endomorphin-2 has been researched along with Glioma* in 2 studies
2 other study(ies) available for endomorphin-2 and Glioma
Article | Year |
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Mu-opioid agonist inhibition of kappa-opioid receptor-stimulated extracellular signal-regulated kinase phosphorylation is dynamin-dependent in C6 glioma cells.
In previous studies we found that mu-opioids, acting via mu-opioid receptors, inhibit endothelin-stimulated C6 glioma cell growth. In the preceding article we show that the kappa-selective opioid agonist U69,593 acts as a mitogen with a potency similar to that of endothelin in the same astrocytic model system. Here we report that C6 cell treatment with mu-opioid agonists for 1 h results in the inhibition of kappa-opioid mitogenic signaling. The mu-selective agonist endomorphin-1 attenuates kappa-opioid-stimulated DNA synthesis, phosphoinositide turnover, and extracellular signal-regulated kinase phosphorylation. To investigate the role of receptor endocytosis in signaling, we have examined the effects of dynamin-1 and its GTPase-defective, dominant suppressor mutant (K44A) on opioid modulation of extracellular signal-regulated kinase phosphorylation in C6 cells. Overexpression of dynamin K44A in C6 cells does not affect kappa-opioid phosphorylation of extracellular signal-regulated kinase. However, it does block the inhibitory action on kappa-opioid signaling mediated by the kappa-opioid receptor. Our results are consistent with a growing body of evidence of the opposing actions of mu- and kappa-opioids and provide new insight into the role of opioid receptor trafficking in signaling. Topics: Animals; Benzeneacetamides; DNA; Dynamin I; Dynamins; Endothelins; Glioma; GTP Phosphohydrolases; Mitogen-Activated Protein Kinases; Morphine; Oligopeptides; Phosphatidylinositols; Phosphorylation; Pyrrolidines; Rats; Receptors, Opioid, kappa; Receptors, Opioid, mu; Tumor Cells, Cultured | 2000 |
Ca2+ channel inhibition by endomorphins via the cloned mu-opioid receptor expressed in NG108-15 cells.
Endomorphin-1 and -2, recently isolated endogenous peptides specific for the mu-opioid receptor, inhibited Ca2+ channel currents with EC50 of 6 and 9 nM, respectively, in NG108-15 cells transformed to express the cloned rat mu-opioid receptor. On the other hand, they elicited no response in nontransfected NG108-15 cells. It is concluded that endomorphin-1 and -2 induce Ca2+ channel inhibition by selectively activating the mu-opioid receptor. Topics: Analgesics, Opioid; Animals; Brain Neoplasms; Calcium Channel Blockers; Glioma; Neuroblastoma; Oligopeptides; Rats; Receptors, Opioid, mu; Recombinant Proteins; Tumor Cells, Cultured | 1997 |