Alpha-methylacyl-CoA racemase (AMACR) primary role involves the racemization of 2-methyl-branched fatty acid CoA esters and the conversion of pristanoyl-CoA and C27-bile acyl-CoAs to their (S)-stereoisomers (1). A central role in all the metabolic pathways is played by AMACR, which regulates metabolism of lipids. AMACR regulates the entry of branched-chain lipids into the peroxisomal and mitochondrial beta-oxidation pathways (2). It has also been proven to be one of the few biomarkers that can help distinguish cancer from benign cells, with high sensitivity and specificity for prostate carcinoma (3). Defects in AMACR are the cause of alpha-methylacyl-CoA racemase deficiency (AMACRD) that results in elevated plasma concentrations of pristanic acid C27-bile-acid intermediates. It can be associated with polyneuropathy, retinitis pigmentosa and epilepsy (1).
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