Evidence map›Paper›PMID 23457524›Full record

ArticlePloS one2013

Immunoproteasome deficiency modifies the alternative pathway of NFκB signaling.

Marcela Maldonado, Rebecca J Kapphahn, Marcia R Terluk, Neal D Heuss, Ching Yuan, Dale S Gregerson, Deborah A Ferrington

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

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  12. Therapeutic Potential of Immunoproteasome Inhibition in Duchenne Muscular Dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2016
    Article
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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

7 authors at 1 institution in 1 country.

Marcela MaldonadoDepartment of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, Minnesota, United States of America.
Rebecca J Kapphahn
Marcia R Terluk
Neal D Heuss
Ching Yuan
Dale S Gregerson
Deborah A Ferrington
University of Minnesota · US

Funding

Visual TestingP30EY011374 · NEI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI NEWMAN, ERIC A · 1996 to 2019
$8.8M
Training Grant: Functional Proteomics of AgingT32AG029796 · NIA · UNIVERSITY OF MINNESOTA · PI EDGAR A ARRIAGA, Douglas G Mashek · 2008 to 2026
$6.6M
Proteasome Function in the Aging RetinaR01EY013623 · NEI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI FERRINGTON, DEBORAH ANN · 2003 to 2010
$2.2M
Local Retinal Antigen PresentationR01EY016376 · NEI · UNIVERSITY OF MINNESOTA · PI GREGERSON, DALE SANNES · 2006 to 2010
$1.8M
Local Generation of Regulatory T Cells to Retinal AntigenR01EY021996 · NEI · UNIVERSITY OF MINNESOTA · PI GREGERSON, DALE SANNES · 2012 to 2014
$1.1M
Smad3 inhibitors for ophthalmic applicationsR21EY019552 · NEI · UNIVERSITY OF MINNESOTA · PI YUAN, CHING · 2009 to 2010
$415k
Immunoproteasome: A key component of the cellular stress responseR21AG032391 · NIA · UNIVERSITY OF MINNESOTA · PI FERRINGTON, DEBORAH ANN · 2008 to 2009
$315k
NEI NIH HHS EY013623NEI NIH HHS EY016376NEI NIH HHS EY019552NEI NIH HHS P30 EY011374NEI NIH HHS P30-EY11374NEI NIH HHS R01 EY013623NEI NIH HHS R01 EY016376NEI NIH HHS R01 EY021996NEI NIH HHS R21 EY019552NIA NIH HHS AG029796NIA NIH HHS AG032391NIA NIH HHS R21 AG032391NIA NIH HHS T32 AG029796
6 · The paper itself

Abstract

Immunoproteasome is a protease abundant in immune cells and also present, albeit at lower concentrations, in cells outside the immune system. Recent evidence supports a novel role for the immunoproteasome in the cellular stress response potentially through regulation of NFκB signaling, which is the primary response to multiple stressors. The current study tests whether the Classical or Alternative Pathways are regulated by immunoproteasome following chronic TNFα exposure in cultured retinal pigment epithelial cells isolated from wild-type mice and mice deficient in one (LMP2, L2) or two (LMP7 and MECL-1, L7M1) immunoproteasome subunits. Assays were performed to assess the expression of NFκB responsive genes, the content and activity of NFκB transcription factors (p65, p50, p52, cRel, RelB), and expression and content of regulatory proteins (IκBα, A20, RPS3). Major findings include distinct differences in expression of NFκB responsive genes in both KO cells. The mechanism responsible for the altered gene expression could not be established for L7M1 since no major differences in NFκB transcription factor content or activation were observed. However, L2 cells exhibited substantially higher content and diminished activation of NFκB transcription factors associated with the Alternative Pathway and delayed termination of the Classical Pathway. These results provide strong experimental evidence supporting a role for immunoproteasome in modulating NFκB signaling.

Indexed as

Signal TransductionAnimalsCells, CulturedCysteine EndopeptidasesGene Expression RegulationGene Knockout TechniquesMiceMice, KnockoutNF-kappa BProteasome Endopeptidase ComplexRetinal Pigment EpitheliumTumor Necrosis Factor-alphaCysteine EndopeptidasesLMP-2 proteinLMP7 proteinNF-kappa BProteasome Endopeptidase ComplexPsmb10 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID23457524
PMCPMC3572990
OpenAlexW2075732775

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.