Evidence map›Paper›PMID 16205639›Full record

ArticleOncogene2006

Regulation of telomerase activity by the p53 family member p73.

M Beitzinger, C Oswald, R Beinoraviciute-Kellner, T Stiewe

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 48 citations in OpenAlex.

  1. Identification of DMP1 as Novel p53 Repressed Transcriptional Target.International journal of molecular sciences · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021
    Review
  7. Review
  8. Review
  9. Review
  10. Differences in telomerase activity between colon and rectal cancer.Canadian journal of surgery. Journal canadien de chirurgie · 2014
    Article
  11. Article
  12. Telomerase as a useful target in cancer fighting-the breast cancer case.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Review
  13. Article
  14. Article
  15. Article
  16. Novel ARF/p53-independent senescence pathways in cancer repression.Journal of molecular medicine (Berlin, Germany) · 2011
    Review
  17. PinX1 inhibits telomerase activity in gastric cancer cells through Mad1/c-Myc pathway.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2010
    Article
  18. Tumor suppression by p53: making cells senescent.Histology and histopathology · 2010
    Review
  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

4 authors at 1 institution in 1 country.

M BeitzingerMolecular Tumor Biology Group, Rudolf-Virchow-Center (DFG Research Center for Experimental Biomedicine), University of Würzburg, Versbacher Strasse 9, Würzburg 97078, Germany.
C Oswald
R Beinoraviciute-Kellner
T Stiewe
University of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The terminal ends of eukaryotic chromosomes, termed telomeres, progressively shorten during each round of cell division eventually leading cells into senescence. Tumor cells typically overcome this barrier to unlimited proliferation by activation of the human telomerase reverse transcriptase (hTERT) gene. In contrast, in most human somatic cells hTERT expression is tightly repressed by multiple tumor suppressors. Here, we studied the regulation of hTERT by the p53 family member p73. We show that forced expression of p73 or activation of endogenous p73 by E2F1 results in the downregulation of telomerase activity. Vice versa, siRNA-mediated knockdown of p73 induces hTERT expression. Responsiveness to p73 is conferred by Sp1 binding sites within the hTERT core promoter. In tumor cells, p73 isoforms lacking the transactivation domain (DeltaNp73) are frequently overexpressed and believed to function as oncogenes. We show that DeltaNp73 antagonizes the repressive effect of the proapoptotic p53 family members on hTERT expression and, in addition, induces hTERT expression in telomerase-negative cells by interfering with E2F-RB-mediated repression of the hTERT core promoter. These data provide evidence that the p73 gene functions as an important regulator of telomerase activity with implications for embryonic development, cellular differentiation and tumorigenesis.

Indexed as

AdenocarcinomaApoptosisBinding SitesCells, CulturedDNA-Binding ProteinsE2F1 Transcription FactorGene Expression Regulation, EnzymologicGenes, Tumor SuppressorHumansLung NeoplasmsNuclear ProteinsPromoter Regions, GeneticProtein Structure, TertiaryRetinoblastoma ProteinRNA, Small InterferingSp1 Transcription Factordelta Np73 protein, humanDNA-Binding ProteinsE2F1 protein, humanE2F1 Transcription FactorNuclear ProteinsRetinoblastoma ProteinRNA, Small InterferingSp1 Transcription FactorTelomeraseTP73 protein, humanTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID16205639
OpenAlexW2045082628

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.