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

Monaldi Arch Chest Dis. 1994 Apr;49(2):125-30.

Abstract

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.

Publication types

  • Review

MeSH terms

  • Asthma / genetics
  • Asthma / metabolism*
  • Asthma / therapy
  • DNA, Complementary / genetics
  • GTP-Binding Proteins / biosynthesis
  • GTP-Binding Proteins / genetics
  • Gene Expression Regulation*
  • Humans
  • Molecular Structure
  • Mutagenesis
  • RNA, Messenger / genetics
  • Receptors, Adrenergic, beta-2 / biosynthesis
  • Receptors, Adrenergic, beta-2 / genetics*
  • Transcription, Genetic
  • Up-Regulation

Substances

  • DNA, Complementary
  • RNA, Messenger
  • Receptors, Adrenergic, beta-2
  • GTP-Binding Proteins