Disease relevance of Aldh4a1

• Thus polyunsaturated fat-cholesterol induced postprandial hypercholesterolemia appeared to be genetically determined by a gene located between the Gpd-1 and Ahd-1 loci, in mice [1].
• In isolated granulomas, activity of proline oxidase was minimal, and P5C dehydrogenase activity was absent [2].

High impact information on Aldh4a1

• The enzymes involved in degradation of proline are proline oxidase and P5C dehydrogenase; both are present in liver cells [2].
• The locus was shown to segregate independently of Ahd-1 (encoding the mitochondrial AHD-A2 isozymes on chromosome 4; HOLMES 1978) [3].
• In this study, non-responsiveness cosegregated with the b allele at the Gpd-1 and Ahd-1 loci [1].
• Genetic variants for liver mitochondrial (AHD-1) and cytoplasmic (AHD-2) isozymes have been used to map the responsible loci (Ahd-1 and Ahd-2) on chromosomes 4 and 19 respectively [4].

Biological context of Aldh4a1

• From this result, we found that the postprandial hypercholesterolemic response to an acute polyunsaturated fat-cholesterol feed, cosegregated with the a allele at the Gpd-1 and Ahd-1 loci, on mouse chromosome 4 [1].

Anatomical context of Aldh4a1

• Mouse ALDH exhibits extensive multiplicity, several forms of which have been characterized, including ALDH1 (liver cytoplasmic/class 1 isozyme); ALDH2 (liver mitochondrial/class 2.); ALDH3 (stomach cytosolic/class 3); ALDH4 (liver microsomal/class 3); and ALDH5 (testis cytosolic/class 3) [5].

Associations of Aldh4a1 with chemical compounds

• Mouse aldehyde dehydrogenase genetics: positioning of Ahd-1 on chromosome 4 [6].
• The genetic locus encoding AHD-A2 (suggested name Ahd-1) is localized on chromosome 4 and was mapped close to je (jerker) and Gpd-1 (encoding the liver and kidney isoenzyme of glucose-6-phosphate dehydrogenase) [7].

References