Fig. 1: Evaluation of S-nitrosylation and GSNOR expression in mouse models of neuromuscular diseases.
From: nNOS/GSNOR interaction contributes to skeletal muscle differentiation and homeostasis
Total homogenates of gastrocnemius from 2-month-old wild-type (WT), Gsnor−/− (KO), mdx mice, and mouse models of fALS expressing the G93A-SOD1 mutant, either systemically (SOD1G93A), or exclusively in the skeletal muscle (MLC-SOD1G93A) were used for: a Biotin-switch assays of S-nitrosylated proteins (PSNOs) revealed, upon biotynilation, by incubation with horseradish peroxidase (HRP)-conjugated streptavidin. b Western blot analyses of GSNOR levels. Lactate dehydrogenase (LDH) was selected as a loading control both in (a) and (b). Results shown are representative of 3 that gave similar results. (c) Densitometry of GSNOR bands shown in (B), calculated by FiJi analysis software. Values shown are the means±SD of n = 3 different experiments normalized to LDH
