Evidence map›Paper›PMID 23966169›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Mitochondrial p53 mediates a transcription-independent regulation of cell respiration and interacts with the mitochondrial F₁F0-ATP synthase.

Marie Bergeaud, Lise Mathieu, Arnaud Guillaume, Ute M Moll, Bernard Mignotte, Nathalie Le Floch, Jean-Luc Vayssière, Vincent Rincheval

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

43 citing papers in PubMed, 64 citations in OpenAlex.

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  15. Natural products and other inhibitors of FEuropean journal of medicinal chemistry · 2020
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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

8 authors at 4 institutions in 2 countries.

Marie BergeaudLaboratoire de génétique et biologie cellulaire (LGBC); Université de Versailles St Quentin-en-Yvelines/Ecole Pratique des Hautes Etudes; UFR des Sciences de la Santé; Montigny-le-Bretonneux, France.
Lise Mathieu
Arnaud Guillaume
Ute M Moll
Bernard Mignotte
Nathalie Le Floch
Jean-Luc Vayssière
Vincent Rincheval
Laboratoire de Génétique Cellulaire · FRÉcole Pratique des Hautes Études · FRLaboratoire de génétique et biologie cellulaireStony Brook University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We and others previously reported that endogenous p53 can be located at mitochondria in the absence of stress, suggesting that p53 has a role in the normal physiology of this organelle. The aim of this study was to characterize in unstressed cells the intramitochondrial localization of p53 and identify new partners and functions of p53 in mitochondria. We find that the intramitochondrial pool of p53 is located in the intermembrane space and the matrix. Of note, unstressed HCT116 p53(+/+) cells simultaneously show increased O₂ consumption and decreased mitochondrial superoxide production compared with their p53-null counterpart. This data was confirmed by stable H1299 cell lines expressing low levels of p53 specifically targeted to the matrix. Using immunoprecipitation and mass spectrometry, we identified the oligomycin sensitivity-conferring protein (OSCP), a subunit of the F₁F₀-ATP synthase complex, as a new partner of endogenous p53, specifically interacting with p53 localized in the matrix. Interestingly, this interaction seems implicated in mitochondrial p53 localization. Moreover, p53 localized in the matrix promotes the assembly of F₁F₀-ATP synthase. Taking into account that deregulations of mitochondrial respiration and reactive oxygen species production are tightly linked to cancer development, we suggest that mitochondrial p53 may be an important regulator of normal mitochondrial and cellular physiology, potentially exerting tumor suppression activity inside mitochondria.

Indexed as

Transcription, GeneticAdenosine TriphosphatasesAmino Acid SequenceCarrier ProteinsCell RespirationEnzyme StabilityGene Knockdown TechniquesHCT116 CellsHumansMembrane ProteinsMitochondriaMitochondrial MembranesMitochondrial Proton-Translocating ATPasesMolecular Sequence DataOxygen ConsumptionProtein BindingAdenosine TriphosphatasesCarrier ProteinsF1F0-ATP synthaseMembrane ProteinsMitochondrial Proton-Translocating ATPasesoligomycin sensitivity-conferring proteinReactive Oxygen SpeciesTumor Suppressor Protein p53cancerenergetic metabolismmitochondriaOSCPoxidative phosphorylationp53reactive oxygen speciesrespirationtumor suppressor

Identifiers

PMID23966169
PMCPMC3899192
OpenAlexW2054257071

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.