Fig 1: Reduced Rac2 and Arhgdib in lesions following Taodan granule (TDG) treatment. (A) Representative images of Rac2 cytoplasm staining (brown) of back lesions from each group (200×). Scale bar = 100 μm. (B) The expression of Arhgdib protein in lesions determined by ELISA. (C) Western blotting of Rac2 and Arhgdib protein in back lesions on day 12. The data are expressed as mean ± SD. Four skin lesions in each group were included for analysis. # p < 0.05, ## p < 0.01, ### p < 0.001, compared with the control group. *p < 0.05, **p < 0.01, ***p < 0.001, compared with the imiquimod (IMQ) group.
Fig 2: Reduced DNA synthesis by Rac2−/− and Rac1BRac2−/− B cells. DNA synthesis was measured by [3H]thymidine uptake of spleen B cells, cultured for 2, 3, and 4 days. Mice were sacrificed 3 days after the last tamoxifen-injection. [3H]thymidine was added for the final 17 h. The values represent the mean of triplicates and bars represent SD. The experiment was repeated at least once with similar results. BG, background. Statistical analysis was done using two-way ANOVA with Tukey’s test for multiple comparisons that includes all time points. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Fig 3: The biological functions of APOBEC3D, TNFRSF14, and RAC2 in BC cells. (a-c) PCR results showed that the model gene expression was lower in MCF-7 and MDA-MB-231 cells. (d-f) Western blotting experiments showed that the APOBEC3D, TNFRSF14, and RAC2 protein expression were weaker in MCF-7 cells. Results of colony formation (g-i) and EdU (j-l) assays revealed that overexpression of APOBEC3D, TNFRSF14, and RAC2 greatly suppressed MCF-7 cell proliferation.
Fig 4: Rac1BRac2−/− mice fail to respond to TNP-conjugated lipopolysaccharide (TNP-LPS). IgM, IgG2b, and IgG3 response to TNP-LPS immunization. Mice were immunized 4 days after the last tamoxifen-injection and bled once a week between day 0 and day 21. Day 0, n = 2 mice per group; day 7, n = 5 mice per group, except nRac2+/− = 6; day 14, n = 5 mice per group, except nWT = 3; day 21, n = 5 mice per group, except nRac2+/− = 3. Statistical analysis done using two-way ANOVA with Sidak’s and Tukey’s tests for multiple comparisons combining all time points. **p < 0.01, ***p < 0.001, ****p < 0.0001. Statistical comparison for IgM: **Rac1B vs WT, ***Rac2+/− vs WT, ***Rac2−/− vs WT, ****Rac1BRac2−/− vs WT. Statistical comparison for IgG2b and IgG3: ***Rac1BRac2−/− vs WT.
Fig 5: The two clusters for prognostic prediction in BC. (a). C1 had the poorest prognosis, whereas C2 had the best prognosis. (b). A total of 1190 DESs were found to be shared by the two groups. (c). APOBEC3D, TNFRSF14, and RAC2 were all found to be risk variables in a forest plot of HRs. (Both d and f). The model was built by Lasso regression.
Supplier Page from Abcam for Anti-RAC2 antibody