Evidence map›Paper›PMID 34824391›Full record

ArticleCell death and differentiation2022

Coordination between cell proliferation and apoptosis after DNA damage in Drosophila.

Mireya Ruiz-Losada, Raul González, Ana Peropadre, Alejandro Gil-Gálvez, Juan J Tena, Antonio Baonza, Carlos Estella

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 71 citations in OpenAlex.

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  6. Cell size modulates ferroptosis susceptibility.bioRxiv : the preprint server for biology · 2026
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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

7 authors at 4 institutions in 2 countries.

Mireya Ruiz-LosadaCentro de Biología Molecular "Severo Ochoa", CSIC-UAM, C/Nicolás Cabrera 1, 28049, Madrid, Spain.ORCID http://orcid.org/0000-0001-5125-4674
Raul GonzálezCentro de Biología Molecular "Severo Ochoa", CSIC-UAM, C/Nicolás Cabrera 1, 28049, Madrid, Spain.
Ana PeropadreDepartment of Biology, Faculty of Sciences, Universidad Autónoma de Madrid, C/Darwin 2, 28049, Madrid, Spain.ORCID http://orcid.org/0000-0002-0787-9391
Alejandro Gil-GálvezCentro Andaluz de Biología del Desarrollo (CABD), CSIC-Universidad Pablo de Olavide-Junta de Andalucía, Seville, Spain.
Juan J TenaCentro Andaluz de Biología del Desarrollo (CABD), CSIC-Universidad Pablo de Olavide-Junta de Andalucía, Seville, Spain.
Antonio BaonzaCentro de Biología Molecular "Severo Ochoa", CSIC-UAM, C/Nicolás Cabrera 1, 28049, Madrid, Spain.ORCID http://orcid.org/0000-0003-3252-0038
Carlos EstellaCentro de Biología Molecular "Severo Ochoa", CSIC-UAM, C/Nicolás Cabrera 1, 28049, Madrid, Spain. cestella@cbm.csic.es.ORCID http://orcid.org/0000-0003-1551-2327
Centro de Biología Molecular Severo Ochoa · ESCentro Andaluz de Biología del Desarrollo · ESHeidelberg University · DEUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to genotoxic stress promotes cell cycle arrest and DNA repair or apoptosis. These "life" or "death" cell fate decisions often rely on the activity of the tumor suppressor gene p53. Therefore, the precise regulation of p53 is essential to maintain tissue homeostasis and to prevent cancer development. However, how cell cycle progression has an impact on p53 cell fate decision-making is mostly unknown. In this work, we demonstrate that Drosophila p53 proapoptotic activity can be impacted by the G2/M kinase Cdk1. We find that cell cycle arrested or endocycle-induced cells are refractory to ionizing radiation-induced apoptosis. We show that p53 binding to the regulatory elements of the proapoptotic genes and its ability to activate their expression is compromised in experimentally arrested cells. Our results indicate that p53 genetically and physically interacts with Cdk1 and that p53 proapoptotic role is regulated by the cell cycle status of the cell. We propose a model in which cell cycle progression and p53 proapoptotic activity are molecularly connected to coordinate the appropriate response after DNA damage.

Indexed as

DrosophilaTumor Suppressor Protein p53AnimalsApoptosisCell CycleCell ProliferationDNA DamageTumor Suppressor Protein p53

Identifiers

PMID34824391
PMCPMC8989919
OpenAlexW3216134382

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.