Down-regulation of μ-Opioid Receptor by Full but Not Partial Agonists Is Independent of G Protein Coupling

1997 ◽  
Vol 52 (5) ◽  
pp. 896-902 ◽  
Author(s):  
Nirmala Yabaluri ◽  
Fedor Medzihradsky
Keyword(s):  
G Protein ◽  
Opioid Receptor ◽  
Down Regulation ◽  
G Protein Coupling ◽  
Protein Coupling ◽  
Partial Agonists ◽  
Μ Opioid Receptor

scholarly journals Selective Interference of β-Arrestin 1 with κ and δ but Not μ Opioid Receptor/G Protein Coupling

1998 ◽  
Vol 273 (38) ◽  
pp. 24328-24333 ◽  
Author(s):  
Zhi-Jie Cheng ◽  
Qing-Ming Yu ◽  
Ya-Lan Wu ◽  
Lan Ma ◽  
Gang Pei
Keyword(s):  
G Protein ◽  
Opioid Receptor ◽  
G Protein Coupling ◽  
Protein Coupling ◽  
Selective Interference ◽  
Μ Opioid Receptor

G-protein coupling of δ-opioid receptors in brains of μ-opioid receptor knockout mice

2003 ◽  
Vol 466 (1-2) ◽  
pp. 91-98 ◽  
Author(s):  
Sarah M. Oakley ◽  
Geza Toth ◽  
Anna Borsodi ◽  
Brigitte L. Kieffer ◽  
Ian Kitchen
Keyword(s):  
G Protein ◽  
Opioid Receptor ◽  
Opioid Receptors ◽  
Knockout Mice ◽  
G Protein Coupling ◽  
Protein Coupling ◽  
Μ Opioid Receptor

scholarly journals Palmitoylation and membrane cholesterol stabilize μ-opioid receptor homodimerization and G protein coupling

2012 ◽  
Vol 13 (1) ◽  
Author(s):  
Hui Zheng ◽  
Elizabeth A Pearsall ◽  
Dow P Hurst ◽  
Yuhan Zhang ◽  
Ji Chu ◽  
...  
Keyword(s):  
G Protein ◽  
Opioid Receptor ◽  
Membrane Cholesterol ◽  
G Protein Coupling ◽  
Protein Coupling ◽  
Μ Opioid Receptor

scholarly journals G-protein coupling of μ-opioid receptors (OP3): elevated basal signalling activity

2000 ◽  
Vol 348 (3) ◽  
pp. 531-537 ◽  
Author(s):  
Neil T. BURFORD ◽  
Danxin WANG ◽  
Wolfgang SADÉE
Keyword(s):  
G Protein ◽  
G Proteins ◽  
Opioid Receptor ◽  
G Protein Coupling ◽  
Hek 293 ◽  
Human Embryonic Kidney Cells ◽  
Protein Coupling ◽  
Protein Levels ◽  
293 Cells ◽  
Μ Opioid Receptor

To determine μ-opioid receptor (OP3) signalling activity, guanosine 5ʹ-[γ-[35S]thio]triphosphate (GTP[35S]) binding to G-proteins was measured in the membranes of human embryonic kidney cells (HEK-293) transfected with μ-opioid receptor (HEK-μ). GTP[35S] binding to HEK-μ membranes was significantly elevated compared with HEK-293 control membranes (without OP3), and this was abolished by pertussis-toxin pretreatment. The irreversible antagonist β-chlornaltrexamine (β-CNA) dose-dependently decreased elevated basal G-protein coupling of HEK-μ to control levels in cells devoid of OP3. This characterizes β-CNA as an inverse OP3 agonist. Immunoprecipitation of solubilized G-proteins with Gi3α antisera demonstrated that basal GTP[35S] binding to Gi3α was also substantially elevated in HEK-μ membranes over the control, whereas Gi3α protein levels were unchanged. Basal GTP[35S] binding to Gi1α/Gi2α and Goα was also increased twofold in HEK-μ membranes over the control. Morphine further increased coupling to each of these Gα proteins with similar potency, but not to Gq/11α or Gsα. These results indicate that the wild-type OP3 can couple constitutively to endogenously expressed Gi3α, Gi1α/Gi2α and Goα subunits of G-proteins in HEK-293 cells.

Allelic Variation S268P of the Human μ-Opioid Receptor Affects Both Desensitization and G Protein Coupling

2000 ◽  
Vol 58 (2) ◽  
pp. 328-334 ◽  
Author(s):  
Thomas Koch ◽  
Thomas Kroslak ◽  
Marco Averbeck ◽  
Peter Mayer ◽  
Helmut Schröder ◽  
...  
Keyword(s):  
G Protein ◽  
Opioid Receptor ◽  
Allelic Variation ◽  
G Protein Coupling ◽  
Protein Coupling ◽  
Μ Opioid Receptor
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