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Article

TAZ encodes tafazzin, a transacylase essential for cardiolipin formation and central to the etiology of Barth syndrome

21 Oct 2019

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Share to Cardiac electrophysiology and arrhythmias
Share to Ion channel regulation and function
Share to Mitochondrial Function and Pathology

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 31647997
DOI: 10.1016/j.gene.2019.144148

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TAZ encodes tafazzin, a transacylase essential for cardiolipin formation and central to the etiology of Barth syndromePMID 31647997Read ↗

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

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

Cardiolipin metabolism and Barth Syndrome.Semantic proximity Read ↗

A novel mutation in TAZ causes mitochondrial respiratory chain disorder without cardiomyopathy.Semantic proximity Read ↗

Defining functional classes of Barth syndrome mutation in humans.Semantic proximity Read ↗

Clinical presentation and natural history of Barth Syndrome: An overview.Semantic proximity Read ↗

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

The Role of Cardiolipin in Cardiovascular HealthSemantic proximity Read ↗

Seven functional classes of Barth syndrome mutation.Semantic proximity Read ↗

Experimental models of Barth syndrome.Semantic proximity Read ↗

The lipid environment modulates cardiolipin and phospholipid constitution in wild type and tafazzin-deficient cells.Semantic proximity Read ↗

A novel TAZ gene mutation and mosaicism in a Polish family with Barth syndrome.Semantic proximity Read ↗

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