The primary focus of the Port lab has been post-transcriptional regulation of beta-adrenergic receptor ( beta-AR ) genes. Responding to endogenous catecholamines, and being targets of beta-blockers for heart failure therapy, these gene products are the primary effectors of changes in heart rate and contractility. Like many highly regulated genes including proto-oncogenes and cytokines, beta-AR genes contain A+U-rich elements in their 3’-untranslated regions (3’UTRs) that make them targets of a number of RNA binding proteins that affect either their stability or translatability. Using biochemical, molecular biological, genetic, and cell biological imaging techniques, we have detailed the interactions of a number of RNA binding proteins with beta-AR mRNAs and how their binding affects beta-AR expression. More recently, we have begun to investigate the effect of microRNAs on beta-AR gene expression and the interaction of RNA binding proteins on the actions of microRNAs. It is hoped that a greater understanding of these basic mechanisms will translate into a more detailed understanding of the biology of heart failure and potentially to new therapeutic modalities.