|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||42387 Da|
|Other Names||Alpha-methylacyl-CoA racemase, 2-methylacyl-CoA racemase, AMACR|
|Target/Specificity||A synthetic peptide corresponding to residues in human AMACR was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||AMACR Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Racemization of 2-methyl-branched fatty acid CoA esters. Responsible for the conversion of pristanoyl-CoA and C27-bile acyl-CoAs to their (S)-stereoisomers.|
|Cellular Location||Peroxisome. Mitochondrion|
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Provided below are standard protocols that you may find useful for product applications.
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).
1. The UniProt Consortium, The Universal Protein Resource (UniProt), Nucleic Acids Res. 36:D190-D195 (2008) 2. Lloyd MD, et al. FEBS J. 275(6):1089-102, 2008 3. Jiang Z, et al. Am J Clin Pathol. 122(2):275-89, 2004
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