Regulation of β2-adrenergic receptors and the implications for bronchial asthma: An update

Cloning and characterization of the gene encoding the β2-adrenergic receptor (β2-AR) have opened new insights into the structure, function and regulation of β2-AR. Deoxyribonucleic acid (DNA) sequencing and site-directed mutagenesis have made it possible to localize the receptor regions, which are essential for β2-AR phosphorylation, sequestration, and downregulation. Furthermore, identification of specific regulatory sites within the nucleotide sequence of the β2-AR gene is contributing to a better understanding of the control of β2-AR gene transcription. All these mechanisms are involved in homologous and heterologous regulation of β2-AR, which accounts for the modulation of β2-AR synthesis and responsiveness mediated by catecholamines, steroid hormones, inflammatory mediators and other agents. Homologous and heterologous regulation of β2-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.