anti-ACSL4 antibody from antibodies-online

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anti-ACSL4 antibody

Description

Product Characteristics:
Acyl-CoA synthetases, also known as long-chain fatty-acid CoA synthases (FACL) or palmitoyl-CoA ligases, include ACSL1-6, which are all single-pass membrane proteins localizing to the mitochondrion, microsome or peroxisome. FACL proteins are important for synthesis of cellular lipids and for -oxidation degradation. Specifically, ACSL proteins catalyze the activation of long-chain fatty acids to acyl-CoAs, which can be metabolized to form CO2, triacylglycerol (TAG), phospholipids (PL) and cholesteryl esters (CE). ACSL3 preferentially utilizes laurate, myristate, arachidonate and eicosapentaenoate among saturated and unsaturated long chain fatty acids. FACL3 is expressed as two isoforms in various tissues, including brain, heart, placenta, prostate, skeletal muscle, testis and thymus. FACL4 preferentially utilizes arachidonate and is abundant in steroidogenic tissues. FACL4 may modulate female fertility and uterine prostaglandin production.

Subcellular location: Cytoplasm, Cell membrane

Synonyms: ACS 4, ACS4, ACSL 4, Acsl4, ACSL4_HUMAN, acyl CoA synthetase 4, Acyl CoA synthetase long chain family member 4, FACL 4, FACL4, Fatty acid Coenzyme A ligase, fatty acid Coenzyme A ligase long-chain 4, LACS 4, LACS4, Lignoceroyl CoA synthase, Long chain 4, long chain acyl CoA synthetase 4, long chain fatty acid CoA ligase 4, long chain fatty acid Coenzyme A ligase 4, Long-chain acyl-CoA synthetase 4, Long-chain-fatty-acid--CoA ligase 4, MRX63, MRX68.

Target Information: The protein encoded by this gene is an isozyme of the long-chain fatty-acid-coenzyme A ligase family. Although differing in substrate specificity, subcellular localization, and tissue distribution, all isozymes of this family convert free long-chain fatty acids into fatty acyl-CoA esters, and thereby play a key role in lipid biosynthesis and fatty acid degradation. This isozyme preferentially utilizes arachidonate as substrate. The absence of this enzyme may contribute to the mental retardation or Alport syndrome. Alternative splicing of this gene generates 2 transcript variants. [provided by RefSeq, Jul 2008]