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. 2022 Mar 28;36(5):e22290. doi: 10.1096/fj.202200154R

FIGURE 1.

FIGURE 1

Loss of UNC‐45A expression increases paracellular permeability of intestinal epithelial cell monolayers. (A, B) Immunoblotting analysis of UNC‐45A and NM‐II isoform expression in HT‐29cf8 (A) and SK‐CO15 (B) human intestinal epithelial cells with CRISPR/Cas9 mediated knockout of UNC‐45A. (C, D) Transepithelial electrical resistance (TEER) of control and UNC‐45A‐depleted HT‐29cf8 (C) and SK‐CO15 (D) cell monolayers at different times post‐plating. (E, F) Transmonolayer flux of FITC‐dextran in control and UNC‐45A‐depleted IEC monolayers on day 9 (HT‐29cf8, E) and day 7 (SK‐CO15, F) post‐plating. Data are presented as means ± SE (n = 3 for HT‐29cf8 and n = 4 for SK‐CO15 cells); *p < .05, **p < .005, ***p < .0005 compared with the control sgRNA groups. (A–F) Data are representative of at least three independent experiments