Parruti G, Ambrosini G, Sallese M, De Blasi A
Laboratory of Receptor Physiopathology, Istituto di Ricerche Farmacologiche Mario Negri, Santa Maria Imbaro, Italy.
J Recept Res. 1993;13(1-4):609-18. doi: 10.3109/10799899309073682.
Receptor phosphorylation is a key step in the process of rapid desensitization. beta-Adrenergic receptor kinase is a specific receptor kinase that is known to phosphorylate and induce desensitization of several G-coupled synaptic receptors only when they are occupied by their agonists. We recently cloned human beta ARK cDNA and reported high levels of beta ARK expression in human peripheral blood leukocytes, also providing the first evidence for its possible functional role in these cells. Complete homologous receptor desensitization by beta ARK requires an additional cytosolic factor, called beta-arrestin. In the present study, we have cloned a 212 bp fragment of the human beta-arrestin cDNA to perform a comparative analysis of beta ARK and beta-arrestin mRNA expression in various human cell types. We found that also beta-arrestin mRNA is abundant in non-innervated tissues and cells. The fact that the entire machinery for G-coupled receptor desensitization is highly expressed in these cells further supports the idea that beta ARK may regulate nonsynaptic as well as synaptic receptors.
受体磷酸化是快速脱敏过程中的关键步骤。β-肾上腺素能受体激酶是一种特异性受体激酶，已知仅当几种G偶联突触受体被其激动剂占据时，它才会使其磷酸化并诱导脱敏。我们最近克隆了人βARK cDNA，并报道了人外周血白细胞中βARK的高表达水平，这也为其在这些细胞中可能的功能作用提供了首个证据。βARK介导的完全同源受体脱敏需要另一种胞质因子，即β-抑制蛋白。在本研究中，我们克隆了人β-抑制蛋白cDNA的一个212 bp片段，以对βARK和β-抑制蛋白mRNA在各种人类细胞类型中的表达进行比较分析。我们发现β-抑制蛋白mRNA在无神经支配的组织和细胞中也很丰富。G偶联受体脱敏的整个机制在这些细胞中高度表达，这一事实进一步支持了βARK可能调节非突触以及突触受体的观点。
