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  1. Chronic and acute modulator treatment restore wild-type-like activity and stability to the primary cystic fibrosis–causing CFTR variant
  2. CFTR potentiators partially restore channel function to A561E‐CFTR, a cystic fibrosis mutant with a similar mechanism of dysfunction as F508del‐CFTR
  3. Revertant mutants modify, but do not rescue, the gating defect of the cystic fibrosis mutant G551D‐CFTR
  4. Loop diuretics are open-channel blockers of the cystic fibrosis transmembrane conductance regulator with distinct kinetics
  5. Acute inhibition of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel by thyroid hormones involves multiple mechanisms
  6. Impact of the cystic fibrosis mutation F508del-CFTR on renal cyst formation and growth