Evidence map›Paper›PMID 18281283›Full record

ArticleThe Journal of biological chemistry2008

Constitutive production of NF-kappaB2 p52 is not tumorigenic but predisposes mice to inflammatory autoimmune disease by repressing Bim expression.

Zhe Wang, Baochun Zhang, Liqun Yang, Jane Ding, Han-Fei Ding

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. 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
1.3field-weighted citation impact, top 17% 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, 43 citations in OpenAlex.

  1. Development of RelB-targeting small-molecule inhibitors of non-canonical NF-κB signaling with antitumor efficacy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Origin of the Functional Distinctiveness of NF-κB/p52.Frontiers in cell and developmental biology · 2021
    Review
  8. Article
  9. Cell Death Pathways in Lymphoid Malignancies.Current oncology reports · 2020
    Review
  10. 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
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. NF-κB signaling mediates homeostatic maturation of new T cells.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  18. Review
  19. Inhibition of pluripotent stem cell-derived teratoma formation by small molecules.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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

5 authors at 1 institution in 1 country.

Zhe WangDepartment of Biochemistry and Cancer Biology, College of Medicine, University of Toledo Health Science Campus, Toledo, Ohio 43614, USA.
Baochun Zhang
Liqun Yang
Jane Ding
Han-Fei Ding
University of Toledo · US

Funding

The Tumor Suppression Potential of NF-kappaB2 p100R01CA106550 · NCI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI DING, HAN-FEI · 2005 to 2008
$907k
NCI NIH HHS R01 CA106550
6 · The paper itself

Abstract

Normal development of the immune system requires regulated processing of NF-kappaB2 p100 to p52, which activates NF-kappaB2 signaling. Constitutive production of p52 has been suggested as a major mechanism underlying lymphomagenesis induced by NF-kappaB2 mutations, which occur recurrently in a variety of human lymphoid malignancies. To test the hypothesis, we generated transgenic mice with targeted expression of p52 in lymphocytes. In contrast to their counterparts expressing the tumor-derived NF-kappaB2 mutant p80HT, which develop predominantly B cell tumors, p52 transgenic mice are not prone to lymphomagenesis. However, they are predisposed to inflammatory autoimmune disease characterized by multiorgan infiltration of activated lymphocytes, high levels of autoantibodies in the serum, and immune complex glomerulonephritis. p52, but not p80HT, represses Bim expression, leading to defects in apoptotic processes critical for elimination of autoreactive lymphocytes and control of immune response. These findings reveal distinct signaling pathways for actions of NF-kappaB2 mutants and p52 and suggest a causal role for sustained NF-kappaB2 activation in the pathogenesis of autoimmunity.

Indexed as

Gene Expression RegulationAnimalsApoptosis Regulatory ProteinsAutoantibodiesBcl-2-Like Protein 11Genetic Predisposition to DiseaseHumansInflammationLymphocytesMembrane ProteinsMiceMice, Inbred C57BLMice, TransgenicMutationNF-kappa B p52 SubunitProto-Oncogene ProteinsApoptosis Regulatory ProteinsAutoantibodiesBCL2L11 protein, humanBcl2l11 protein, mouseBcl-2-Like Protein 11Membrane ProteinsNF-kappa B p52 SubunitProto-Oncogene Proteins

Identifiers

PMID18281283
PMCPMC3762532
OpenAlexW2072537237

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.