Evidence map›Paper›PMID 9314550›Full record

ArticleThe Journal of experimental medicine1997

Gastric hyperplasia and increased proliferative responses of lymphocytes in mice lacking the COOH-terminal ankyrin domain of NF-kappaB2.

H Ishikawa, D Carrasco, E Claudio, R P Ryseck, R Bravo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

85 citing papers in PubMed, 174 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. American journal of physiology. Gastrointestinal and liver physiology · 2022
    Article
  7. Review
  8. Origin of the Functional Distinctiveness of NF-κB/p52.Frontiers in cell and developmental biology · 2021
    Review
  9. NF-κB Signaling Regulates Physiological and Pathological Chondrogenesis.International journal of molecular sciences · 2019
    Review
  10. Article
  11. 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
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

25 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

H IshikawaThe Department of Oncology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000, USA.
D Carrasco
E Claudio
R P Ryseck
R Bravo
Bristol-Myers Squibb (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nfkb2 gene encodes the p100 precursor which produces the p52 protein after proteolytic cleavage of its COOH-terminal domain. Although the p52 product can act as an alternative subunit of NF-kappaB, the p100 precursor is believed to function as an inhibitor of Rel/NF-kappaB activity by cytoplasmic retention of Rel/NF-kappaB complexes, like other members of the IkappaB family. However, the physiological relevance of the p100 precursor as an IkappaB molecule has not been understood. To assess the role of the precursor in vivo, we generated, by gene targeting, mice lacking p100 but still containing a functional p52 protein. Mice with a homozygous deletion of the COOH-terminal ankyrin repeats of NF-kappaB2 (p100(-/-)) had marked gastric hyperplasia, resulting in early postnatal death. p100(-/-) animals also presented histopathological alterations of hematopoietic tissues, enlarged lymph nodes, increased lymphocyte proliferation in response to several stimuli, and enhanced cytokine production in activated T cells. Dramatic induction of nuclear kappaB-binding activity composed of p52-containing complexes was found in all tissues examined and also in stimulated lymphocytes. Thus, the p100 precursor is essential for the proper regulation of p52-containing Rel/NF-kappaB complexes in various cell types and its absence cannot be efficiently compensated for by other IkappaB proteins.

Indexed as

I-kappa B ProteinsAnimalsAnkyrinsBlotting, WesternCell DivisionCytokinesDimerizationDNA-Binding ProteinsDNA PrimersFlow CytometryGene TargetingHyperplasiaIn Situ HybridizationLymphocyte ActivationMiceMice, KnockoutAnkyrinsCytokinesDNA-Binding ProteinsDNA PrimersI kappa B beta proteinI-kappa B ProteinsNF-kappa BNF-kappa B p52 SubunitProtein PrecursorsProto-Oncogene ProteinsProto-Oncogene Proteins c-relRNA, Messenger

Identifiers

PMID9314550
PMCPMC2199059
OpenAlexW2046265685

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.