Evidence map›Paper›PMID 16702954›Full record

ArticleOncogene2006

Differential effects of NF-kappaB on apoptosis induced by DNA-damaging agents: the type of DNA damage determines the final outcome.

E Strozyk, B Pöppelmann, T Schwarz, D Kulms

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. ZIP1 Is a Critical DNA Damage-Responsive Zinc Transporter Induced by Bleomycin via the TNFα-NF-κB Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  6. Memory-Enhancing Effects ofAntioxidants (Basel, Switzerland) · 2020
    Article
  7. Article
  8. p53 and the Carcinogenicity of Chronic Inflammation.Cold Spring Harbor perspectives in medicine · 2016
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Necrosis-like death can engage multiple pro-apoptotic Bcl-2 protein family members.Apoptosis : an international journal on programmed cell death · 2012
    Article
  17. Article
  18. Review
  19. Article
  20. 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 at 3 institutions in 1 country.

E StrozykDepartment of Dermatology, University of Muenster, Muenster, Germany.
B Pöppelmann
T Schwarz
D Kulms
University of Münster · DEKiel University · DEUniversity of Stuttgart · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor nuclear factor kappa-B (NF-kappaB) is generally regarded as an antiapoptotic factor. Accordingly, NF-kappaB activation inhibits death ligand-induced apoptosis. In contrast, ultraviolet light B (UVB)-induced apoptosis is not inhibited but even enhanced upon NF-kappaB activation by interleukin-1 (IL-1). This study was performed to identify the molecular mechanisms underlying this switch of NF-kappaB. Enhancement of UVB-induced apoptosis was always associated with increased release of tumour necrosis factor-alpha (TNF-alpha), which was dependent on NF-kappaB activation. The same was observed when UVA and cisplatin were used, which like UVB induce base modifications. In contrast, apoptosis caused by DNA strand breaks was not enhanced by IL-1, indicating that the type of DNA damage is critical for switching the effect of NF-kappaB on apoptosis. Surprisingly, activated NF-kappaB induced TNF-alpha mRNA expression in the presence of all DNA damage-inducing agents. However, in the presence of DNA strand breaks, there was no release of the TNF-alpha protein, which is so crucial for enhancing apoptosis. Together, this indicates that induction of DNA damage may have a significant impact on biological effects but it is the type of DNA damage that determines the final outcome. This may have implications for the role of NF-kappaB in carcinogenesis and for the application of NF-kappaB inhibitors in anticancer therapy.

Indexed as

DNA DamageAcetylcysteineAntineoplastic AgentsApoptosisChromosome BreakageCisplatinComet AssayDoxorubicinEtoposideGamma RaysGene Expression RegulationHumansI-kappa B KinaseI-kappa B ProteinsInterleukin-1Interleukin-63-(4-methylphenylsulfonyl)-2-propenenitrileAcetylcysteineAntineoplastic Agentsbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCisplatinDoxorubicinEtoposideI-kappa B KinaseI-kappa B ProteinsInterleukin-1Interleukin-6lactacystinLeupeptinsNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanNitrilesProteasome InhibitorsReceptors, Tumor Necrosis Factor, Type IRNA, MessengerSulfonesTumor Necrosis Factor-alpha

Identifiers

PMID16702954
OpenAlexW2087984134

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.