Beta-hydroxybutyrate mitigates bioenergetic deficits in the Tafazzin shRNA mouse model of Barth Syndrome
The respiratory profile of tafazzin-deficient cells is robust against lipid supplementation-induced alterations of mitochondrial membranes
Use of novel iPSC-derived skeletal muscle model to understand mitochondrial phenotypes of TAFAZZIN-deficiency in Barth syndrome
Barth syndorme, tafazzin and mitochondrial lyso-PC acyltransferase.
