4 GO Annotations
| GO Term | Gene Name |
|---|---|
| GO:0003997 | IPR002655 |
| GO:0006635 | IPR002655 |
| GO:0055114 | IPR002655 |
| GO:0005777 | IPR002655 |
4 Ontology Annotations
| GO Term | Gene Name |
|---|---|
| GO:0003997 | IPR002655 |
| GO:0006635 | IPR002655 |
| GO:0055114 | IPR002655 |
| GO:0005777 | IPR002655 |
| Type: | Domain | Name: | Acyl-CoA oxidase, C-terminal |
| Description: | Acyl-CoA oxidase (ACO) acts on CoA derivatives of fatty acids with chain lengths from 8 to 18. It catalyses the first and rate-determining step of the peroxisomal beta-oxidation of fatty acids [].Acyl-CoA oxidase is a homodimer and the polypeptide chain of the subunit is folded into the N-terminal alpha-domain, beta-domain, and C-terminal alpha-domain []. Functional differences between the peroxisomal acyl-CoA oxidases and the mitochondrial acyl-CoA dehydrogenases are attributed to structural differences in the FAD environments []. Experimental data indicate that, in the pumpkin, the expression pattern of ACOX is very similar to that of the glyoxysomal enzyme 3-ketoacyl-CoA thiolase []. In humans, defects in ACOX1 are the cause of pseudoneonatal adrenoleukodystrophy, also known as peroxisomal acyl-CoA oxidase deficiency. Pseudo-NALD is a peroxisomal single-enzyme disorder. Clinical features include mental retardation, leukodystrophy, seizures, mild hepatomegaly and hearing deficit. Pseudo-NALD is characterised by increased plasma levels of very-long chain fatty acids due to a decrease in, or absence of, peroxisome acyl-CoA oxidase activity, despite the peroxisomes being intact and functioning.This entry represents the Acyl-CoA oxidase C-terminal. | Short Name: | Acyl-CoA_oxidase_C |
| GO Term | Gene Name |
|---|---|
| GO:0003997 | IPR002655 |
| GO:0006635 | IPR002655 |
| GO:0055114 | IPR002655 |
| GO:0005777 | IPR002655 |
| GO Term | Gene Name |
|---|---|
| GO:0003997 | IPR002655 |
| GO:0006635 | IPR002655 |
| GO:0055114 | IPR002655 |
| GO:0005777 | IPR002655 |
