The control of cytochrome P-450 gene expression by dioxin.

Many chemicals produce their biological effects by binding to specific 'receptor' macromolecules on or within the cell. Much current research in pharmacology and toxicology is aimed at the molecular mechanisms by which such ligand-receptor interactions elicit cellular responses. Studies of the mechanism by which TCDD (dioxin) activates CYP1A1 gene transcription demonstrate the usefulness of applying recombinant DNA and gene transfer methods to analyse these fundamental problems. In this article, James Whitlock summarizes the evidence that the Ah receptor functions as a ligand-dependent transcription factor during the induction of aryl hydrocarbon hydroxylase activity by TCDD.