Purines, Pyrimidines and Nucleic Acid Metabolism
In a patient with cystic fibrosis caused by the Δ F508 mutation, the mutant cystic fibrosis transmembrane conductance regulator (CFTR) protein folds incorrectly. The patient's cells modify this abnormal protein by attaching ubiquitin molecules to it. What is the fate of this modified CFTR protein?
|A||It performs its normal function, as the ubiquitin largely corrects for the effect of the mutation.|
|B||It is secreted from the cell.|
|C||It is placed into storage vesicles.|
|D||It is degraded by the proteasome.|
Ubiquitination usually marks old, damaged, or misfolded proteins for destruction by the proteasome. There is no known cellular mechanism for repair of damaged proteins.