Basic Information

Symbol
SLC27A2
RNA class
mRNA
Alias
Solute Carrier Family 27 Member 2 ACSVL1 FATP2 VLACS VLCS HsT17226 HFACVL1 FACVL1 Solute Carrier Family 27 (Fatty Acid Transporter), Member 2 Fatty-Acid-Coenzyme A Ligase, Very Long-Chain 1 Long-Chain Fatty Acid Transport Protein 2 Very Long-Chain-Fatty-Acid-CoA Ligase Very Long-Chain Acyl-CoA Synthetase Long-Chain-Fatty-Acid--CoA Ligase Fatty Acid Transport Protein 2 Arachidonate--CoA Ligase Phytanate--CoA Ligase THCA-CoA Ligase EC 6.2.1.7 FATP-2 Very Long-Chain Fatty-Acid-Coenzyme A Ligase 1 EC 6.2.1.15 EC 6.2.1.24 EC 6.2.1.3 EC 6.2.1.- EC 6.2.1
Location (GRCh38)
Forensic tag(s)
Other applications

MANE select

Transcript ID
NM_003645.4
Sequence length
2384.0 nt
GC content
0.4887

Transcripts

ID Sequence Length GC content
AGUCCUGCCCGGAACCCCCGGCAACGCGCAUACGACUACACCUGCUCCG… 2225 nt 0.4903
AGUCCUGCCCGGAACCCCCGGCAACGCGCAUACGACUACACCUGCUCCG… 2384 nt 0.4887
Summary

The protein encoded by this gene is an isozyme of 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 activates long-chain, branched-chain and very-long-chain fatty acids containing 22 or more carbons to their CoA derivatives. It is expressed primarily in liver and kidney, and is present in both endoplasmic reticulum and peroxisomes, but not in mitochondria. Its decreased peroxisomal enzyme activity is in part responsible for the biochemical pathology in X-linked adrenoleukodystrophy. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Apr 2009]

Forensic Context

A study in humans demonstrated that the SLC27A2 gene, involved in lipid and fatty acid metabolic processes, was the most downregulated transcript in subcutaneous adipose tissue of heavier co-twins from BMI-discordant monozygotic twin pairs, with a fold change of 0.1848 [Muniandy et al. DOI:10.1038/ijo.2017.95]. Subsequent multiomics research in human adipose tissue from similar twin cohorts confirmed the downregulation of the SLC27A2 in heavier individuals, associating this molecular change with broader mitochondrial dysfunction and altered lipid metabolism in acquired obesity [van der Kolk et al. DOI:10.1016/j.xcrm.2021.100226].