TCDB is operated by the Saier Lab Bioinformatics Group
TRANSPORTERS FROM HUMANS:
Transporter Information:
Name: solute carrier family 27 (fatty acid transporter), member 3
Symbol: SLC27A3
TC: 9.B.17.1.5
Locations: 1q21.1
Aliases: FATP3, MGC4365
MGI: MGI:1347358
GenBank: BC003041
Swiss-Prot: Q9BTY5
Accession Number: NM_024330
GDBGDB:9956098
LocusLink11000
OMIM604193
PubMed (9671728): Hirsch D, Stahl A, Lodish HF. A family of fatty acid transporters conserved from mycobacterium to man.Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8625-9. PMID: 9671728 [PubMed - indexed for MEDLINE]

Long chain fatty acids (LCFAs) are an important source of energy for most organisms. They also function as blood hormones, regulating key metabolic functions such as hepatic glucose production. Although LCFAs can diffuse through the hydrophobic core of the plasma membrane into cells, this nonspecific transport cannot account for the high affinity and specific transport of LCFAs exhibited by cells such as cardiac muscle, hepatocytes, and adipocytes. Transport of LCFAs across the plasma membrane is facilitated by fatty acid transport protein (FATP), a plasma membrane protein that increases LCFA uptake when expressed in cultured mammalian cells [Schaffer, J. E. & Lodish, H. F. (1994) Cell 79, 427-436]. Here, we report the identification of four novel murine FATPs, one of which is expressed exclusively in liver and another only in liver and kidney. Both genes increase fatty acid uptake when expressed in mammalian cells. All five murine FATPs have homologues in humans in addition to a sixth FATP gene. FATPs are found in such diverse organisms as Fugu rubripes, Caenorhabditis elegans, Drosophila melanogaster, Saccharomyces cerevisiae, and Mycobacterium tuberculosis. The function of the FATP gene family is conserved throughout evolution as the C. elegans and mycobacterial FATPs facilitate LCFA uptake when overexpressed in COS cells or Escherichia coli, respectively. The identification of this evolutionary conserved fatty acid transporter family will allow us to gain a better understanding of the mechanisms whereby LCFAs traverse the lipid bilayer as well as yield insight into the control of energy homeostasis and its dysregulation in diseases such as diabetes and obesity.