[Recent detailed studies of the biochemical properties of the mutant CYP17 enzymes from patients with isolated 17,20-lyase deficiency demonstrate that alterations in the interaction of CYP17 with its redox partner proteins P450-oxidoreductase and cytochrome b5 form the biochemical basis for these selective enzyme defects.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
Gene-disease associations inferred from text-mining the literature.
DisGeNET evidence - LITERATURE