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 | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
mitochondrion | - |
Homo sapiens | 5739 | - |
Metals/Ions | Comment | Organism | Structure |
---|---|---|---|
Mg2+ | required | Homo sapiens |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + hexadecanoate + CoA | Homo sapiens | - |
AMP + diphosphate + hexadecanoyl-CoA | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
isozyme ACSL5 | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
Hep-G2 cell | - |
Homo sapiens | - |
liver | - |
Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + hexadecanoate + CoA | - |
Homo sapiens | AMP + diphosphate + hexadecanoyl-CoA | - |
? |
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 Maximum [°C] | Comment | Organism |
---|---|---|---|
30 | - |
assay at | Homo sapiens |
pH Optimum Minimum | pH Optimum Maximum | Comment | Organism |
---|---|---|---|
7.5 | - |
assay at | Homo sapiens |
Cofactor | Comment | Organism | Structure |
---|---|---|---|
ATP | - |
Homo sapiens |
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 | 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 |