Cloned (Comment) | Organism |
---|---|
gene acs-3, expression as GFP-tagged protein in worm embryos | Caenorhabditis elegans |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Caenorhabditis elegans | - |
isozyme ACS-3, gene acs-3 | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
adult | tissue expression patterns of acs-3, overview | Caenorhabditis elegans | - |
epidermal cell | - |
Caenorhabditis elegans | - |
larva | tissue expression patterns of acs-3, overview | Caenorhabditis elegans | - |
seam cell | - |
Caenorhabditis elegans | - |
Synonyms | Comment | Organism |
---|---|---|
ACS-3 | - |
Caenorhabditis elegans |
acyl-CoA synthase-3 | - |
Caenorhabditis elegans |
General Information | Comment | Organism |
---|---|---|
malfunction | loss of ACS-3, a long-chain acyl-CoA synthase, causes enhanced intestinal lipid uptake, de novo fat synthesis, and accumulation of enlarged, neutral lipid-rich intestinal depots. Acs-3 mutant phenotypes require the nuclear hormone receptor NHR-25, a key regulator of Caenorhabditis elegans molting | Caenorhabditis elegans |
additional information | mutation of nhr-25 suppresses the fatty acid uptake phenotypes of acs-3(ft5) animals, overview | Caenorhabditis elegans |
physiological function | regulation of Caenorhabditis elegans fat uptake and storage by acyl-CoA synthase-3 is dependent on NR5A family nuclear hormone receptor nhr-25, overview. ACS-3-derived long-chain fatty acyl-CoAs, perhaps incorporated into complex ligands such as phosphoinositides, modulate NHR-25 function, which in turn regulates an endocrine program of lipid uptake and synthesis | Caenorhabditis elegans |