Evidence map›Paper›PMID 11930006›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

The combined absence of NF-kappa B1 and c-Rel reveals that overlapping roles for these transcription factors in the B cell lineage are restricted to the activation and function of mature cells.

Thomas Pohl, Raffi Gugasyan, Raelene J Grumont, Andreas Strasser, Donald Metcalf, David Tarlinton, William Sha, David Baltimore, Steve Gerondakis

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.7field-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

58 citing papers in PubMed, 110 citations in OpenAlex.

  1. Trial
  2. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
  3. Review
  4. Regulation of BCR-mediated CaScience immunology · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Regulation of B-cell function by NF-kappaB c-Rel in health and disease.Cellular and molecular life sciences : CMLS · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Sensing danger through a "finger".The Journal of experimental medicine · 2018
    Article
  16. Review
  17. PTIP chromatin regulator controls development and activation of B cell subsets to license humoral immunity in mice.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  18. Article
  19. Article
  20. The Paracaspase MALT1.Biochimie · 2016
    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

9 authors at 4 institutions in 2 countries.

Thomas PohlThe Walter and Eliza Hall Institute of Medical Research, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.
Raffi Gugasyan
Raelene J Grumont
Andreas Strasser
Donald Metcalf
David Tarlinton
William Sha
David Baltimore
Steve Gerondakis
University of California, Berkeley · USWalter and Eliza Hall Institute of Medical Research · AUThe Royal Melbourne Hospital · AUCalifornia Institute of Technology · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription factors NF-kappaB1 and c-Rel, individually dispensable during embryogenesis, serve similar, yet distinct, roles in the function of mature hemopoietic cells. Redundancy among Rel/NF-kappaB family members prompted an examination of the combined roles of c-Rel and NF-kappaB1 by using mice that lack both proteins. Embryonic development and the maturation of hemopoietic progenitors were unaffected in nfkb1(-/-)c-rel(-/-) mice. Peripheral T cell populations developed normally, but follicular, marginal zone, and CD5(+) peritoneal B cell populations all were reduced. In culture, a failure of mitogen-stimulated nfkb1(-/-)c-rel(-/-) B cells to proliferate was caused by a cell cycle defect in early G(1) that prevented growth. In vivo, defects in humoral immunity and splenic architecture seen in nfkb1(-/-) and c-rel(-/-) mice were exacerbated in the double mutant mice. These findings demonstrate that in the B lineage overlapping roles for NF-kappaB1 and c-Rel appear to be restricted to regulating the activation and function of mature cells.

Indexed as

Cell LineageLymphocyte ActivationAnimalsAntibody FormationB-LymphocytesCell DivisionHematopoiesisMiceMice, Inbred C57BLNF-kappa BProto-Oncogene Proteins c-relNF-kappa BProto-Oncogene Proteins c-rel

Identifiers

PMID11930006
PMCPMC123679
OpenAlexW2005318103

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.