Evidence map›Paper›PMID 22898807›Full record

ArticleCell death and differentiation2013

Drosophila p53 isoforms differentially regulate apoptosis and apoptosis-induced proliferation.

M-L Dichtel-Danjoy, D Ma, P Dourlen, G Chatelain, F Napoletano, M Robin, M Corbet, C Levet, H Hafsi, P Hainaut and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. The Dynamic Alliance of p53 and Metabolism in the Tumor Microenvironment Shapes Tumor Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022
    Review
  7. eLife · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Conformational stability and dynamics of the cancer-associated isoform Δ133p53β are modulated by p53 peptides and p53-specific DNA.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  16. P53 and Apoptosis in the Drosophila Model.Advances in experimental medicine and biology · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. p53 on the crossroad between regeneration and cancer.Cell death and differentiation · 2017
    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

13 authors at 5 institutions in 3 countries.

M-L Dichtel-DanjoyGroup Apoptosis and Neurogenetics, Laboratory of Molecular Biology of the Cell, CNRS UMR5239, Ecole Normale Supérieure de Lyon, UMS3444 Biosciences Lyon Gerland, Université de Lyon, Lyon, France.
D Ma
P Dourlen
G Chatelain
F Napoletano
M Robin
M Corbet
C Levet
H Hafsi
P Hainaut
H D Ryoo
J-C Bourdon
B Mollereau
Université Claude Bernard Lyon 1 · FRCentre international de recherche sur le cancer · FRNew York University · USUniversity of Dundee · GBUniversity of Strathclyde · GB

Funding

Coordination of Apoptosis and Cell Proliferation in DrosophilaR01GM079425 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RYOO, HYUNG D · 2007 to 2011
$1.8M
NIGMS NIH HHS R01 GM079425NIGMS NIH HHS R01GM079425
6 · The paper itself

Abstract

Irradiated or injured cells enter apoptosis, and in turn, promote proliferation of surrounding unaffected cells. In Drosophila, apoptotic cells have an active role in proliferation, where the caspase Dronc and p53 induce mitogen expression and growth in the surrounding tissues. The Drosophila p53 gene structure is conserved and encodes at least two protein isoforms: a full-length isoform (Dp53) and an N-terminally truncated isoform (DΔNp53). Historically, DΔNp53 was the first p53 isoform identified and was thought to be responsible for all p53 biological activities. It was shown that DΔNp53 induces apoptosis by inducing the expression of IAP antagonists, such as Reaper. Here we investigated the roles of Dp53 and DΔNp53 in apoptosis and apoptosis-induced proliferation. We found that both isoforms were capable of activating apoptosis, but that they each induced distinct IAP antagonists. Expression of DΔNp53 induced Wingless (Wg) expression and enhanced proliferation in both 'undead cells' and in 'genuine' apoptotic cells. In contrast to DΔNp53, Dp53 did not induce Wg expression in the absence of the endogenous p53 gene. Thus, we propose that DΔNp53 is the main isoform that regulates apoptosis-induced proliferation. Understanding the roles of Drosophila p53 isoforms in apoptosis and in apoptosis-induced proliferation may shed new light on the roles of p53 isoforms in humans, with important implications in cancer biology.

Indexed as

AnimalsAnimals, Genetically ModifiedApoptosisCell Growth ProcessesDrosophilaProtein IsoformsSignal TransductionTumor Suppressor Protein p53Protein IsoformsTumor Suppressor Protein p53

Identifiers

PMID22898807
PMCPMC3524635
OpenAlexW2008004544

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.