Evidence map›Paper›PMID 23197645›Full record

ArticleMolecular pharmacology2013

Modulation of μ-opioid receptor signaling by RGS19 in SH-SY5Y cells.

Qin Wang, John R Traynor

Open access · bronzeAbstract read
In one paragraph

Article in Molecular pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Qin WangDepartment of Pharmacology, University of Michigan, Ann Arbor, MI 48109-5632, USA.
John R Traynor
University of Michigan–Ann Arbor · US

Funding

OPIOID RECEPTOR MECHANISMSR01DA004087 · NIDA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TRAYNOR, JOHN R. · 1987 to 2010
$2.5M
RGS modulation of 5HT1A receptor signaling in depressionR21MH097012 · NIMH · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TRAYNOR, JOHN R. · 2012 to 2013
$418k
Cellular Mechanisms in Animal Models of DepressionR01MH083754 · NIMH · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TRAYNOR, JOHN R. · 2011 to 2011
$386k
NIDA NIH HHS DA04087NIDA NIH HHS R01 DA004087NIMH NIH HHS MH083754NIMH NIH HHS R01 MH083754NIMH NIH HHS R21 MH097012
6 · The paper itself

Abstract

Regulator of G-protein signaling protein 19 (RGS19), also known as Gα-interacting protein (GAIP), acts as a GTPase accelerating protein for Gαz as well as Gαi/o subunits. Interactions with GAIP-interacting protein N-terminus and GAIP-interacting protein C-terminus (GIPC) link RGS19 to a variety of intracellular proteins. Here we show that RGS19 is abundantly expressed in human neuroblastoma SH-SY5Y cells that also express µ- and δ- opioid receptors (MORs and DORs, respectively) and nociceptin receptors (NOPRs). Lentiviral delivery of short hairpin RNA specifically targeted to RGS19 reduced RGS19 protein levels by 69%, with a similar reduction in GIPC. In RGS19-depleted cells, there was an increase in the ability of MOR (morphine) but not of DOR [(4-[(R)-[(2S,5R)-4-allyl-2,5-dimethylpiperazin-1-yl](3-methoxyphenyl)methyl]-N,N-diethylbenzamide (SNC80)] or NOPR (nociceptin) agonists to inhibit forskolin-stimulated adenylyl cyclase and increase mitogen-activated protein kinase (MAPK) activity. Overnight treatment with either MOR [D-Ala, N-Me-Phe, Gly-ol(5)-enkephalin (DAMGO) or morphine] or DOR (D-Pen(5)-enkephalin or SNC80) agonists increased RGS19 and GIPC protein levels in a time- and concentration-dependent manner. The MOR-induced increase in RGS19 protein was prevented by pretreatment with pertussis toxin or the opioid antagonist naloxone. Protein kinase C (PKC) activation alone increased the level of RGS19 and inhibitors of PKC 5,6,7,13-tetrahydro-13-methyl-5-oxo-12H-indolo[2,3-a]pyrrolo[3,4-c]carbazole-12-propanenitrile and mitogen-activated protein kinase kinase 1 2-(2-amino-3-methoxyphenyl)-4H-chromen-4-one, but not protein kinase A (H89), completely blocked DAMGO-induced RGS19 protein accumulation. The findings show that RGS19 and GIPC are jointly regulated, that RGS19 is a GTPase accelerating protein for MOR with selectivity over DOR and NOPR, and that chronic MOR or DOR agonist treatment increases RGS19 levels by a PKC and the MAPK pathway-dependent mechanism.

Indexed as

Adaptor Proteins, Signal TransducingAdenylyl CyclasesAnimalsBenzamidesColforsinEnkephalin, Ala(2)-MePhe(4)-Gly(5)-HEK293 CellsHumansMitogen-Activated Protein KinasesMorphineNociceptinNociceptin ReceptorOpioid PeptidesPC12 CellsPiperazinesProtein Kinase C4-(alpha-(4-allyl-2,5-dimethyl-1-piperazinyl)-3-methoxybenzyl)-N,N-diethylbenzamideAdaptor Proteins, Signal TransducingAdenylyl CyclasesBenzamidesColforsinEnkephalin, Ala(2)-MePhe(4)-Gly(5)-GIPC1 protein, humanMitogen-Activated Protein KinasesMorphineNociceptinNociceptin ReceptorOpioid PeptidesPiperazinesProtein Kinase CReceptors, OpioidReceptors, Opioid, deltaReceptors, Opioid, muregulator of G-protein signalling 19RGS Proteins

Identifiers

PMID23197645
PMCPMC3558815
OpenAlexW2106859021

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.