Evidence map›Paper›PMID 24162663›Full record

ArticleCell death and differentiation2014

β-arrestin protects neurons by mediating endogenous opioid arrest of inflammatory microglia.

X Feng, C-Y Wu, F H Burton, H H Loh, L-N Wei

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 21% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  15. Epiisopiloturine, an Alkaloid fromOxidative medicine and cellular longevity · 2023
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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

5 authors at 1 institution in 1 country.

X FengDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
C-Y WuDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
F H BurtonDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
H H LohDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
L-N WeiDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
University of Minnesota Medical Center · US

Funding

Subcellular Targeting/Packaging of Opioids/ReceptorsP50DA011806 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LOH, HORACE · 1998 to 2012
$14.0M
Studies of nuclear receptor corepressor, NRIP1, in vitamin A signaling pathwaysR01DK060521 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 2002 to 2022
$6.9M
Structural and Functions Studies of Mu Opiate Receptors: Regulation of its GeneR01DA001583 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LOH, HORACE · 1985 to 2017
$6.5M
TR2 NUCLEAR RECEPTOR IN VITAMIN A SIGNALING PATHWAYSR01DK054733 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 1999 to 2021
$5.7M
Studies of Mouse Kappa Opioid Receptor Gene RegulationR01DA011190 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 1997 to 2011
$3.3M
STRUCTURAL AND FUNCTIONAL STUDIES OF MU OPIOID RECEPTORSR37DA001583 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LOH, HORACE H · 1987 to 1996
–
NIDA NIH HHS DA01583NIDA NIH HHS DA11190NIDA NIH HHS DA11806NIDA NIH HHS P50 DA011806NIDA NIH HHS R01 DA001583NIDA NIH HHS R01 DA011190NIDDK NIH HHS DK54733NIDDK NIH HHS DK60521NIDDK NIH HHS R01 DK054733NIDDK NIH HHS R01 DK060521
6 · The paper itself

Abstract

Microglial activation worsens neuronal loss and contributes to progressive neurological diseases like Parkinson's disease (PD). This inflammatory progression is countered by dynorphin (Dyn), the endogenous ligand of the kappa-opioid receptor (KOR). We show that microglial β-arrestin mediates the ability of Dyn/KOR to limit endotoxin-elicited production of pro-inflammatory effectors and cytokines, subsequently protecting neurons from inflammation-induced neurotoxicity. Agonist-activated KOR enhances the interaction of β-arrestin2 with transforming growth factor-beta-activated kinase 1 (TAK1)-binding protein 1 (TAB1), disrupting TAK1-TAB1 mediated pro-inflammatory gene expression. We reveal a new physiological role for β-arrestin in neuroprotection via receptor internalization-triggered blockade of signal effectors of microglial inflammatory neurotoxicity. This result offers novel drug targets in the convergent KOR/β-arrestin2 and inflammatory pathways for treating microglial inflammatory neuropathologies like PD.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsArrestinsbeta-ArrestinsCell DeathCytokinesDynorphinsFemaleInflammationMaleMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceMice, Inbred C57BLMicrogliaNeuronsAdaptor Proteins, Signal TransducingArrestinsbeta-ArrestinsCytokinesDynorphinsMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesOpioid PeptidesReceptors, Opioid, kappaTab1 protein, mouse

Identifiers

PMID24162663
PMCPMC3921587
OpenAlexW2013359545

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.