Table 1.

Characteristics of the ACSL family.

Name	Chromosome Localization	Size (Number of Amino Acids)	Molecular Mass (Da)	Preferential Substrate	Tissue Expression (Most Abundant)	Subcellular Distribution (Most Abundant)	Function
ACSL1	4q35.1	698	77,943	Palmitoleate, oleate and linoleate	Liver	Endoplasmic reticulum, mitochondrion	Catalyzes the conversion of long-chain fatty acids to their activated acyl-CoA forms for both cellular lipid synthesis and degradation via beta-oxidation.
ACSL3	2q36.1	720	80,420	Myristate, laurate, arachidonate and eicosapentaenoate	Nervous system	Golgi apparatus, endoplasmic reticulum	Activates long-chain fatty acids for both cellular lipid synthesis and degradation via beta-oxidation. Promotes hepatic lipogenesis and the incorporation of fatty acids into phosphatidylcholine.
ACSL4	Xq23	711	79,188	Arachidonate and eicosapentaenoate	Eye, stomach	Endoplasmic reticulum, mitochondrion, plasma membrane	Catalyzes the conversion of long-chain fatty acids to their activated acyl-CoA forms for both cellular lipid synthesis and degradation via beta-oxidation.
ACSL5	10q25.2	683	75,991	A wide range of saturated fatty acids and a preference for C16–C18 unsaturated fatty acids	Intestine	Endoplasmic reticulum, nucleus, mitochondrion, plasma membrane	Catalyzes the conversion of long-chain fatty acids to their activated acyl-CoA forms for both cellular lipid synthesis and degradation via beta-oxidation. Activates fatty acids from exogenous sources for the synthesis of triacylglycerol, which is destined for intracellular storage.
ACSL6	5q31	697	77,752	Equal preference for saturated and polyunsaturated fatty acids with a backbone of C16–C20	Nervous system	Endoplasmic reticulum, plasma membrane	Catalyzes the conversion of long-chain fatty acids to their activated acyl-CoA forms for both cellular lipid synthesis and degradation via beta-oxidation.