Evidence map›Paper›PMID 25112869›Full record

ArticleThe Journal of biological chemistry2014

The role of constitutive nitric-oxide synthase in ultraviolet B light-induced nuclear factor κB activity.

Lingying Tong, Shiyong Wu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Role of constitutive nitric oxide synthases in the dynamic regulation of the autophagy response of keratinocytes upon UVB exposure.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2020
    Article
  6. Anticancer Activity ofNutrients · 2020
    Review
  7. Potential Immunoregulatory and Antiviral/SARS-CoV-2 Activities of Nitric Oxide.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

2 authors at 2 institutions in 1 country.

Lingying TongDepartment of Chemistry and Biochemistry, Edison Biotechnology Institute and Molecular and Cellular Biology Program, Ohio University, Athens, Ohio 45701.
Shiyong WuDepartment of Chemistry and Biochemistry, Edison Biotechnology Institute and Molecular and Cellular Biology Program, Ohio University, Athens, Ohio 45701. Electronic address: wus1@ohio.edu.
Biotechnology Institute · USOhio University · US

Funding

NCI NIH HHS R01 CA86926
6 · The paper itself

Abstract

NF-κB is a transcription factor involved in many signaling pathways that also plays an important role in UV-induced skin tumorigenesis. UV radiation can activate NF-κB, but the detailed mechanism remains unclear. In this study, we provided evidence that the activation of constitutive nitric-oxide synthase plays a role in regulation of IκB reduction and NF-κB activation in human keratinocyte HaCaT cells in early phase (within 6 h) post-UVB. Treating the cells with l-NAME, a selective inhibitor of constitutive nitric-oxide synthase (cNOS), can partially reverse the IκB reduction and inhibit the DNA binding activity as well as nuclear translocation of NF-κB after UVB radiation. A luciferase reporter assay indicates that UVB-induced NF-κB activation is totally diminished in cNOS null cells. The cNOS-mediated reduction of IκB is likely due to the imbalance of nitric oxide/peroxynitrite because treating the cells with lower (50 μm), but not higher (100-500 μm), concentration of S-nitroso-N-acetylpenicillamine (SNAP) can reverse the effect of l-NAME in partial restore IκB level post-UVB. Our data also showed that NF-κB activity was required for maintaining a stable IκB kinase α subunit (IKKα) level because treating the cells with NF-κB or cNOS inhibitors could reduce IKKα level upon UVB radiation. In addition, our data demonstrated that although NF-κB protects cells from UVB-induced death, its pro-survival activity was likely neutralized by the pro-death activity of peroxynitrite after UVB radiation.

Indexed as

ApoptosisEnzyme ActivationHEK293 CellsHeLa CellsHumansI-kappa B KinaseNF-kappa BNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase Type IIIProtein BindingProtein BiosynthesisProtein Processing, Post-TranslationalSignal TransductionTranscriptional ActivationUltraviolet RaysI-kappa B KinaseNF-kappa BNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase Type IIINOS3 protein, humanApoptosisKeratinocytesNF-kappa B (NF-KB)Nitric OxideNitric-oxide SynthaseSuperoxide Ion

Identifiers

PMID25112869
PMCPMC4176213
OpenAlexW2032909115

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.