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. 2018 Feb 5;128(3):903–905. doi: 10.1172/JCI99799

Figure 1. Schematic summarizing the effects of CLDN18 deficiency in type 2 alveolar epithelial (AT2) cells.

Figure 1

(A) Normally CLDN18 in AT2 cells is found as part of a membrane complex in epithelial apical tight junctions, bound to the tight junction (TJ) protein ZO-1, as well bound to Hippo kinases (p-LATS), and phosphorylated YAP (p-YAP). The phosphorylation of YAP by p-LATS sequesters p-YAP protein in the cytoplasm bound to CLDN18 in the apical junction protein complex. (B) In contrast, loss of CLDN18 in AT2 cells results in loss of tight junction epithelial barrier function as well as loss of p-LATS activity, allowing dephosphorylated YAP to translocate to the nucleus where it promotes proliferation.