Abstract

The ORL1 receptors stably expressed in HEK 293 cells can utilize PTX-resistant mutants of GαoA/B to inhibit adenylyl cyclase (AC) and stimulate extracellular signal-regulated protein kinases (ERKs). However, development of AC superactivation and loss of ERK1/2 responsiveness induced by chronic activation of the ORL1 receptors remained PTXsensitive.

Keywords: Adenylyl cyclase, ERK, G proteins, ORL1 receptor, signal transduction, superactivation