Neural Plasticity / 2018 / Article / Fig 3

Research Article

Activation of Phosphotyrosine-Mediated Signaling Pathways in the Cortex and Spinal Cord of SOD1G93A, a Mouse Model of Familial Amyotrophic Lateral Sclerosis

Figure 3

Effects of G93A mutation in SOD1 mice on PTP and STEP activities. (a) PTP activity was measured in synaptosomes obtained from the cortex and spinal cord of control, SOD1WT, and SOD1G93A animals. The activity is expressed as percentage variation of control values. The bar graphs represent the means ± SEM of five independent experiments for each group. §Significantly different from SOD1WT and control (, Kruskal-Wallis followed by Dunn’s test). (b) STEP protein was immunoprecipitated by a specific polyclonal antibody from solubilized synaptosomes prepared from the cortex and spinal cord of SOD1G93A and control mice. The phosphatase activity of the STEP-immunocomplex is expressed as percentage variation of control values (100%). The bar graphs represent the means ± SEM of four independent preparations. Significantly different from control (, Mann–Whitney test). (c) Western blot analysis with an anti-STEP polyclonal antibody of solubilized synaptosomes prepared from the cortex and spinal cord of control and SOD1G93A mice. The nitrocellulose was also probed with an anti-β-actin antibody to evaluate the amount of loaded proteins (lower panel). The immunoreactive bands were detected by ECL. The results shown are representative of four independent experiments.
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