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. 2021 Feb 11;8(1):ENEURO.0358-20.2020. doi: 10.1523/ENEURO.0358-20.2020

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Copyright © 2021 Chang et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 3. — Exogenous Sox11^K91A leads to more RGC death than Sox11 in vivo. Control AAV2-GFP-Ctrl, AAV2-Sox11, or AAV2-Sox11^K91A were injected intravitreally in control eyes and in eyes two weeks before optic nerve crush. Two weeks after injection in controls, or two weeks after optic nerve crush (four weeks after injection), eyes were harvested and retinas flat-mounted and immunostained against RGC-specific marker RBPMS (A). Both Sox11 and Sox11^K91A significantly increased RGC death in sham (B) and optic nerve crush (C) eyes, with Sox11^K91A showing significantly greater effect than wild-type Sox11 (N ≥ 4 experimental replicates, *p < 0.05, **p < 0.01, ***p < 0.001, by one-way ANOVA with post hoc t test with Tukey correction; mean ± SEM shown; scale bar: 100 μm).