ArticleMolecular pharmacology2010
Phosphorylation of the mu-opioid receptor at tyrosine 166 (Tyr3.51) in the DRY motif reduces agonist efficacy.
Article in Molecular pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Trace amine associated receptor 1: predicted effects of single nucleotide variants on structure-function in geographically diverse populations.Human genomics · 2024Article
- Repurposing EGFR Inhibitors for Oral Cancer Pain and Opioid Tolerance.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Additive Anticonvulsant Profile and Molecular Docking Analysis of 5,5'-Diphenylhydantoin Schiff Bases and Phenytoin.Biomedicines · 2023Article
- Quantitative Systems Pharmacology and Biased Agonism at Opioid Receptors: A Potential Avenue for Improved Analgesics.International journal of molecular sciences · 2022Review
- Mu-opioid receptor and receptor tyrosine kinase crosstalk: Implications in mechanisms of opioid tolerance, reduced analgesia to neuropathic pain, dependence, and reward.Frontiers in systems neuroscience · 2022Review
- Molecular mechanisms of opioid tolerance: From opioid receptors to inflammatory mediators (Review).Experimental and therapeutic medicine · 2021Review
- Relevance of Mu-Opioid Receptor Splice Variants and Plasticity of Their Signaling Sequelae to Opioid Analgesic Tolerance.Cellular and molecular neurobiology · 2021Review
- Modulation of Pathological Pain by Epidermal Growth Factor Receptor.Frontiers in pharmacology · 2021Review
- Spinal Opioid Tolerance Depends upon Platelet-Derived Growth Factor Receptor-Molecular pharmacology · 2020Article
- Regulation and Functional Implications of Opioid Receptor Splicing in Opioid Pharmacology and HIV Pathogenesis.Journal of cellular physiology · 2016Review
- STEP signaling pathway mediates psychomotor stimulation and morphine withdrawal symptoms, but not for reward, analgesia and tolerance.Experimental & molecular medicine · 2016Article
- Cellular signalling of non-synonymous single-nucleotide polymorphisms of the human μ-opioid receptor (OPRM1).British journal of pharmacology · 2015Review
- Opioid receptor desensitization: mechanisms and its link to tolerance.Frontiers in pharmacology · 2014Review
- Regulation of μ-opioid receptors: desensitization, phosphorylation, internalization, and tolerance.Pharmacological reviews · 2013Review
- Epigenetics of µ-opioid receptors: intersection with HIV-1 infection of the central nervous system.Journal of cellular physiology · 2012Review
- Identification of critical residues involved in ligand binding and G protein signaling in human somatostatin receptor subtype 2.Endocrinology · 2012Article
- Functional selectivity at the μ-opioid receptor: implications for understanding opioid analgesia and tolerance.Pharmacological reviews · 2011Review
- Molecular mechanisms of opioid receptor-dependent signaling and behavior.Anesthesiology · 2011Review
- Signaling events initiated by kappa opioid receptor activation: quantification and immunocolocalization using phospho-selective KOR, p38 MAPK, and K(IR) 3.1 antibodies.Methods in molecular biology (Clifton, N.J.) · 2011Article
- Ligand-directed c-Jun N-terminal kinase activation disrupts opioid receptor signaling.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The effects of phosphorylation of the tyrosine residue in the highly conserved DRY motif expressed in the putative second cytoplasmic loop of the mu-opioid receptor were assessed after expression in human embryonic kidney (HEK) 293 cells. Tyrosine kinase activation by epidermal growth factor (EGF) or hydrogen peroxide treatment effectively increased phosphorylation of the tyrosine-166 in the mu-opioid receptor (MOR-Tyr166p) as measured by a novel phosphoselective antibody. We were surprised to find that the increase in MOR-Tyr166p immunoreactivity (ir) required coactivation by the opioid agonist [D-Ala(2),methyl-Phe(4),Gly(5)-ol]enkephalin (DAMGO), as demonstrated by both Western blot imaging of membrane proteins and confocal microscopy of transfected cells; MOR-Tyr166p-ir did not significantly increase after either DAMGO, EGF, or H(2)O(2) treatment alone. The increase in MOR-Tyr166p-ir was blocked by pretreatment with the opioid antagonist naloxone or the Src kinase inhibitor 4-amino-5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine. Consistent with these data, mutation of the tyrosine-166 to phenylalanine blocked the increased immunoreactivity, and untransfected HEK293 cells did not increase MOR-Tyr166p-ir after treatment. DAMGO increased guanosine 5'-O-(3-[(35)S]thio)triphosphate ([(35)S]GTP gamma S) binding to membranes from cells expressing wild-type MOR or MOR-Y166F receptors in a dose-dependent manner. Pretreatment of the wild-type MOR-expressing cells with the combination of DAMGO and EGF completely blocked subsequent DAMGO stimulation of [(35)S]GTP gamma S binding membranes, whereas [(35)S]GTP gamma S binding to membranes from cells expressing mutated MOR(Y166F) was only partially inhibited. These results suggest that G-protein activation as measured by [(35)S]GTP gamma S binding can be regulated by DAMGO and EGF by convergent mechanisms and support the hypothesis that tyrosine phosphorylation within the DRY motif may reduce mu-opioid receptor-G-protein coupling efficiency.
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