Evidence map›Paper›PMID 23555623›Full record

ArticlePloS one2013

Frequent engagement of RelB activation is critical for cell survival in multiple myeloma.

Françoise Cormier, Hélène Monjanel, Claire Fabre, Katy Billot, Elène Sapharikas, Fanny Chereau, Didier Bordereaux, Thierry J Molina, Hervé Avet-Loiseau, Véronique Baud

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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. A Suite of EightbioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Mouse models of human multiple myeloma subgroups.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Substrate complex competition is a regulatory motif that allows NFκB RelA to license but not amplify NFκB RelB.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  13. Article
  14. Review
  15. Review
  16. A link betweenOncotarget · 2017
    Article
  17. Review
  18. Article
  19. Article
  20. Article
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

10 authors at 8 institutions in 1 country.

Françoise CormierINSERM, U1016, Institut Cochin, Paris, France.
Hélène Monjanel
Claire Fabre
Katy Billot
Elène Sapharikas
Fanny Chereau
Didier Bordereaux
Thierry J Molina
Hervé Avet-Loiseau
Véronique Baud
Centre National de la Recherche Scientifique · FRCentre Hospitalier Universitaire de Toulouse · FRDélégation Paris 5 · FRHôtel-Dieu de Paris · FRInserm · FRInstitut Cochin · FRInstitut Curie · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NF-κB family of transcription factors has emerged as a key player in the pathogenesis of multiple myeloma (MM). NF-κB is activated by at least two major signaling pathways. The classical pathway results in the activation of mainly RelA containing dimers, whereas the alternative pathway leads to the activation of RelB/p52 and RelB/p50 heterodimers. Activating mutations in regulators of the alternative pathway have been identified in 17% of MM patients. However, the status of RelB activation per se and its role in the regulation of cell survival in MM has not been investigated. Here, we reveal that 40% of newly diagnosed MM patients have a constitutive RelB DNA-binding activity in CD138(+) tumor cells, and we show an association with increased expression of a subset of anti-apoptotic NF-κB target genes, such as cIAP2. Furthermore, we demonstrate that RelB exerts a crucial anti-apoptotic activity in MM cells. Our findings indicate that RelB activation is key for promoting MM cell survival through the upregulation of anti-apoptotic proteins. Altogether, our study provides the framework for the development of new molecules targeting RelB in the treatment of MM.

Indexed as

Gene Expression Regulation, NeoplasticTranscription, GeneticAdultAgedAged, 80 and overApoptosisBaculoviral IAP Repeat-Containing 3 ProteinCell SurvivalDNAFemaleHumansInhibitor of Apoptosis ProteinsMaleMiddle AgedMultiple MyelomaPrimary Cell CultureBaculoviral IAP Repeat-Containing 3 ProteinBIRC3 protein, humanDNAInhibitor of Apoptosis ProteinsRELA protein, humanRELB protein, humanSDC1 protein, humanSyndecan-1Transcription Factor RelATranscription Factor RelBUbiquitin-Protein Ligases

Identifiers

PMID23555623
PMCPMC3610937
OpenAlexW2034580886

What OpenQuestion holds

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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.