DUSP1/MKP1 Antibody - #AF5286

Figure 8 Construction of risk model and functional validation of critical genes. (A) Differential analysis between clust1 and no_clust1 in TCGA dataset; (B) Differential analysis between clust2 and no_clust2 in TCGA dataset; (C) Differential analysis between clust3 and no_clust3 in TCGA dataset; (D) A total of 961 promising candidates were identified among the differentially expressed genes; (E) Trajectory of each independent variable as lambda changes; (F) Confidence interval under lambda; (G) Coefficients of prognostic-related genes obtained from multivariate Cox analysis; (H) Western blot assay of DUSP1 protein expression in 786-O cell after transfection of Si-DUSP1; (I) Colony formation assay was carried out to evaluate the proliferation of 786-O cell; (J, K) Transwell assay was used to assess the migration and invasion of 786-O cell. (L) Western blot assay of p21 and p53 protein expression in 786-O cell after transfection of Si-DUSP1. *, p< 0.05; (M) SA-β-gal staining of 786-O cell. *, p< 0.05.

FIGURE 3 MKP‐1 expression lowered in Alzheimer's disease (AD) model mice and AD model cells. (A) Immunofluorescence staining was performed in the brain of wild‐type (WT), AD mice. Iba1 (red) for microglia, green for MKP‐1, and 4′,6‐diamidino‐2‐phenylindole (DAPI) (blue) for nuclei. Scale bar: 50 μm. (B, C) Testing MKP‐1 positive area (%) and MKP‐1+ Iba1+/Iba1+ ratio in WT and AD mice. (D–F) Immunoblotting examined MKP‐1 and amyloid precursor protein (APP) protein levels in the brains of WT and AD mice. (G, H) Western blot analyses of BV2 microglia cell lines treated with amyloid‐β (Aβ) in a gradient level of 0, 2.5, 5, 10, and 20 μM. The results are displayed as the mean values ± SEM, n = 4 per group.

FIGURE 3 MKP‐1 expression lowered in Alzheimer's disease (AD) model mice and AD model cells. (A) Immunofluorescence staining was performed in the brain of wild‐type (WT), AD mice. Iba1 (red) for microglia, green for MKP‐1, and 4′,6‐diamidino‐2‐phenylindole (DAPI) (blue) for nuclei. Scale bar: 50 μm. (B, C) Testing MKP‐1 positive area (%) and MKP‐1+ Iba1+/Iba1+ ratio in WT and AD mice. (D–F) Immunoblotting examined MKP‐1 and amyloid precursor protein (APP) protein levels in the brains of WT and AD mice. (G, H) Western blot analyses of BV2 microglia cell lines treated with amyloid‐β (Aβ) in a gradient level of 0, 2.5, 5, 10, and 20 μM. The results are displayed as the mean values ± SEM, n = 4 per group.

Fig. 5 RA upregulates retinal expression of MKP-1 and inhibits JNK phosphorylation induced by light exposure. a, d Western blots of p-NF- κB/NF-κB, p-JNK/JNK and MKP-1 expression levels in the control and RA-treated groups unexposed to light and at 3 days and 7 days after light exposure. b, c, e Quantitative analysis of western blotting of the phosphorylation levels of NF-κB (b), JNK (c), and MKP-1 (e). Oneway ANOVA analysis followed by Dunnett’s test was used. n = 3 per group, *P < 0.05 and **P < 0.01. LI, light injury; RA, all-trans retinoic acid; JNK, c-Jun N-terminal kinase; NF-κB, nuclear factor-κB; MKP-1, mitogen-activated protein kinase phosphatase-1

Figure 3: |MKP-1 immunofluorescence staining of cochlear spiral ganglion of pigs in the AP group. MKP-1 stained in the spiral ganglion cell (white arrows). Blue: nuclei stained with DAPI;green: MKP-1 stained in inner hair cell (IHC) and outer hair cell (OHC). Scale bars = 10 μm. The red marker is the stereocilia of hair cells, and the blue marker is the cell nucleus.

Figure 6:| The protein expression of (a) MKP-1 and GR, (b) p38 and p-p38, and (c) NF-κB and p-NF-κB p65 was determined by western blot analysis. Bar graphs show the quantification of the indicated proteins. Data are shown as means ± SD from at least three independent experiments, #p < 0 05 vs. AP group; ##p < 0 01 vs. AP group; ∗p < 0 05 vs. LPS+DEX group; ∗∗p < 0 01 vs. LPS+DEX group.