Molecule Information

General Information of the Molecule (ID: Mol01946)

• Name: Very long-chain acyl-CoA synthetase (S27A2) ,Homo sapiens
• Synonyms: SLC27A2; ACSVL1; FACVL1; FATP2; VLACS
• Molecule Type: Protein
• Gene Name: S27A2
• Gene ID: 11001
• Location: chr15:50,182,196-50,236,385[+]
• Sequence:
  MLSAIYTVLAGLLFLPLLVNLCCPYFFQDIGYFLKVAAVGRRVRSYGKRRPARTILRAFL
  EKARQTPHKPFLLFRDETLTYAQVDRRSNQVARALHDHLGLRQGDCVALLMGNEPAYVWL
  WLGLVKLGCAMACLNYNIRAKSLLHCFQCCGAKVLLVSPELQAAVEEILPSLKKDDVSIY
  YVSRTSNTDGIDSFLDKVDEVSTEPIPESWRSEVTFSTPALYIYTSGTTGLPKAAMITHQ
  RIWYGTGLTFVSGLKADDVIYITLPFYHSAALLIGIHGCIVAGATLALRTKFSASQFWDD
  CRKYNVTVIQYIGELLRYLCNSPQKPNDRDHKVRLALGNGLRGDVWRQFVKRFGDICIYE
  FYAATEGNIGFMNYARKVGAVGRVNYLQKKIITYDLIKYDVEKDEPVRDENGYCVRVPKG
  EVGLLVCKITQLTPFNGYAGAKAQTEKKKLRDVFKKGDLYFNSGDLLMVDHENFIYFHDR
  VGDTFRWKGENVATTEVADTVGLVDFVQEVNVYGVHVPDHEGRIGMASIKMKENHEFDGK
  KLFQHIADYLPSYARPRFLRIQDTIEITGTFKHRKMTLVEEGFNPAVIKDALYFLDDTAK
  MYVPMTEDIYNAISAKTLKL
• Function: Acyl CoA synthetase that activates long-chain and very long-chain fatty acids (VLCFAs) by catalyzing the formation of fatty acyl-CoA. Can also activate branched-chain fatty acids such as phytanic acid and pristanic acid. Does not activate C24 bile acids, cholate and chenodeoxycholate. In vitro, activates 3-alpha,7-alpha,12-alpha-trihydroxy-5-beta-cholestanate (THCA), the C27 precursor of cholic acid deriving from the de novo synthesis from cholesterol. Exhibits long-chain fatty acids (LCFA) transport activity and plays an important role in hepatic fatty acid uptake.
• Uniprot ID: S27A2_HUMAN
• Ensembl ID: ENSG00000140284

Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens

Type(s) of Resistant Mechanism of This Molecule

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Drug

Approved Drug(s) 1 drug(s) in total

Insulin

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Disease Class: Type 2 diabetes mellitus [1]

• Sensitive Disease: Type 2 diabetes mellitus [ICD-11: 5A11.0]
• Sensitive Drug: Insulin
• Molecule Alteration: Expression; Down-regulation
• Experimental Note: Identified from the Human Clinical Data
• Mechanism Description: Several studies have shown that lipid accumulation in liver and skeletal muscle caused by short-term HFD feeding or lipid/heparin infusions induce insulin resistance in rats. In addition, overexpression of lipoprotein lipase (LPL) in liver or muscle induced peripheral insulin resistance and the accumulation of lipid in respective tissues, and skeletal muscle-specific LPL deletion enhanced insulin signaling in HFD challenged muscle. Furthermore, deleting fat transport proteins such as CD36 or FATP-1 increased insulin-mediated glucose uptake in skeletal muscle, and liver-specific knockdown of FATP2 or FATP5 significantly reduced HFD-induced hepatosteatosis and increased glucose tolerance.

Disease- and Tissue-specific Abundances of This Molecule

ICD Disease Classification 05

Type 2 diabetes mellitus [ICD-11: 5A11]

Differential expression of molecule in resistant diseases

• The Studied Tissue: Omental adipose tissue
• The Specified Disease: Obesity related type 2 diabetes
• The Expression Level of Disease Section Compare with the Healthy Individual Tissue: p-value: 7.25E-01; Fold-change: -1.91E-02; Z-score: -3.10E-02
• The Studied Tissue: Liver
• The Specified Disease: Type 2 diabetes mellitus
• The Expression Level of Disease Section Compare with the Healthy Individual Tissue: p-value: 6.57E-01; Fold-change: 1.68E-01; Z-score: 5.07E-01

References

• Ref 1: Insulin Resistance: From Mechanisms to Therapeutic Strategies .Diabetes Metab J. 2022 Jan;46(1):15-37. doi: 10.4093/dmj.2021.0280. Epub 2021 Dec 30. 10.4093/dmj.2021.0280