Evidence map›Paper›PMID 25497099›Full record

ArticleCell reports2014

A pathway switch directs BAFF signaling to distinct NFκB transcription factors in maturing and proliferating B cells.

Jonathan V Almaden, Rachel Tsui, Yi C Liu, Harry Birnbaum, Maxim N Shokhirev, Kim A Ngo, Jeremy C Davis-Turak, Dennis Otero, Soumen Basak, Robert C Rickert and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.6field-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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Computational modelling of aggressive B-cell lymphoma.Biochemical Society transactions · 2025
    Review
  3. Article
  4. Review
  5. Review
  6. RTF: an R package for modelling time course data.Bioinformatics (Oxford, England) · 2024
    Article
  7. Review
  8. NF-kB and the CLL microenvironment.Frontiers in oncology · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. An epithelialProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Article
  16. 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
  17. Article
  18. Review
  19. Article
  20. Review
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 4 institutions in 2 countries.

Jonathan V AlmadenSignaling Systems Laboratory and San Diego Center for Systems Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Rachel TsuiSignaling Systems Laboratory and San Diego Center for Systems Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Yi C LiuDepartment of Microbiology, Immunology, and Molecular Genetics and Institute for Quantitative and Computational Biosciences, University of California, Los Angeles, Los Angeles, CA 90025, USA.
Harry BirnbaumSignaling Systems Laboratory and San Diego Center for Systems Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA; Department of Microbiology, Immunology, and Molecular Genetics and Institute for Quantitative and Computational Biosciences, University of California, Los Angeles, Los Angeles, CA 90025, USA.
Maxim N ShokhirevSignaling Systems Laboratory and San Diego Center for Systems Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Kim A NgoSignaling Systems Laboratory and San Diego Center for Systems Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA; Department of Microbiology, Immunology, and Molecular Genetics and Institute for Quantitative and Computational Biosciences, University of California, Los Angeles, Los Angeles, CA 90025, USA.
Jeremy C Davis-TurakSignaling Systems Laboratory and San Diego Center for Systems Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Dennis OteroDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Soumen BasakSystems Immunology Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi 110067, India.
Robert C RickertProgram on Inflammatory Disease Research, Infectious and Inflammatory Disease Center, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA.
Alexander HoffmannSignaling Systems Laboratory and San Diego Center for Systems Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA; Department of Microbiology, Immunology, and Molecular Genetics and Institute for Quantitative and Computational Biosciences, University of California, Los Angeles, Los Angeles, CA 90025, USA. Electronic address: ahoffmann@ucla.edu.
University of California, San Diego · USUniversity of California, Los Angeles · USNational Institute of Immunology · INSanford Burnham Prebys Medical Discovery Institute · US

Funding

SYNTHETIC SYSTEMSP50GM085764 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HASTY, JEFF M, IDEKER, TREY · 2010 to 2018
$23.3M
STRUCTURE AND STABILITY OF IKB/NF-KB COMPLEXESP01GM071862 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KOMIVES, ELIZABETH A. · 2006 to 2016
$14.9M
IKK:Biophysical basis of dynamic regulationR01CA141722 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GHOSH, GOURISANKAR, HOFFMANN, ALEXANDER · 2009 to 2013
$2.7M
Regulation of signaling via the lkB-NF-kB interactionR01GM071573 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HOFFMANN, ALEXANDER · 2005 to 2013
$2.2M
The NF-kB signaling system as a regulator of B-cell activationR01AI083453 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HOFFMANN, ALEXANDER · 2010 to 2014
$1.7M
NCI NIH HHS NCI R01 CA141722NCI NIH HHS R01 CA141722NIAID NIH HHS R01 AI083453NIGMS NIH HHS P01 GM071862NIGMS NIH HHS P01GM071862NIGMS NIH HHS P50 GM085764NIGMS NIH HHS R01 GM071573PHS HHS NIAID R01 AI083453PHS HHS NIGMS R01 GM071573
6 · The paper itself

Abstract

BAFF, an activator of the noncanonical NFκB pathway, provides critical survival signals during B cell maturation and contributes to B cell proliferation. We found that the NFκB family member RelB is required ex vivo for B cell maturation, but cRel is required for proliferation. Combined molecular network modeling and experimentation revealed Nfkb2 p100 as a pathway switch; at moderate p100 synthesis rates in maturing B cells, BAFF fully utilizes p100 to generate the RelB:p52 dimer, whereas at high synthesis rates, p100 assembles into multimeric IκBsome complexes, which BAFF neutralizes in order to potentiate cRel activity and B cell expansion. Indeed, moderation of p100 expression or disruption of IκBsome assembly circumvented the BAFF requirement for full B cell expansion. Our studies emphasize the importance of p100 in determining distinct NFκB network states during B cell biology, which causes BAFF to have context-dependent functional consequences.

Indexed as

Cell ProliferationSignal TransductionAnimalsB-Cell Activating FactorB-LymphocytesCell DifferentiationI-kappa B ProteinsMiceModels, BiologicalNF-kappa BProtein SubunitsB-Cell Activating FactorI-kappa B ProteinsNF-kappa BProtein SubunitsTnfsf13b protein, mouse

Identifiers

PMID25497099
PMCPMC4889572
OpenAlexW2077107480

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.