Regulation of beta 2-adrenergic receptors and the implications for bronchial asthma: an update

Cloning and characterization of the gene encoding the beta 2-adrenergic receptor (beta 2-AR) have opened new insights into the structure, function and regulation of beta 2-AR. Deoxyribonucleic acid (DNA) sequencing and site-directed mutagenesis have made it possible to localize the receptor regions, which are essential for beta 2-AR phosphorylation, sequestration, and downregulation. Furthermore, identification of specific regulatory sites within the nucleotide sequence of the beta 2-AR gene is contributing to a better understanding of the control of beta 2-AR gene transcription. All these mechanisms are involved in homologous and heterologous regulation of beta 2-AR, which accounts for the modulation of beta 2-AR synthesis and responsiveness mediated by catecholamines, steroid hormones, inflammatory mediators and other agents. Homologous and heterologous regulation of beta 2-AR, along with modulation of expression and turnover of the G proteins coupled to adenylyl cyclase, may play an important role in the pathogenesis, evolution, and management of bronchial asthma.