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Primary antibodies against the following proteins were used: anti-phospho GSK-3�� (Ser9) (pGSK-3��, 1:1000), anti-GSK-3�� (1:1000), and anti-��-actin (1:1000). The membranes were then incubated with horseradish peroxidase-conjugated anti-rabbit antibody (1:1000). The chemioluminescence (ECL) was detected using X-ray films (Kodak X-Omat). Films were scanned and the percentage of band intensity was analyzed using Optiquant software (Packard Instrument). For each experiment, the test groups (treated with GM1, fibrillar A��25�C35, or simultaneously treated with both GM1 and fibrillar A��25�C35), were compared to control cultures (exposed neither to A��25�C35 nor to GM1), which were considered 100%, thus assuring the same signal intensity for control and test groups. Data are expressed as percentage of phosphorylated protein for selleck screening library GSK3��, which was obtained by the ratio of the phospho-protein (pGSK-3��) with its whole amount (GSK-3��) (Frozza et al., 2009). Protein contents were measured by the method of Peterson (1977). In order to normalize the value of protein, we detected ��-actin in the same analysis. Data are expressed as mean?��?S.D. One-way or two-way analysis of variance (ANOVA) was applied to the means to determine statistical differences HDAC phosphorylation between experimental groups. Post hoc comparisons were performed using the Tukey test for multiple comparisons. Differences between mean values were considered significant when p?3-mercaptopyruvate sulfurtransferase as observed in Fig. 1A. The quantification of PI incorporation is shown in Fig. 1B. We did not observe any increase in fluorescence in hippocampal slices exposed to the reverse sequence of peptides (A��35�C25) at 25?��M (data not shown). Although neither the fibrillar nor the non-fibrillar ��-amyloid forms were able to cause any change to total radiolabeling (Fig. 2A), chromatographic and densitometric analysis revealed that they exerted distinct effects on the profile and distribution of expressed gangliosides. While non-fibrillar A�� caused a significant increase in GM1 expression (p?