Evidence map›Paper›PMID 32976891›Full record

ArticleNeuropharmacology2020

Pharmacological and phosphoproteomic approaches to roles of protein kinase C in kappa opioid receptor-mediated effects in mice.

Jeffrey J Liu, Yi-Ting Chiu, Chongguang Chen, Peng Huang, Matthias Mann, Lee-Yuan Liu-Chen

Open access · greenAbstract read
In one paragraph

Article in Neuropharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

6 citing papers in PubMed, 7 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

6 authors at 2 institutions in 2 countries.

Jeffrey J LiuDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152, Martinsried, Germany.
Yi-Ting ChiuCenter for Substance Abuse Research & Department of Pharmacology, Temple University Lewis Katz School of Medicine, Philadelphia, PA, 19140, USA.
Chongguang ChenCenter for Substance Abuse Research & Department of Pharmacology, Temple University Lewis Katz School of Medicine, Philadelphia, PA, 19140, USA.
Peng HuangCenter for Substance Abuse Research & Department of Pharmacology, Temple University Lewis Katz School of Medicine, Philadelphia, PA, 19140, USA.
Matthias MannDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152, Martinsried, Germany.
Lee-Yuan Liu-ChenCenter for Substance Abuse Research & Department of Pharmacology, Temple University Lewis Katz School of Medicine, Philadelphia, PA, 19140, USA. Electronic address: lliuche@temple.edu.
Temple University · USMax Planck Institute of Biochemistry · DE

Funding

Pilot Projects Core (PPC)P30DA013429 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI Munir Gunes Kutlu · 2000 to 2026
$34.6M
Pharmacology of Kappa Opioid ReceptorR01DA041359 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI LIU-CHEN, LEE-YUAN · 2017 to 2021
$2.9M
Kappa opioid receptor in claustrumR21DA045274 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI LIU-CHEN, LEE-YUAN · 2018 to 2019
$436k
NIDA NIH HHS P30 DA013429NIDA NIH HHS R01 DA041359NIDA NIH HHS R21 DA045274
6 · The paper itself

Abstract

Kappa opioid receptor (KOR) agonists possess adverse dysphoric and psychotomimetic effects, thus limiting their applications as non-addictive anti-pruritic and analgesic agents. Here, we showed that protein kinase C (PKC) inhibition preserved the beneficial antinociceptive and antipruritic effects of KOR agonists, but attenuated the adverse condition placed aversion (CPA), sedation, and motor incoordination in mice. Using a large-scale mass spectrometry-based phosphoproteomics of KOR-mediated signaling in the mouse brain, we observed PKC-dependent modulation of G protein-coupled receptor kinases and Wnt pathways at 5 min; stress signaling, cytoskeleton, mTOR signaling and receptor phosphorylation, including cannabinoid receptor CB1 at 30 min. We further demonstrated that inhibition of CB1 attenuated KOR-mediated CPA. Our results demonstrated the feasibility of in vivo biochemical dissection of signaling pathways that lead to side effects.

Indexed as

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerAnimalsAvoidance LearningG-Protein-Coupled Receptor KinasesMaleMiceMotor ActivityPhosphoproteinsPhosphorylationProtein Kinase CProtein Kinase InhibitorsProteomicsReceptor, Cannabinoid, CB1Receptors, G-Protein-CoupledReceptors, Opioid, kappaSignal Transduction3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerG-Protein-Coupled Receptor KinasesmTOR protein, mousePhosphoproteinsProtein Kinase CProtein Kinase InhibitorsReceptor, Cannabinoid, CB1Receptors, G-Protein-CoupledReceptors, Opioid, kappaTOR Serine-Threonine KinasesCB1mTORPhosphoproteomicsProtein kinase CWntκ opioid receptor

Identifiers

PMID32976891
PMCPMC8148297
OpenAlexW3089321665

What OpenQuestion holds

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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.