Evidence map›Paper›PMID 27075172›Full record

ArticleMolecular biology of the cell2016

NFκB is a central regulator of protein quality control in response to protein aggregation stresses via autophagy modulation.

Mathieu Nivon, Loïc Fort, Pascale Muller, Emma Richet, Stéphanie Simon, Baptiste Guey, Maëlenn Fournier, André-Patrick Arrigo, Claudio Hetz, Julie D Atkin and 1 more

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

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  11. The Links between ALS and NF-κB.International journal of molecular sciences · 2021
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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

11 authors at 3 institutions in 3 countries.

Mathieu NivonUniversité de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France.
Loïc FortUniversité de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France.
Pascale MullerUniversité de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France.
Emma RichetUniversité de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France.
Stéphanie SimonUniversité de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France.
Baptiste GueyUniversité de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France.
Maëlenn FournierUniversité de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France.
André-Patrick ArrigoUniversité de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France.
Claudio HetzBiomedical Neuroscience Institute, Faculty of Medicine, University of Chile, 70086 Santiago, Chile Center for Geroscience, Brain Health and Metabolism, 70086 Santiago, Chile.
Julie D AtkinDepartment of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW 2109, Australia.
Carole Kretz-RemyUniversité de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France carole.kretz@univ-lyon1.fr.
Université Claude Bernard Lyon 1 · FRCenter for Climate and Resilience Research · CLMacquarie University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During cell life, proteins often misfold, depending on particular mutations or environmental changes, which may lead to protein aggregates that are toxic for the cell. Such protein aggregates are the root cause of numerous diseases called "protein conformational diseases," such as myofibrillar myopathy and familial amyotrophic lateral sclerosis. To fight against aggregates, cells are equipped with protein quality control mechanisms. Here we report that NFκB transcription factor is activated by misincorporation of amino acid analogues into proteins, inhibition of proteasomal activity, expression of the R120G mutated form of HspB5 (associated with myofibrillar myopathy), or expression of the G985R and G93A mutated forms of superoxide dismutase 1 (linked to familial amyotrophic lateral sclerosis). This noncanonical stimulation of NFκB triggers the up-regulation of BAG3 and HspB8 expression, two activators of selective autophagy, which relocalize to protein aggregates. Then NFκB-dependent autophagy allows the clearance of protein aggregates. Thus NFκB appears as a central and major regulator of protein aggregate clearance by modulating autophagic activity. In this context, the pharmacological stimulation of this quality control pathway might represent a valuable strategy for therapies against protein conformational diseases.

Indexed as

Adaptor Proteins, Signal Transducingalpha-Crystallin B ChainApoptosis Regulatory ProteinsAutophagyHeLa CellsHumansMotor NeuronsNF-kappa BProtein ConformationProtein FoldingProtein Serine-Threonine KinasesStress, PhysiologicalSuperoxide Dismutase-1Transcriptional ActivationUp-RegulationAdaptor Proteins, Signal Transducingalpha-Crystallin B ChainApoptosis Regulatory ProteinsBAG3 protein, humanCRYAB protein, humanNF-kappa BProtein Serine-Threonine KinasesSuperoxide Dismutase-1

Identifiers

PMID27075172
PMCPMC4884063
OpenAlexW2337886805

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.