Evidence map›Paper›PMID 19959593›Full record

ArticleMolecular pharmacology2010

Phosphorylation of the mu-opioid receptor at tyrosine 166 (Tyr3.51) in the DRY motif reduces agonist efficacy.

Cecilea C Clayton, Michael R Bruchas, Michael L Lee, Charles Chavkin

Abstract readComparative Study
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 35 citations in OpenAlex.

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  20. 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 · 2010
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Cecilea C ClaytonDepartment of Pharmacology, University of Washington School of Medicine, Seattle, WA 98195-7280, USA.
Michael R Bruchas
Michael L Lee
Charles Chavkin
University of Washington · US

Funding

Regulation of Opioid Signaling by Tyr-PhosphorylationR37DA011672 · NIDA · UNIVERSITY OF WASHINGTON · PI CHAVKIN, CHARLES · 2004 to 2013
$2.5M
Dynorphins and Kappa Opioid Receptors in the Stress ResponseK05DA020570 · NIDA · UNIVERSITY OF WASHINGTON · PI CHAVKIN, CHARLES · 2006 to 2015
$1.2M
MODELS OF OPIOID RECEPTOR DESENSITIZATION MECHANISMSR01DA011672 · NIDA · UNIVERSITY OF WASHINGTON · PI CHAVKIN, CHARLES · 1999 to 2003
$902k
NIDA NIH HHS DA11672NIDA NIH HHS K05 DA020570NIDA NIH HHS R01 DA011672NIDA NIH HHS R37 DA011672
6 · The paper itself

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.

Indexed as

Amino Acid MotifsAmino Acid SequenceAnalgesics, OpioidAnimalsCell LineEnkephalin, Ala(2)-MePhe(4)-Gly(5)-HumansMiceMolecular Sequence DataMutationPhosphorylationReceptors, Opioid, muTyrosineAnalgesics, OpioidEnkephalin, Ala(2)-MePhe(4)-Gly(5)-Receptors, Opioid, muTyrosine

Identifiers

PMID19959593
PMCPMC2835424
OpenAlexW2170110211

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.