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We have identified by the first time in a young patient and his only sister a familiar genetic defect of an enzyme called ACOX2, which participates in the transformation of cholesterol into bile acids as a cause of increased serum transaminases in the absence of any other symptomatology.
Results found an ACOX2 variant present in a subset of human breast cancers and associated with improved outcome ER+ tumors suggesting it as a potential novel therapeutic biomarker in ER+ breast tumors.
Our results suggest that downregulation of ACOX2 is a shared risk factor for PE and CVD.
The product of this gene belongs to the acyl-CoA oxidase family. It encodes the branched-chain acyl-CoA oxidase which is involved in the degradation of long branched fatty acids and bile acid intermediates in peroxisomes. Deficiency of this enzyme results in the accumulation of branched fatty acids and bile acid intermediates, and may lead to Zellweger syndrome, severe mental retardation, and death in children.
acyl-CoA oxidase 2, branched chain
, peroxisomal acyl-coenzyme A oxidase 2-like
, acyl-Coenzyme A oxidase 2, branched chain
, peroxisomal acyl-coenzyme A oxidase 2
, 3-alpha,7-alpha,12-alpha-trihydroxy-5-beta-cholestanoyl-CoA 24-hydroxylase
, 3-alpha,7-alpha,12-alpha-trihydroxy-5-beta-cholestanoyl-CoA oxidase
, THCA-CoA oxidase
, peroxisomal branched chain acyl-CoA oxidase
, trihydroxycoprostanoyl-CoA oxidase
, 3alfa, 7alfa 12alfa-trihydroxy-5beta-cholestanoyl-CoA oxidase
, branched chain acyl-CoA oxidase