NUDT1 Antibody - #DF7359

Fig. 4 Dysregulated protein phosphorylation in MTH1-deficient platelets after thrombin stimulation. a MTH1fl/fl or MTH1−/− platelets were treated with thrombin (1 U/ml) for 3 min followed by quantitative phosphoproteomics assay. b Differentially expressed phosphopeptides between two groups were presented as volcano map. X-axis shows the fold change (logarithmic conversion based on 2) and Y-axis shows the P-value (logarithmic conversion based on 10). Red dots represented the differentially upregulated phosphopeptides with significance and Blue dots showed the differentially downregulated phosphopeptides with significance. KEGG pathway analysis between control and MTH1-deficient platelets under the condition of resting (MA/NA) (c) or stimulation (MB/NB) (d). e MTH1fl/fl or MTH1−/− platelets were stimulated with thrombin (1 U/ml) followed by measuring the phosphorylation level of p38 MAPK, AKT, PLCβ3 and RhoA. The data were quantified based on three independent experiments (mean ± SD, n = 3 independent isolated platelets, two-way ANOVA with Sidak multiple comparisons test). f The number of differentially expressed phosphopeptides among the four groups. g Details of the 2 differentially expressed phosphopeptides localized in the mitochondria with significance identified from the comparison of control and MTH1-deficient platelets after thrombin stimulation (n = 3 independent experiments, two-tailed unpaired Student’s t test).

Fig. 5. TSG promotes cell survival and decreases Aβ deposition. TSG treatment increases antioxidative ability in hippocampus. (A) The protein expression levels of Aβ, GSS, Peroxiredoxin 1, SOD1, SOD2 and iNOS were assessed by western blotting analysis. The levels were normalized to β-actin. (B) 8-OHdG, NeuN and DAPI fluorescence staining co-localization of WT, APP/PS1 and TSG 60 mg/kg group. P # < 0.05, P ## < 0.01 vs WT group. P* < 0.05, P ** < 0.01, P *** < 0.001 vs APP/PS1 group. 2×, 100 × magnification, scare bar: 500 and 100 μ m, n = 5/group.