ACSL5
ACSL5 (acyl-CoA synthetase long chain family member 5, also known as ACS5, ACS2 and FACL5) is a long-chain-fatty-acid--CoA ligase that converts long-chain fatty acids into their active acyl-CoA form. It supports both lipid synthesis and fatty acid degradation. Browse Assay Genie's current range of ACSL5 research reagents below, or read on for the biology behind the target.
ACSL5 catalyses the conversion of long-chain fatty acids to acyl-CoAs, the active form needed both for the synthesis of cellular lipids and for degradation by beta-oxidation. It may activate fatty acids taken up from exogenous sources for the synthesis of triacylglycerol destined for intracellular storage, and it has also been suggested to stimulate fatty acid oxidation. The enzyme uses a wide range of saturated fatty acids, with a preference for C16-C18 unsaturated fatty acids.
The ACSL5 gene encodes one isozyme of the long-chain fatty-acid-coenzyme A ligase family. Members of this family differ in substrate specificity, subcellular localisation and tissue distribution, but all convert free long-chain fatty acids into fatty acyl-CoA esters. The ACSL5 protein belongs to the ATP-dependent AMP-binding enzyme family and is annotated at the mitochondrion, the endoplasmic reticulum, the mitochondrial outer membrane, the endoplasmic reticulum membrane and the cell membrane. It is highly expressed in uterus and spleen, and only in trace amounts in normal brain. Three transcript variants encoding two different isoforms have been described.
ACSL5 has also been linked to cell fate. At the villus tip of the crypt-villus axis in the small intestine, it may sensitise epithelial cells to apoptosis triggered by the death ligand TRAIL. Levels are markedly increased in malignant gliomas, where the gene mediates fatty acid-induced glioma cell growth and the protein may contribute to glioma cell survival. Earlier names for the gene include fatty-acid-Coenzyme A ligase, long-chain 5.
ACSL5 may activate exogenous fatty acids for triacylglycerol synthesis and intracellular storage, making it relevant to studies of cellular lipid handling.
By producing acyl-CoAs for beta-oxidation, and possibly stimulating fatty acid oxidation, ACSL5 is a candidate node in fatty acid catabolism research.
ACSL5 is markedly raised in malignant gliomas and mediates fatty acid-induced glioma cell growth, with a suggested role in glioma cell survival.
At the small intestinal villus tip, ACSL5 may sensitise epithelial cells to TRAIL-triggered apoptosis, linking lipid metabolism to cell death.
ACSL5 converts long-chain fatty acids into acyl-CoAs, the active form used for lipid synthesis and for beta-oxidation. It may channel exogenous fatty acids into triacylglycerol storage and prefers C16-C18 unsaturated fatty acids, though it uses a wide range of saturated ones.
ACSL5 is also called ACS5, ACS2 and FACL5, and its UniProt name is long-chain-fatty-acid--CoA ligase 5. A previous gene name was fatty-acid-Coenzyme A ligase, long-chain 5. Three transcript variants encode two different isoforms.
ACSL5 levels are markedly increased in malignant gliomas, and the gene mediates fatty acid-induced glioma cell growth. Orthologues exist as Acsl5 in mouse and rat; check the datasheet of any product for its validated reactivity.
Other long-chain acyl-CoA synthetase family members and lipid metabolism targets with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q9ULC5; product specifications from Assay Genie datasheets.