Mitochondrial cardiolipin involved in outer-membrane protein biogenesis: implications for Barth syndrome.
Barth syndrome: an X-linked cause of fetal cardiomyopathy and stillbirth.
Mitochondrial dysfunction and organic aciduria in five patients carrying mutations in the Ras-MAPK pathway.
Cardiac and skeletal muscle defects in a mouse model of human Barth syndrome.
Characterization of a transgenic short hairpin RNA-induced murine model of Tafazzin deficiency.
Barth syndrome mutations that cause tafazzin complex lability.
Impaired cardiac reserve and severely diminished skeletal muscle O(2) utilization mediate exercise intolerance in Barth syndrome.
Substrate metabolism during basal and hyperinsulinemic conditions in adolescents and young-adults with Barth syndrome.