Evidence map›Paper›PMID 26397130›Full record

ArticleCell cycle (Georgetown, Tex.)2015

p53-mediated control of gene expression via mRNA translation during Endoplasmic Reticulum stress.

Ignacio López, Anne-Sophie Tournillon, Karin Nylander, Robin Fåhraeus

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Foxg1 and companions: Not only transcription factors.Neural regeneration research · 2026
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  5. Development of novel pyrimidine nucleoside analogs as potential anticancer agents: Synthesis, characterization, and In-vitro evaluation against pancreatic cancer.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2024
    Article
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  13. HSP90 inhibitors in the context of heat shock and the unfolded protein response: effects on a primary canine pulmonary adenocarcinoma cell line.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2017
    Article
  14. Review
  15. Article
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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

4 authors at 3 institutions in 3 countries.

Ignacio Lópeza Équipe Labellisée Ligue Contre le Cancer; Université Paris 7; INSERM UMR 1162 "Génomique fonctionnelle des tumeurs solides" ; Paris , France
Anne-Sophie Tournillona Équipe Labellisée Ligue Contre le Cancer; Université Paris 7; INSERM UMR 1162 "Génomique fonctionnelle des tumeurs solides" ; Paris , France
Karin Nylanderb Department of Medical Biosciences ; Umeå University ; Umeå , Sweden.
Robin Fåhraeusa Équipe Labellisée Ligue Contre le Cancer; Université Paris 7; INSERM UMR 1162 "Génomique fonctionnelle des tumeurs solides" ; Paris , France
Umeå University · SEInserm · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53 is activated by different stress and damage pathways and regulates cell biological responses including cell cycle arrest, repair pathways, apoptosis and senescence. Following DNA damage, the levels of p53 increase and via binding to target gene promoters, p53 induces expression of multiple genes including p21(CDKN1A) and mdm2. The effects of p53 on gene expression during the DNA damage response are well mimicked by overexpressing p53 under normal conditions. However, stress to the Endoplasmic Reticulum (ER) and the consequent Unfolded Protein Response (UPR) leads to the induction of the p53/47 isoform that lacks the first 40 aa of p53 and to an active suppression of p21(CDKN1A) transcription and mRNA translation. We now show that during ER stress p53 also suppresses MDM2 protein levels via a similar mechanism. These observations not only raise questions about the physiological role of MDM2 during ER stress but it also reveals a new facet of p53 as a repressor toward 2 of its major target genes during the UPR. As suppression of p21(CDKN1A) and MDM2 protein synthesis is mediated via their coding sequences, it raises the possibility that p53 controls mRNA translation via a common mechanism that might play an important role in how p53 regulates gene expression during the UPR, as compared to the transcription-dependent gene regulation taking place during the DNA damage response.

Indexed as

Endoplasmic Reticulum StressGene Expression Regulation, NeoplasticCyclin-Dependent Kinase Inhibitor p21Down-RegulationEndoplasmic Reticulum Chaperone BiPGene Knockdown TechniquesHCT116 CellsHeat-Shock ProteinsHumansNeoplasmsProto-Oncogene Proteins c-mdm2RNA, MessengerSignal TransductionTransfectionTumor Suppressor Protein p53Unfolded Protein ResponseCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Endoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsMDM2 protein, humanProto-Oncogene Proteins c-mdm2RNA, MessengerTP53 protein, humanTumor Suppressor Protein p53ER stressMDM2mRNA translationp53p53/47

Identifiers

PMID26397130
PMCPMC4825612
OpenAlexW2172764194

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.