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Tafazzin is a transacylase involved in cardiolipin remodeling.1 It is composed of a transmembrane domain, an HX4D motif, two targeting domains flanking the transacylase active site, and a membrane anchor. Tafazzin is expressed in a wide variety of tissues, including cardiac and skeletal muscle, and is localized to the inner and outer mitochondrial membranes.1,2 It transfers acyl chains from phospholipids to monolysocardiolipin (MLCL) to form mature cardiolipin, with a preference for transferring linoleic acid from phosphatidylcholine to MLCL.1,3 Due to its role in determining cardiolipin composition, tafazzin activity indirectly affects mitochondrial function, including oxidative phosphorylation, oxidative stress repair, and apoptosis.1 Mutations in TAFAZZIN are associated with Barth syndrome, an X-linked disorder characterized by cardiovascular, musculoskeletal, and neurological pathologies.3 Cayman’s Tafazzin Polyclonal Antibody can be used for immunohistochemistry using paraffin-embedded samples (IHC-P), immunoprecipitation (IP), and Western blot (WB) applications.
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1. TAZ encodes tafazzin, a transacylase essential for cardiolipin formation and central to the etiology of Barth syndrome. Gene 726, 144148 (2020).
2. Complex expression pattern of the Barth syndrome gene product tafazzin in human cell lines and murine tissues. Biochem. Cell Biol. 82(5), 569-576 (2004).
3. Role of Tafazzin in mitochondrial function, development and disease. J. Dev. Biol. 8(2), 10 (2020).