Fig. S1
- ID
- ZDB-FIG-170505-18
- Publication
- Di Stefano et al., 2017 - NMN Deamidase Delays Wallerian Degeneration and Rescues Axonal Defects Caused by NMNAT2 Deficiency In Vivo
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Protection of injured axons in NMN deamidase transgenic mice, related to Figure 3. (A) Western blot showing the extent of NF-H degradation in distal tibial nerve of founder 14207 and 14208 (NMNdhemi) mice 3 days after cut (relative to uncut and cut wild-type (wt) nerves). (B) Western blot showing NF-H degradation 7 days after cut in a founder 14208-derived NMNdhemi mouse (sterile offspring of founder 14208). (C) Comparison of NF-H degradation in NMNdhemi and NMNdhomo mice (founder 14209-derived line) at 2 weeks after cut. In all the blots, histone H3 was used as a loading control. (D) Light microscopy images of sciatic nerves of an NMNdhomo mouse (founder 14209-derived line) 28 days after axotomy and (E) a founder 14208-derived NMNdhemi mouse 7 days after cut. Of note, protection at 7 days in the 14208-derived NMNdhemi mouse appears stronger than that observed in line 14209-derived NMNdhemi mice (Figure 3C). This is consistent with the higher enzymatic activity detected in tissue from founder 14208 compared to line 14209. |