Fig. 3
From: Targeting PDZ domains as potential treatment for viral infections, neurodegeneration and cancer
A Airway epithelial cells in normal conditions (red) and cystic fibrosis (light blue). Interaction of NHERF and CAL with CFTR mediated by the PDZ domains is shown. In normal condition, NHERF stabilizes CFTR to the plasma membrane, while CAL promotes the CFTR degradation in lysosomes. In cistic fibrosis the ΔF508A mutation in CFTR causes its rapid degradation mediated by CAL, with consequent absence of the CFTR at the plasma membrane. Inhibitors of the interaction of CAL with CFTR could restore the presence of CFTR at the plasma membrane. B 3D structure of the complex formed by iCAL36 10 (in orange) and PDZ CAL (in green). The box shows the hydrogen bonds between the main chain functional groups of the peptide with the β2 strand of PDZ CAL. (Figure designed through BioRender.com online tool)