Evidence map›Paper›PMID 12235210›Full record

ArticleThe Journal of experimental medicine2002

DeltaNp73, a dominant-negative inhibitor of wild-type p53 and TAp73, is up-regulated in human tumors.

Alex I Zaika, Neda Slade, Susan H Erster, Christine Sansome, Troy W Joseph, Michael Pearl, Eva Chalas, Ute M Moll

Expression of concernOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 146 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 1 pooled it
11.2field-weighted citation impact, top 1% 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

146 citing papers in PubMed, 1 synthesis or guideline pooled it, 317 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Dichotomous transactivation domains contribute to growth inhibitory and promotion functions of TAp73.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Article
  10. Article
  11. p53 Family in Resistance to Targeted Therapy of Melanoma.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. AlternativeBiomolecules · 2022
    Article
  16. 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
  17. Article
  18. Pathogenic Effect ofNeurology · 2021
    Article
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Alex I ZaikaDepartment of Pathology, Stony Brook University, Stony Brook, NY 11794, USA.
Neda Slade
Susan H Erster
Christine Sansome
Troy W Joseph
Michael Pearl
Eva Chalas
Ute M Moll
Stony Brook University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p73 has significant homology to p53. However, tumor-associated up-regulation of p73 and genetic data from human tumors and p73-deficient mice exclude a classical Knudson-type tumor suppressor role. We report that the human TP73 gene generates an NH(2) terminally truncated isoform. DeltaNp73 derives from an alternative promoter in intron 3 and lacks the transactivation domain of full-length TAp73. DeltaNp73 is frequently overexpressed in a variety of human cancers, but not in normal tissues. DeltaNp73 acts as a potent transdominant inhibitor of wild-type p53 and transactivation-competent TAp73. DeltaNp73 efficiently counteracts transactivation function, apoptosis, and growth suppression mediated by wild-type p53 and TAp73, and confers drug resistance to wild-type p53 harboring tumor cells. Conversely, down-regulation of endogenous DeltaNp73 levels by antisense methods alleviates its suppressive action and enhances p53- and TAp73-mediated apoptosis. DeltaNp73 is complexed with wild-type p53, as demonstrated by coimmunoprecipitation from cultured cells and primary tumors. Thus, DeltaNp73 mediates a novel inactivation mechanism of p53 and TAp73 via a dominant-negative family network. Deregulated expression of DeltaNp73 can bestow oncogenic activity upon the TP73 gene by functionally inactivating the suppressor action of p53 and TAp73. This trait might be selected for in human cancers.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBase SequenceDNADNA-Binding ProteinsDNA DamageDrug Resistance, NeoplasmGenes, Tumor SuppressorHumansMiceMolecular Sequence DataMutationNuclear ProteinsTumor Protein p73Tumor Suppressor Protein p53delta Np73 protein, humanDNADNA-Binding ProteinsNuclear ProteinsTP73 protein, humanTrp73 protein, mouseTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID12235210
PMCPMC2194062
OpenAlexW2165454946

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.