Evidence map›Paper›PMID 29796387›Full record

ArticleMicrobial cell (Graz, Austria)2018

Decreasing cytosolic translation is beneficial to yeast and human Tafazzin-deficient cells.

Maxence de Taffin de Tilques, Jean-Paul Lasserre, François Godard, Elodie Sardin, Marine Bouhier, Marina Le Guedard, Roza Kucharczyk, Patrice X Petit, Eric Testet, Jean-Paul di Rago and 1 more

Open access · goldAbstract read
In one paragraph

Article in Microbial cell (Graz, Austria), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  5. Article
  6. Article
  7. Experimental models of Barth syndrome.Journal of inherited metabolic disease · 2022
    Review
  8. 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

11 authors at 3 institutions in 4 countries.

Maxence de Taffin de TilquesInstitut de Biochimie et Génétique Cellulaires, CNRS UMR 5095, Université de Bordeaux, 1 rue Camille Saint-Saëns, 33077 Bordeaux cedex, France.
Jean-Paul LasserreInstitut de Biochimie et Génétique Cellulaires, CNRS UMR 5095, Université de Bordeaux, 1 rue Camille Saint-Saëns, 33077 Bordeaux cedex, France.
François GodardInstitut de Biochimie et Génétique Cellulaires, CNRS UMR 5095, Université de Bordeaux, 1 rue Camille Saint-Saëns, 33077 Bordeaux cedex, France.
Elodie SardinInstitut de Biochimie et Génétique Cellulaires, CNRS UMR 5095, Université de Bordeaux, 1 rue Camille Saint-Saëns, 33077 Bordeaux cedex, France.
Marine BouhierInstitut de Biochimie et Génétique Cellulaires, CNRS UMR 5095, Université de Bordeaux, 1 rue Camille Saint-Saëns, 33077 Bordeaux cedex, France.
Marina Le GuedardLaboratoire de Biogenèse Membranaire, CNRS UMR 5200, Université de Bordeaux, INRA Bordeaux Aquitaine, Villenave d'Ornon, France.
Roza KucharczykInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland.
Patrice X PetitCNRS FR3636 Fédération de recherché en Neuroscience, Université Paris-Descartes, 45, rue des Saints-Pères, 75006 Paris, France.
Eric TestetLaboratoire de Biogenèse Membranaire, CNRS UMR 5200, Université de Bordeaux, INRA Bordeaux Aquitaine, Villenave d'Ornon, France.
Jean-Paul di RagoInstitut de Biochimie et Génétique Cellulaires, CNRS UMR 5095, Université de Bordeaux, 1 rue Camille Saint-Saëns, 33077 Bordeaux cedex, France.
Déborah Tribouillard-TanvierInstitut de Biochimie et Génétique Cellulaires, CNRS UMR 5095, Université de Bordeaux, 1 rue Camille Saint-Saëns, 33077 Bordeaux cedex, France.
Centre National de la Recherche Scientifique · FRDélégation Paris 5 · FRInstitute of Biochemistry and Biophysics, Polish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiolipin (CL) optimizes diverse mitochondrial processes, including oxidative phosphorylation (OXPHOS). To function properly, CL needs to be unsaturated, which requires the acyltransferase Tafazzin (TAZ). Loss-of-function mutations in the TAZ gene are responsible for the Barth syndrome (BTHS), a rare X-linked cardiomyopathy, presumably because of a diminished OXPHOS capacity. Herein we show that a partial inhibition of cytosolic protein synthesis, either chemically with the use of cycloheximide or by specific genetic mutations, fully restores biogenesis and the activity of the oxidative phosphorylation system in a yeast BTHS model (

Indexed as

Barth syndromecycloheximide; cardiolipin remodelingcytosolic protein synthesismitochondrial diseaseoxidative phosphorylation

Identifiers

PMID29796387
PMCPMC5961916
OpenAlexW2789988471

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.