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Updated: Jul 15, 2025

Functional Reconstitution and Channel Activity Measurements of Purified Wildtype and Mutant CFTR Protein
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Small molecule correctors divert CFTR-F508del from ERAD by stabilizing sequential folding states

Celeste Riepe1, Magda Wąchalska1, Kirandeep K Deol2,3,4

  • 1Department of Biology, Stanford University, Stanford, CA, USA 94305.

Biorxiv : the Preprint Server for Biology
|September 25, 2023
PubMed
Summary

Cystic fibrosis (CF) treatments target the F508del mutation in cystic fibrosis transmembrane conductance regulator (CFTR) protein. This study identifies key molecular machinery involved in CFTR-F508del degradation, revealing how correctors improve CFTR protein levels.

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