Evidence map›Paper›PMID 25987726›Full record

ArticleThe Journal of experimental medicine2015

BAFF activation of the ERK5 MAP kinase pathway regulates B cell survival.

Emilie Jacque, Edina Schweighoffer, Victor L J Tybulewicz, Steven C Ley

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2015. 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
1.2field-weighted citation impact, top 22% 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, 34 citations in OpenAlex.

  1. Review
  2. Review
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  4. Posttranscriptional control of the B cell receptor by HuR is essential for innate B cell maintenance and function.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Article
  7. [Research advances on B-cell activating factor and its targeted agents in inflammatory bowel disease].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
    Review
  8. Review
  9. FCRL1 Regulates B Cell Receptor-Induced ERK Activation through GRB2.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  10. Review
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  18. SATB2 suppresses gastric cancer cell proliferation and migration.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  19. 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

4 authors.

Emilie JacqueDivision of Immune Cell Biology, MRC National Institute for Medical Research London, London NW7 1AA, England, UK.
Edina SchweighofferDivision of Immune Cell Biology, MRC National Institute for Medical Research London, London NW7 1AA, England, UK.
Victor L J TybulewiczDivision of Immune Cell Biology, MRC National Institute for Medical Research London, London NW7 1AA, England, UK.
Steven C LeyDivision of Immune Cell Biology, MRC National Institute for Medical Research London, London NW7 1AA, England, UK steve.ley@crick.ac.uk.

Funding

Medical Research Council MC_U117527252Medical Research Council MC_U117584209
6 · The paper itself

Abstract

B cell activating factor (BAFF) stimulation of the BAFF receptor (BAFF-R) is essential for the homeostatic survival of mature B cells. Earlier in vitro experiments with inhibitors that block MEK 1 and 2 suggested that activation of ERK 1 and 2 MAP kinases is required for BAFF-R to promote B cell survival. However, these inhibitors are now known to also inhibit MEK5, which activates the related MAP kinase ERK5. In the present study, we demonstrated that BAFF-induced B cell survival was actually independent of ERK1/2 activation but required ERK5 activation. Consistent with this, we showed that conditional deletion of ERK5 in B cells led to a pronounced global reduction in mature B2 B cell numbers, which correlated with impaired survival of ERK5-deficient B cells after BAFF stimulation. ERK5 was required for optimal BAFF up-regulation of Mcl1 and Bcl2a1, which are prosurvival members of the Bcl-2 family. However, ERK5 deficiency did not alter BAFF activation of the PI3-kinase-Akt or NF-κB signaling pathways, which are also important for BAFF to promote mature B cell survival. Our study reveals a critical role for the MEK5-ERK5 MAP kinase signaling pathway in BAFF-induced mature B cell survival and homeostatic maintenance of B2 cell numbers.

Indexed as

Gene Expression Regulation, EnzymologicAnimalsB-Cell Activating FactorB-LymphocytesBone Marrow CellsCell SurvivalEnzyme ActivationExtracellular Signal-Regulated MAP KinasesFemaleFlow CytometryGene DeletionMaleMAP Kinase Kinase 5MAP Kinase Signaling SystemMiceMice, Inbred C57BLAkt1 protein, mouseB-Cell Activating FactorBCL2-related protein A1Extracellular Signal-Regulated MAP KinasesMap2k5 protein, mouseMAP Kinase Kinase 5Mcl1 protein, mouseMinor Histocompatibility AntigensMitogen-Activated Protein Kinase 7Myeloid Cell Leukemia Sequence 1 ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Tnfsf13b protein, mouse

Identifiers

PMID25987726
PMCPMC4451135
OpenAlexW1915104373

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.