Evidence map›Paper›PMID 14602923›Full record

ArticleNucleic acids research2003

DNA damage induces transcriptional activation of p73 by removing C-EBPalpha repression on E2F1.

Mirko Marabese, Faina Vikhanskaya, Cristina Rainelli, Toshiyuki Sakai, Massimo Broggini

Open access · bronzeAbstract read
In one paragraph

Article in Nucleic acids research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Targeting Cryptochromes in Chronic Diseases.Cell biology international · 2025
    Review
  2. Review
  3. p73α1, a p73 C-terminal isoform, regulates tumor suppression and the inflammatory response via Notch1.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Autophagy and genomic integrity.Cell death and differentiation · 2013
    Review
  9. Article
  10. Article
  11. Article
  12. Circadian clock disruption improves the efficacy of chemotherapy through p73-mediated apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  13. p73 in Cancer.Genes & cancer · 2011
    Article
  14. p73 as a pharmaceutical target for cancer therapy.Current pharmaceutical design · 2011
    Review
  15. Article
  16. Article
  17. Therapeutic prospects for p73 and p63: rising from the shadow of p53.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
    Review
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

5 authors at 1 institution in 1 country.

Mirko MarabeseLaboratory of Molecular Pharmacology, Istituto di Ricerche Farmacologiche Mario Negri, via Eritrea 62, 20157 Milan, Italy.
Faina Vikhanskaya
Cristina Rainelli
Toshiyuki Sakai
Massimo Broggini
Mario Negri Institute for Pharmacological Research · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p73 is a member of the p53 family often overexpressed in human cancer. Its regulation, particularly following DNA damage, is different from that of p53. Following DNA damage, we found induction of p73 at both the protein and mRNA levels. Furthermore, by using different p73 promoter fragments, we found a role for E2F1 in mediating transcription of p73. However, this observation alone does not account for the observed DNA damage-induced activation of p73 in the cells used in these experiments. By analyzing the p73 promoter sequence, we revealed a new mechanism of p73 induction associated with the removal of transcriptional repression from the p73 promoter. We found, in fact, that treatment of cells with DNA damaging agents induced nuclear export of the transcription factor C-EBPalpha and blockage of this export abolished drug-induced p73 activation. We also show that C-EBPalpha has a direct repressive activity on transfactor E2F1, and for this repression the binding of C-EBPalpha to its consensus sequence in the DNA is required. These data suggest that in normal conditions a repressor complex involving C-EBPalpha, E2F1 and perhaps other proteins is present on the p73 promoter. This repressor complex is destroyed following damage by removal of C-EBPalpha from nuclei.

Indexed as

Cell Cycle ProteinsDNA DamageAntibiotics, AntineoplasticBinding SitesCCAAT-Enhancer-Binding Protein-alphaCell Line, TumorCell NucleusCytoplasmDNA-Binding ProteinsDoxorubicinE2F1 Transcription FactorE2F Transcription FactorsGenes, Tumor SuppressorHumansLuciferasesMutationAntibiotics, AntineoplasticCCAAT-Enhancer-Binding Protein-alphaCell Cycle ProteinsDNA-Binding ProteinsDoxorubicinE2F1 protein, humanE2F1 Transcription FactorE2F Transcription FactorsLuciferasesNuclear ProteinsRecombinant Fusion ProteinsRNA, MessengerTP73 protein, humanTranscription FactorsTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID14602923
PMCPMC275563
OpenAlexW2164938315

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.