|Application ||WB, IF, E|
|Other Accession||NP_001986, 40807491|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||77 kDa|
|Application Notes||ACSL1 antibody can be used for detection of ACSL1 by Western blot at 1 - 2 µg/mL. For immunofluorescence start at 20 µg/mL.|
|Target/Specificity||ACSL1; At least three isoforms of ACSL1 are known to exist; this antibody will detect all three isoforms.|
|Reconstitution & Storage||ACSL1 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||ACSL1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||FACL1, FACL2, LACS, LACS1, LACS2|
|Function||Activation of long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. Preferentially uses palmitoleate, oleate and linoleate.|
|Cellular Location||Mitochondrion outer membrane; Single-pass type III membrane protein. Peroxisome membrane; Single-pass type III membrane protein. Microsome membrane; Single-pass type III membrane protein. Endoplasmic reticulum membrane; Single-pass type III membrane protein|
|Tissue Location||Highly expressed in liver, heart, skeletal muscle, kidney and erythroid cells, and to a lesser extent in brain, lung, placenta and pancreas.|
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Provided below are standard protocols that you may find useful for product applications.
ACSL1 Antibody: Long-chain acyl coenzyme A synthetase 1 (ACSL1) catalyzes the synthesis of acyl-CoA from long-chain fatty acids in an ATP-dependent manner. ACSL1 is a member of a family of long-chain acyl-CoA synthetases which differ in substrate preference, tissue expression, and subcellular localization. In mouse, ASCL1 is the major acyl-CoA enzyme in the heart, providing 60-90% of heart ATP. Loss of ASCL1 either globally or in heart ventricles resulted in impaired fatty acid oxidation, activation of the mammalian target of rapamycin (mTOR), and cardiac hypertrophy.
Black PN and DiRusso CC. Transmembrane movement of exogenous long-chain fatty acids: proteins, enzymes, and vectorial esterification. Microbiol. Mol. Biol. Rev. 2003; 67:454-72.
Coleman RA, Lewin TM, Van Horn CG, et al. Do acyl-CoA synthetases regulate fatty acid entry into synthetic versus degradative pathways? J. Nutr. 2002; 132:2123-6.
Clark H, Carling D, and Saggerson D. Covalent activation of heart AMP-activated protein kinase in response to physiological concentrations of long-chain fatty acids. Eur. J. Biochem. 2004; 271:2215-24
Ellis JM, Mentock SM, DePetrillo MA, et al. Mouse cardiac acyl Coenzyme A synthetase 1 deficiency impairs fatty acid oxidation and induces cardiac hypertrophy. Mol. Cell. Biol. 2011; 31:1252-62.
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