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Article

The mitochondrial quality control protein Yme1 is necessary to prevent defective mitophagy in a yeast model of Barth syndrome.

The Journal of biological chemistry - 3 Apr 2015

Gaspard Gerard J, McMaster Christopher R

Abstract excerpt

The Saccharomyces cerevisiae TAZ1 gene is an orthologue of human TAZ; both encode the protein tafazzin. Tafazzin is a transacylase that transfers acyl chains with unsaturated fatty acids from phospholipids to monolysocardiolipin to generate cardiolipin with unsaturated fatty acids. Mutations in human TAZ cause Barth syndrome, a fatal childhood cardiomyopathy biochemically characterized by reduced cardiolipin mass...

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Identifiers

PMID: 25688091
DOI: 10.1074/jbc.M115.641878
PMCID: PMC4423712

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

The mitochondrial quality control protein Yme1 is necessary to prevent defective mitophagy in a yeast model of Barth syndrome.PMID 25688091Read ↗

Cardiolipin remodeling by TAZ/tafazzin is selectively required for the initiation of mitophagy.Semantic proximity Read ↗

Barth syndrome cellular models have dysregulated respiratory chain complex I and mitochondrial quality control due to abnormal cardiolipinSemantic proximity Read ↗

Tafazzin Mutation Affecting Cardiolipin Leads to Increased Mitochondrial Superoxide Anions and Mitophagy Inhibition in Barth Syndrome.Semantic proximity Read ↗

Taz1, an outer mitochondrial membrane protein, affects stability and assembly of inner membrane protein complexes: implications for Barth Syndrome.Semantic proximity Read ↗

Barth syndrome mutations that cause tafazzin complex lability.Semantic proximity Read ↗

Blocking phosphatidylglycerol degradation in yeast defective in cardiolipin remodeling results in a new model of the Barth syndrome cellular phenotype.Semantic proximity Read ↗

Barth syndrome: cellular compensation of mitochondrial dysfunction and apoptosis inhibition due to changes in cardiolipin remodeling linked to tafazzin (TAZ) gene mutation.Semantic proximity Read ↗

The Function of Tafazzin, a Mitochondrial Phospholipid-Lysophospholipid Acyltransferase.Semantic proximity Read ↗

Deacylation on the matrix side of the mitochondrial inner membrane regulates cardiolipin remodeling.Semantic proximity Read ↗

Tafazzin-Mediated Cardiolipin Remodeling Controls Metabolic Stress Response and Effector Function of Inflammatory T CellsSemantic proximity Read ↗

The human TAZ gene complements mitochondrial dysfunction in the yeast taz1Delta mutant. Implications for Barth syndrome.Semantic proximity Read ↗

Restoration of mitophagy ameliorates cardiomyopathy in Barth syndromeSemantic proximity Read ↗

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