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. 2017 Nov 28;27(3):463–474. doi: 10.1093/hmg/ddx415

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© The Author(s) 2017. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — Homozygous hFUS (+/+) transgenic mice show a loss of NMJs by the end stage of disease. (A, C) Co-localization of BTX with FUS revealed an abundance of FUS at the NMJs in P56 NTg and hFUS (+/−) transgenic mice whilst homozygous hFUS (+/+) mice, who have severe hind limb paralysis by this age, show a significant decrease in FUS and BTX co-localization (**P < 0.001) (scale bar 15 μm). (B, D) Synaptophysin (SYP) staining shows that the NMJ is retained in P56 mice from NTg and hFUS (+/−) mice but that there is a significant loss of SYP and BTX co-localization in hFUS (+/+) animals by P56 (**P < 0.001) (scale bar 15 μm). Significance was determined using a 2-way ANOVA with Holm-Sidak post hoc test.

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