Evidence map›Paper›PMID 23159862›Full record

ArticleCell cycle (Georgetown, Tex.)2012

Tissue-specific expression of p73 C-terminal isoforms in mice.

Francesca Grespi, Ivano Amelio, Paola Tucci, Margherita Annicchiarico-Petruzzelli, Gerry Melino

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

27 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. 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
  7. Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022
    Review
  8. Review
  9. Article
  10. Regulation of Adult Neurogenesis in Mammalian Brain.International journal of molecular sciences · 2020
    Review
  11. The C terminus of p73 is essential for hippocampal development.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. P73 C-terminus is dispensable for multiciliogenesis.Cell cycle (Georgetown, Tex.) · 2020
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. TAp73 upregulates IL-1β in cancer cells: Potential biomarker in lung and breast cancer?Biochemical and biophysical research communications · 2017
    Article
  19. How Does p73 Cause Neuronal Defects?Molecular neurobiology · 2016
    Review
  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

5 authors at 4 institutions in 3 countries.

Francesca GrespiMedical Research Council, Toxicology Unit, Leicester University, Leicester, UK.
Ivano Amelio
Paola Tucci
Margherita Annicchiarico-Petruzzelli
Gerry Melino
University of Leicester · GBGhent University Hospital · BEMedical Research Council · GBUniversity of Rome Tor Vergata · IT

Funding

Medical Research Council MC_U132670600
6 · The paper itself

Abstract

p73 is a p53 family transcription factor. Due to the presence in the 5' flanking region of two promoters, there are two N-terminal variants, TAp73, which retains a fully active transactivation domain (TA), and ΔNp73, in which the N terminus is truncated. In addition, extensive 3' splicing gives rise to at least seven distinctive isoforms; TAp73-selective knockout highlights its role as a regulator of cell death, senescence and tumor suppressor. ΔNp73-selective knockout, on the other hand, highlights anti-apoptotic function of ΔNp73 and its involvement in DNA damage response. In this work, we investigated the expression pattern of murine p73 C-terminal isoforms. By using a RT-PCR approach, we were able to detect mRNAs of all the C-terminal isoforms described in humans. We characterized their in vivo expression profile in mouse organs and in different mouse developmental stages. Finally, we investigated p73 C-terminal expression profile following DNA damage, ex vivo after primary cultures treatment and in vivo after systemic administration of cytotoxic compounds. Overall, our study first elucidates spatio-temporal expression of mouse p73 isoforms and provides novel insights on their expression-switch under triggered conditions.

Indexed as

AnimalsAntineoplastic AgentsCells, CulturedCisplatinDNA-Binding ProteinsDNA DamageEmbryonic DevelopmentEtoposideGene ExpressionMiceNuclear ProteinsProtein IsoformsProtein Structure, TertiaryReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSpleenAntineoplastic AgentsCisplatindelta Np73 protein, humanDNA-Binding ProteinsEtoposideNuclear ProteinsProtein IsoformsRNA, MessengerTP73 protein, humanTrp73 protein, mouseTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID23159862
PMCPMC3552929
OpenAlexW2057217501

What OpenQuestion holds

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LicenceCC BY-NC
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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.