Evidence map›Paper›PMID 9566896›Full record

ArticleMolecular and cellular biology1998

Tumor suppressor p53 can participate in transcriptional induction of the GADD45 promoter in the absence of direct DNA binding.

Q Zhan, I T Chen, M J Antinore, A J Fornace

Erratum issuedAbstract read
In one paragraph

Article in Molecular and cellular biology, 1998. 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 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.5field-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

60 citing papers in PubMed, 152 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Shared gene targets of the ATF4 and p53 transcriptional networks.bioRxiv : the preprint server for biology · 2023
    Article
  5. Article
  6. GADD45 in Stress Signaling, Cell Cycle Control, and Apoptosis.Advances in experimental medicine and biology · 2022
    Article
  7. Cancer and Apoptosis.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  8. Gadd45 in Neuronal Development, Function, and Injury.Advances in experimental medicine and biology · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. BET and HDAC inhibitors induce similar genes and biological effects and synergize to kill in Myc-induced murine lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  16. Beyond transcriptional silencing: is methylcytosine a widely conserved eukaryotic DNA elimination mechanism?BioEssays : news and reviews in molecular, cellular and developmental biology · 2014
    Article
  17. Apoptosis and molecular targeting therapy in cancer.BioMed research international · 2014
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Q ZhanDivision of Basic Sciences, National Cancer Institute, Bethesda, Maryland 20892-4255, USA.
I T Chen
M J Antinore
A J Fornace
National Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The GADD45 gene is a growth arrest-associated gene that is induced by certain DNA-damaging agents and other stresses, such as starvation, in all mammalian cells. In addition to a strong p53-binding element in an intronic sequence, we have recently found that p53, while not required or sufficient alone, may contribute to the stress responsiveness of the promoter. Much of the responsiveness was localized to a GC-rich motif in the proximal promoter which contains multiple Egr1 sites and a larger WT1 site; this 20-bp WT1 motif is identical to the WT1-binding site in the PDGF-A gene. In extracts from a human breast carcinoma cell line expressing p53 and WT1, which is known to associate with p53 in vivo, evidence was obtained that these proteins are in a complex that binds this 20-bp element. A combination of p53 and WT1 expression vectors strongly induced a GADD45-reporter construct, while mutation of the WT1-Egr1 site in the promoter prevented this induction. Abrogation of p53 function by a dominant-negative vector or abrogation of WT1 function by an antisense vector markedly reduced the induction of this promoter. Since p53 does not bind directly to the promoter, these results indicate that p53 can contribute to the positive regulation of a promoter by protein-protein interactions.

Indexed as

Immediate-Early ProteinsPromoter Regions, GeneticAntisense Elements (Genetics)Binding SitesDNA-Binding ProteinsEarly Growth Response Protein 1GADD45 ProteinsGene Expression RegulationGenes, ReporterHumansIntracellular Signaling Peptides and ProteinsProtein BindingProtein BiosynthesisProteinsRecombinant Fusion ProteinsStress, PhysiologicalAntisense Elements (Genetics)DNA-Binding ProteinsEarly Growth Response Protein 1EGR1 protein, humanGADD45 ProteinsImmediate-Early ProteinsIntracellular Signaling Peptides and ProteinsProteinsRecombinant Fusion ProteinsTranscription FactorsTumor Suppressor Protein p53WT1 Proteins

Identifiers

PMID9566896
PMCPMC110656
OpenAlexW2164678989

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.