Evidence map›Paper›PMID 9950682›Full record

ArticleMolecular biology of the cell1999

NF-kappaB and AP-1 activation by nitric oxide attenuated apoptotic cell death in RAW 264.7 macrophages.

A von Knethen, D Callsen, B Brüne

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 160 citations in OpenAlex.

  1. Article
  2. Ethanol Extract ofMolecules (Basel, Switzerland) · 2023
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  4. Structural and Functional Properties of Activator Protein-1 in Cancer and Inflammation.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Role of PARP-1 as a novel transcriptional regulator of MMP-9 in diabetic retinopathy.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Article
  10. Article
  11. Article
  12. Article
  13. Sustained nitric oxide (NO)-releasing compound reverses dysregulated NO signal transduction in priapism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  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

3 authors at 1 institution in 1 country.

A von KnethenUniversity of Erlangen-Nürnberg, Faculty of Medicine, Department of Medicine IV-Experimental Division, Erlangen, Germany.
D Callsen
B Brüne
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A toxic dose of the nitric oxide (NO) donor S-nitrosoglutathione (GSNO; 1 mM) promoted apoptotic cell death of RAW 264.7 macrophages, which was attenuated by cellular preactivation with a nontoxic dose of GSNO (200 microM) or with lipopolysaccharide, interferon-gamma, and NG-monomethyl-L-arginine (LPS/IFN-gamma/NMMA) for 15 h. Protection from apoptosis was achieved by expression of cyclooxygenase-2 (Cox-2). Here we investigated the underlying mechanisms leading to Cox-2 expression. LPS/IFN-gamma/NMMA prestimulation activated nuclear factor (NF)-kappaB and promoted Cox-2 expression. Cox-2 induction by low-dose GSNO demanded activation of both NF-kappaB and activator protein-1 (AP-1). NF-kappaB supershift analysis implied an active p50/p65 heterodimer, and a luciferase reporter construct, containing four copies of the NF-kappaB site derived from the murine Cox-2 promoter, confirmed NF-kappaB activation after NO addition. An NF-kappaB decoy approach abrogated not only Cox-2 expression after low-dose NO or after LPS/IFN-gamma/NMMA but also inducible protection. The importance of AP-1 for Cox-2 expression and cell protection by low-level NO was substantiated by using the extracellular signal-regulated kinase inhibitor PD98059, blocking NO-elicited Cox-2 expression, but leaving the cytokine signal unaltered. Transient transfection of a dominant-negative c-Jun mutant further attenuated Cox-2 expression by low-level NO. Whereas cytokine-mediated Cox-2 induction relies on NF-kappaB activation, a low-level NO-elicited Cox-2 response required activation of both NF-kappaB and AP-1.

Indexed as

AnimalsApoptosisBase SequenceCalcium-Calmodulin-Dependent Protein KinasesCell LineCyclooxygenase 2Enzyme InhibitorsFlavonoidsGene ExpressionGlutathioneInterferon-gammaIsoenzymesLipopolysaccharidesMacrophagesMiceNF-kappa B2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneCalcium-Calmodulin-Dependent Protein KinasesCyclooxygenase 2Enzyme InhibitorsFlavonoidsGlutathioneInterferon-gammaIsoenzymesLipopolysaccharidesNF-kappa BNitric OxideNitric Oxide DonorsNitroso CompoundsOligodeoxyribonucleotidesomega-N-MethylarginineProstaglandin-Endoperoxide SynthasesRecombinant ProteinsS-NitrosoglutathioneTranscription Factor AP-1Tumor Suppressor Protein p53

Identifiers

PMID9950682
PMCPMC25174
OpenAlexW2009386000

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.