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Literature summary for 6.2.1.3 extracted from

  • Reinartz, A.; Ehling, J.; Leue, A.; Liedtke, C.; Schneider, U.; Kopitz, J.; Weiss, T.; Hellerbrand, C.; Weiskirchen, R.; Knuechel, R.; Gassler, N.
    Lipid-induced up-regulation of human acyl-CoA synthetase 5 promotes hepatocellular apoptosis (2010), Biochim. Biophys. Acta, 1801, 1025-1035.
    View publication on PubMed
Search for more literature for 6.2.1.3

Protein Variants

Protein Variants Comment Organism
additional information overexpression of ACSL5 decreases HepG2 cell viability and increases susceptibility to TRAIL- and TNFalpha-, but not FAS- induced apoptosis, whereas knockdown of ACSL5 reduces apoptosis susceptibility Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion
-
 Homo sapiens 5739
-

Metals/Ions

Metals/Ions Comment Organism Structure
Mg2+ required Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
ATP + hexadecanoate + CoA Homo sapiens
-
 AMP + diphosphate + hexadecanoyl-CoA
-
 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
 isozyme ACSL5
-

Source Tissue

Source Tissue Comment Organism Textmining
Hep-G2 cell
-
 Homo sapiens
-
liver
-
 Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + hexadecanoate + CoA
-
 Homo sapiens AMP + diphosphate + hexadecanoyl-CoA
-
 ?

Synonyms

Synonyms Comment Organism
ACSL5
-
 Homo sapiens
acyl-CoA synthetase 5
-
 Homo sapiens
More the enzyme is a member of the ACSL gene family that catalyzes the activation of long-chain fatty acids for lipid biosynthesis Homo sapiens

Temperature Optimum [°C]

Temperature Optimum [°C] Temperature Optimum Maximum [°C] Comment Organism
30
-
 assay at Homo sapiens

pH Optimum

pH Optimum Minimum pH Optimum Maximum Comment Organism
7.5
-
 assay at Homo sapiens

Cofactor

Cofactor Comment Organism Structure
ATP
-
 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens lipid-induced up-regulation of acyl-CoA synthetase 5 promotes hepatocellular apoptosis. ACSL5 expression is enhanced in steatotic liver up

General Information

General Information Comment Organism
malfunction lipid-induced up-regulation of acyl-CoA synthetase 5 promotes hepatocellular apoptosis. High ACSL5 activity results in enhanced caspase-3/7 activity, but is not accompanied by up-regulation of death receptors, DR4, DR5 or TNF-R1 Homo sapiens
metabolism acyl-CoA synthetase 5 is involved in the activation of long-chain fatty acids for lipid biosynthesis, and it is the only ACSL isoform that is both, located on mitochondria and functionally involved in enterocyte apoptosis. Analysis of regulation of ACSL5 in hepatocellular fatty acid degeneration and its involvement in hepatocyte apoptosis using models of in vitro and in vivo steatosis as well as plasmid-mediated stable gene transfer and RNAi-mediated gene silencing Homo sapiens
physiological function ACSL5 plays a role in promoting fatty acid-induced lipoapoptosis in hepatocytes as important mechanism in fatty liver-related disorders Homo sapiens