2016 Aug 9;44(22):10929–10945. doi: 10.1093/nar/gkw703

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© The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 5. — Splicing defect in OPMD mouse induces decreased calcium sensitivity. (A) Tnnt3 splicing defect is present in OPMD mouse model. RT-PCR analysis of endogenous Tnnt3 exons 16 and 17 isoforms in soleus (Sol) muscles of wild-type (WT) and A17.1 (OPMD) mice. (B) PABPN1 staining following KCl treatment revealed intranuclear aggregates in the soleus muscle of A17.1 mouse (red: dystrophin, green: PABPN1, blue: dapi), whereas no aggregate are observed in control mice. Aggregates are indicated with an arrow (see also inset boxes). Scale bar = 30 μm. (C) Deregulation of Tnnt3 exon 16 and 17 induces decreased calcium sensitivity in mice slow fibers, as measured by pCa/Tension relationship. * indicates P< 0.05, ** indicates P< 0.01.