INT27529
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
As described for most of GPCRs, opioid receptor desensitization involves their phosphorylation by kinases and their uncoupling from G-proteins realized by arrestins. | |||||||||||||||
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Also, the role of G-protein coupled receptor kinases in opioid-receptor phosphorylation is discussed. | |||||||||||||||
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Here we review the current understandings of opioid-receptor phosphorylation, endocytosis and desensitization after repeated agonist treatments. | |||||||||||||||
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Disruption of Cdk5-associated phosphorylation of residue threonine-161 of the delta-opioid receptor: impaired receptor function and attenuated morphine antinociceptive tolerance. | |||||||||||||||
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Receptor trafficking induced by mu-opioid-receptor phosphorylation. | |||||||||||||||
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Mu- and delta-opioid receptor agonists inhibit DARPP-32 phosphorylation in distinct populations of striatal projection neurons. | |||||||||||||||
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Previous studies have shown that once phosphoryled, the opioid receptor binds to ? | |||||||||||||||
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Finally, highly purified recombinant betaARK1 proved active to phosphorylate enriched delta-opioid receptor preparations in an opioid agonist-dependent manner. | |||||||||||||||
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Agonist-mediated tyrosine phosphorylation of isoforms of the shc adapter protein by the delta opioid receptor. | |||||||||||||||
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Recent studies have shown that during its biosynthesis in bovine adrenal medulla, the opioid precursor proenkephalin A, may be both N-glycosylated and phosphorylated. | |||||||||||||||
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Besides, the opioid receptor desensitization involves phosphorylation of receptors and subsequent binds to beta-arrestin. | |||||||||||||||
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Withdrawal caused by an opioid receptor antagonist - naloxone - attenuated phosphorylation of ERK1/2. | |||||||||||||||
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These results represent the identification of the GRK phosphorylation site on an opioid receptor for the first time and demonstrate that GRK is the prominent kinase responsible for agonist-induced opioid receptor phosphorylation in vivo. | |||||||||||||||
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In this study, the mouse delta-opioid receptor (delta OR) was used in a model system to investigate the role of opioid receptor phosphorylation in receptor desensitization. | |||||||||||||||
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Taken together, we have demonstrated that agonist-induced opioid receptor phosphorylation occurs exclusively at two phosphate acceptor sites (T358 and S363) of GRK2 at the DOR carboxyl terminus. | |||||||||||||||
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The role of opioid receptor phosphorylation and trafficking in adaptations to persistent opioid treatment. | |||||||||||||||
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Heterologous activation of protein kinase C stimulates phosphorylation of delta-opioid receptor at serine 344, resulting in beta-arrestin- and clathrin-mediated receptor internalization. | |||||||||||||||
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These results represent the identification of the GRK phosphorylation site on an opioid receptor for the first time and demonstrate that GRK is the prominent kinase responsible for agonist-induced opioid receptor phosphorylation in vivo. | |||||||||||||||
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Our previous research suggested that agonist-induced delta-opioid receptor (DOR) phosphorylation occurs at the receptor carboxyl terminal domain. | |||||||||||||||
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Identification of G protein-coupled receptor kinase 2 phosphorylation sites responsible for agonist-stimulated delta-opioid receptor phosphorylation. | |||||||||||||||
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