作者: Rüdiger Schulz , Daniela A. Eisinger , Andrea Wehmeyer
DOI: 10.1016/J.EJPHAR.2004.07.010
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摘要: Activation of G protein-coupled receptors (GPCRs) may result in phosphorylation extracellular signal-regulated kinases 1/2 (ERK 1/2). The signaling pathway involves ectodomain shedding, generating epidermal growth factor (EGF)-like ligands, which turn stimulate the mitogen-activated protein kinase (MAPK) via EGF receptors. present study investigates into control MAPKs by opioidergic GPCRs human embryonic kidney cells (HEK 293). Experiments were conducted with expressing opioid receptors, receptor kinases, and ERKs. outcome our studies let us suggest that EGF-like ligands released stimulation utilize different to phosphorylate ERKs, while utilizes type 1 Differences between multiple are apparent respect activation rapidly triggers internalization fluorescent 1, but we failed observe any sequestration this upon exposure an opioid, since opioids most likely trigger a type. In conclusion, MAPK cascade similar fashion as described for non-opioid GPCRs, although distinct differences exist μ-, δ- κ-receptors. EGF-induced ERK is mediated seems brings about