Evidence map›Paper›PMID 18805989›Full record

ArticleGenes & development2008

TAp73 knockout shows genomic instability with infertility and tumor suppressor functions.

Richard Tomasini, Katsuya Tsuchihara, Margareta Wilhelm, Masashi Fujitani, Alessandro Rufini, Carol C Cheung, Fatima Khan, Annick Itie-Youten, Andrew Wakeham, Ming-Sound Tsao and 7 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 279 papers.

0numbers the graph read from it
0cells of the map it votes in
279citing papers in PubMed
–field-weighted citation impact
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

279 citing papers in PubMed, 430 citations in OpenAlex.

  1. Article
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  3. Metabolomic Analysis Identifies Betaine as a Key Mediator ofInternational journal of molecular sciences · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. 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
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Regulation of Oocyte Apoptosis: A View from Gene Knockout Mice.International journal of molecular sciences · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. p53 Controls Meiotic Prophase Progression and Crossover Formation.International journal of molecular sciences · 2022
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 9 institutions in 5 countries.

Richard TomasiniThe Campbell Family Institute for Breast Cancer Research, Princess Margaret Hospital, Toronto, Ontario M5G 2C1, Canada.
Katsuya Tsuchihara
Margareta Wilhelm
Masashi Fujitani
Alessandro Rufini
Carol C Cheung
Fatima Khan
Annick Itie-Youten
Andrew Wakeham
Ming-Sound Tsao
Juan L Iovanna
Jeremy Squire
Igor Jurisica
David Kaplan
Gerry Melino
Andrea Jurisicova
Tak W Mak
Princess Margaret Cancer Centre · CAUniversity of Toronto · CAInserm · FRMount Sinai Hospital · CADiscovery Centre · CAHospital for Sick Children · CAMedical Research Council · GBNational Cancer Center Hospital East · JPUniversity of Rome Tor Vergata · IT

Funding

Medical Research Council MC_U132670600
6 · The paper itself

Abstract

The Trp53 gene family member Trp73 encodes two major groups of protein isoforms, TAp73 and DeltaNp73, with opposing pro- and anti-apoptotic functions; consequently, their relative ratio regulates cell fate. However, the precise roles of p73 isoforms in cellular events such as tumor initiation, embryonic development, and cell death remain unclear. To determine which aspects of p73 function are attributable to the TAp73 isoforms, we generated and characterized mice in which exons encoding the TAp73 isoforms were specifically deleted to create a TAp73-deficient (TAp73(-/-)) mouse. Here we show that mice specifically lacking in TAp73 isoforms develop a phenotype intermediate between the phenotypes of Trp73(-/-) and Trp53(-/-) mice with respect to incidence of spontaneous and carcinogen-induced tumors, infertility, and aging, as well as hippocampal dysgenesis. In addition, cells from TAp73(-/-) mice exhibit genomic instability associated with enhanced aneuploidy, which may account for the increased incidence of spontaneous tumors observed in these mutants. Hence, TAp73 isoforms exert tumor-suppressive functions and indicate an emerging role for Trp73 in the maintenance of genomic stability.

Indexed as

Genomic InstabilityAgingAneuploidyAnimalsBase SequenceDNA PrimersEmbryonic DevelopmentFemaleGenes, Tumor SuppressorHippocampusInfertility, FemaleMaleMiceMice, Inbred C57BLMice, KnockoutNeoplasmsdelta Np73, mouseDNA PrimersNuclear ProteinsTumor Suppressor Protein p53

Identifiers

PMID18805989
PMCPMC2559903
OpenAlexW2100610935

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.