Kai Du

TL;DR: Screening of 150,000 chemically diverse compounds and more than 1,500 analogs of active compounds yielded several classes of DeltaF508-CFTR correctors with micromolar potency that produced greater apical membrane chloride current than did low-temperature rescue.

TL;DR: Curcumin treatment may be able to correct defects associated with the homozygous expression of ΔF508 CFTR, which results in the production of a misfolded CFTR protein that is retained in the endoplasmic reticulum and targeted for degradation.

TL;DR: Using functional small-interfering RNA screens in cells expressing the common cystic fibrosis mutation F508CFTR, the authors identified a pair of chaperones that promoted clearance of defective proteins from the plasma membrane that will also need to be overcome to increase the effectiveness of strategies to overcome protein misfolding disorders.

TL;DR: It is suggested that hydrophobic side chain interactions of Phe508 are required for vectorial folding of NBD2 and the domain-domain assembly of CFTR, representing a combined co- and post-translational folding mechanism that may be used by other multidomain membrane proteins.

TL;DR: It is shown that the folding state of CFTR determines the post-endocytic trafficking of the channel and a paradigm for the quality control of plasma membrane proteins involving the coordinated function of ubiquitination and the Ub-dependent endosomal sorting machinery is suggested.