Title : Cardiac and skeletal muscle defects in a mouse model of human Barth syndrome.

Pub. Date : 2011 Jan 14

PMID : 21068380






1 Functional Relationships(s)
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1 Tafazzin knockdown mice provide the first mammalian model system for Barth syndrome in which the pathophysiological relationships between altered content of mitochondrial phospholipids, ultrastructural abnormalities, myocardial and mitochondrial dysfunction, and clinical outcome can be completely investigated. Phospholipids tafazzin, phospholipid-lysophospholipid transacylase Mus musculus