Skip to main content
. 2021 Feb 15;131(4):e135296. doi: 10.1172/JCI135296

Figure 8. Sema3G deficiency increases the instability of β-catenin.

Figure 8

(A and B) GO terms and KEGG pathway analysis of the differentially expressed genes between control and Sema3G-silenced HRMECs. (C) Schematic of the Cas9-sgRNA–targeting sites in the human Sema3G gene. The gray shaded region labels the sgRNA-targeting sequences. (D) β-catenin (green), VE-cadherin (red), phalloidin (magenta), and DAPI (blue) staining of control and Sema3G knockout (Sema3G-KO) HRMECs with or without lentivirus-mediated β-catenin overexpression (β-catenin OE). (E) Fluorescence signal intensities of β-catenin staining quantified from D (n = 5 independent experiments). (F–J) Immunoblot analysis and quantification of β-catenin and VE-cadherin protein levels in control and Sema3G-KO HRMECs with or without lentivirus-mediated β-catenin OE (n = 4 independent experiments). Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; 1-way ANOVA with Tukey’s multiple comparisons test. Scale bars: 50 μm (D); magnified images: 10 μm (D). PAM, protospacer adjacent motif; p-β-catenin, phosphorylated β-catenin.