Evidence map›Paper›PMID 21525290›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

The canonical nuclear factor-κB pathway regulates cell survival in a developmental model of spinal cord motoneurons.

Stefka Mincheva, Ana Garcera, Myriam Gou-Fabregas, Mario Encinas, Xavier Dolcet, Rosa M Soler

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-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

19 citing papers in PubMed, 28 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 1 country.

Stefka MinchevaUnitat de Senyalització Neuronal, Departament de Ciències Mèdiques Bàsiques, Facultat de Medicina, Universitat de Lleida-Institut de Recerca Biomèdica de Lleida (IRBLLEIDA), 25008 Lleida, Spain.
Ana Garcera
Myriam Gou-Fabregas
Mario Encinas
Xavier Dolcet
Rosa M Soler
Biomedical Research Institute of Lleida · ESHospital Universitari Arnau de Vilanova · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In vivo and in vitro motoneuron survival depends on the support of neurotrophic factors. These factors activate signaling pathways related to cell survival or inactivate proteins involved in neuronal death. In the present work, we analyzed the involvement of the nuclear factor-κB (NF-κB) pathway in mediating mouse spinal cord motoneuron survival promoted by neurotrophic factors. This pathway comprises ubiquitously expressed transcription factors that could be activated by two different routes: the canonical pathway, associated with IKKα/IKKβ kinase phosphorylation and nuclear translocation RelA (p65)/p50 transcription factors; and the noncanonical pathway, related to IKKα kinase homodimer phosphorylation and RelB/p52 transcription factor activation. In our system, we show that neurotrophic factors treatment induced IKKα and IKKβ phosphorylation and RelA nuclear translocation, suggesting NF-κB pathway activation. Protein levels of different members of the canonical or noncanonical pathways were reduced in a primary culture of isolated embryonic motoneurons using an interference RNA approach. Even in the presence of neurotrophic factors, selective reduction of IKKα, IKKβ, or RelA proteins induced cell death. In contrast, RelB protein reduction did not have a negative effect on motoneuron survival. Together these results demonstrated that the canonical NF-κB pathway mediates motoneuron survival induced by neurotrophic factors, and the noncanonical pathway is not related to this survival effect. Canonical NF-κB blockade induced an increase of Bim protein level and apoptotic cell death. Bcl-x(L) overexpression or Bax reduction counteracted this apoptotic effect. Finally, RelA knockdown causes changes of CREB and Smn protein levels.

Indexed as

Analysis of VarianceAnimalsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11bcl-X ProteinCells, CulturedCell SurvivalChromonesCREB-Binding ProteinEmbryo, MammalianEnzyme ActivationEnzyme InhibitorsFemaleGene Expression Regulation, DevelopmentalGreen Fluorescent Proteins2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl2l11 protein, mouseBcl-2-Like Protein 11bcl-X ProteinChromonesCREB-Binding ProteinEnzyme InhibitorsGreen Fluorescent ProteinsI-kappa B KinaseMembrane ProteinsMorpholinesNerve Growth FactorsNF-kappa BPeptidesProto-Oncogene ProteinsRela protein, mouseSN50 peptideTranscription Factor RelA

Identifiers

PMID21525290
PMCPMC6622684
OpenAlexW1977817949

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.