Evidence map›Paper›PMID 12673210›Full record

ArticleOncogene2003

Identification of NF-kappa B-regulated genes induced by TNFalpha utilizing expression profiling and RNA interference.

Anwu Zhou, Shane Scoggin, Richard B Gaynor, Noelle Sevilir Williams

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 173 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Clonally expanded CD38Science immunology · 2023
    Article
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  7. Article
  8. Article
  9. Article
  10. Cytokine Receptors-Regulators of Antimycobacterial Immune Response.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Current evidence for vitamin D in intestinal function and disease.Experimental biology and medicine (Maywood, N.J.) · 2019
    Review
  18. Article
  19. Article
  20. The roles of TNFAIP2 in cancers and infectious diseases.Journal of cellular and molecular medicine · 2018
    Review

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

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Anwu ZhouDepartment of Medicine, Harold Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas 75390-8594, USA.
Shane Scoggin
Richard B Gaynor
Noelle Sevilir Williams
The University of Texas Southwestern Medical Center · USEli Lilly (Singapore) · SG

Funding

PROPERTIES TO THE HTLV I TAX PROTEINR01CA074128 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI WILLIAMS, NOELLE SEVILIR · 1997 to 2001
$486k
NCI NIH HHS CA74128
6 · The paper itself

Abstract

Tumor necrosis factor alpha (TNF alpha) is a proinflammatory cytokine with important roles in regulating inflammatory responses as well as cell cycle proliferation and apoptosis. Although TNFalpha stimulates apoptosis, it also activates the transcription factor NF-kappa B, and studies have shown that inhibition of NF-kappa B potentiates the cytotoxicity of TNFalpha. Since several chemotherapy agents act like TNFalpha to both promote apoptosis and activate NF-kappa B, understanding the role of NF-kappa B in suppressing apoptosis may have significant clinical applications. To understand the effects of stimulation with TNFalpha and the role of NF-kappa B in regulating this response, a 23k human cDNA microarray was used to screen TNFalpha-inducible genes in HeLa cells. Real-time PCR verified expression changes in 16 of these genes and revealed three distinct temporal patterns of expression after TNFalpha stimulation. Using RNA interference to disrupt expression of the p65 subunit of NF-kappa B, all but two of the genes were shown to depend on this transcription factor for their expression, which correlated well with the existence of NF-kappa B binding sites in most of their promoters. Inflammatory, proapoptotic, and antiapoptotic genes were all shown to be regulated by NF-kappa B, demonstrating the wide variety of targets activated by NF-kappa B signaling and the necessity of differentiating among these genes for therapeutic purposes.

Indexed as

Gene Expression ProfilingGene Expression RegulationRNA InterferenceComputer SystemsHeLa CellsHumansNeoplasm ProteinsNF-kappa BOligonucleotide Array Sequence AnalysisPolymerase Chain ReactionPromoter Regions, GeneticTranscription Factor RelATumor Necrosis Factor-alphaNeoplasm ProteinsNF-kappa BTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID12673210
OpenAlexW2016909880

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.