Fig 1: TLN increased MBP, MPZ, and Sox10 in vivo and in vitro to ameliorate schwannopathy. (A)Western blotting of Sox10 and MBP in sciatic nerves of DPN rats and quantifications of these proteins. The results were normalized to the values of the control group, n = 6 for each group. β-actin images are reused. (B) Representative images of immunofluorescence staining on MPZ (green) and S100β (purple). Scale bar, 20 μm, and quantification of MPZ, n = 6 for each group. ΔΔ P< 0.01, Δ P< 0.05 vs. control group; ## P < 0.01, #P< 0.05 vs. model group (C–E) Representative images of immunofluorescence staining on Sox10 (green), MPZ (green), MBP (green), and nucleus (blue). Scale bar, 5 μm, and quantification of Sox10, MPZ, and MBP, n = 4 for each group. ΔΔ P< 0.01, Δ P< 0.05 vs. 25 mM glucose group; ## P < 0.01, # P< 0.05 vs. 150 mM glucose group.
Fig 2: The functional role of MPZ, SCARA3, MPP2 and PBXIP1 in CRC cells. The results indicated that the inhibition of MPZ, SCARA3, MPP2 and PBXIP1 expression inhibited the colony formation ability of SW620 cells A in vitro and B-C tumorigenicity in vivo. D IHC analysis of xenografted tumour tissues revealed that MPZ, SCARA3, MPP2 and PBXIP1 expression was low in the SW620/sh-MPZ, SW620/sh-SCARA3, SW620/sh-MPP2 and SW620/sh-PBXIP1 groups
Fig 3: The expression of the unreported model genes. The results of A-D qPCR and E–H IHC analysis showed that the expression of MPZ, SCARA3, MPP2 and PBXIP1 was high in CRC tissues
Supplier Page from Abcam for Anti-Myelin Protein Zero antibody [EPR20383]