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. 2017 Aug 15;7:8296. doi: 10.1038/s41598-017-08373-4

Figure 4.

Figure 4

Loss of KRIT1 promotes NF-κB signaling. (A) NF-κB p65 expression in lysates of KRIT1 null (KO) and reconstituted (9/6) MEFs. Tubulin is shown as loading control. Representative blots were cropped for space considerations, n = 5. (B) Densitometry analysis of (A). Expression of NF-κB normalized to loading control tubulin, *p < 0.05 by two-tailed t-test. (C) NF-κB reporter activity in negative control (NC) and anti-KRIT1 siRNA transfected HPAEC treated with 10 µM VAS2870, 100 µM YAv1, 25 ng/ml TNF-α, or both YAv1 and TNF-α. KRIT1 (rescue) = cells transfected with KRIT1 siRNA and a rescue plasmid containing a silent mutation of the siRNA target sequence. Data shown are normalized to vehicle-treated siNC. p < 0.0001 by ANOVA; using Tukey’s post-hoc test *p < 0.05 vs. siNC vehicle, **p < 0.05 vs. siKRIT1 vehicle, #p < 0.05 vs. TNF-α treatment, n.s.- not significant, n = 5.