Disease relevance of Dao1

• Then, real-time PCR was employed to screen for lambda phages carrying D-amino-acid oxidase gene from mouse genomic library [1].
• The effects of testosterone (10 micrograms/100g body weight) on renal PAO and DAO activities were also studied [2].

Psychiatry related information on Dao1

• The Morris water maze learning and the LTP in the CA1 area of the hippocampal slice were observed in wild-type mice and mutant mice lacking D-amino-acid oxidase [3].

High impact information on Dao1

• At low concentrations and pH 7.4, the cysteamine-glyoxylate substrate (presumably thiazolidine-2-carboxylic acid) reacts an order of magnitude faster than any other known D-amino acid oxidase substrate [4].
• Reactions of cysteamine and other amine metabolites with glyoxylate and oxygen catalyzed by mammalian D-amino acid oxidase [4].
• Interestingly, it was shown that the monoclonal antibody was cross-reactive with FAD-dependent enzymes such as salicylate hydroxylase (EC 1.14.13.1) and D-amino acid oxidase (EC 1.4.3.3), and that it was specific for the FAD-binding sites of these enzymes [5].
• We have confirmed that this strain lacks DAO activity and shown for the first time it has increased occupancy of the NMDAR glycine site due to elevated extracellular D-serine levels and has enhanced NMDAR function in vivo [6].
• Urine from mutant mice which lack D-amino-acid oxidase contained a large amount of D-alanine [7].

Biological context of Dao1

• Thus Dao is not linked to previously mapped peroxisomal enzyme loci, Hao-1 and Cs, closely localized on chromosome 2 [8].
• Genetics and ontogeny of butyryl CoA dehydrogenase in the mouse and linkage of Bcd-1 with Dao-1 [9].
• Spatial learning and long-term potentiation of mutant mice lacking D-amino-acid oxidase [3].
• These results indicate that the single base-pair substitution is the cause of the loss of DAO activity in the ddY/DAO- mice [10].
• After cDNA encoding DAO was amplified by the polymerase chain reaction it was cloned into a plasmid and sequenced [10].

Anatomical context of Dao1

• In the brains of ddY/DAO+ mice, a relatively high amount of D-leucine has been observed in the pineal gland compared with other regions [11].
• Free D-serine, D-aspartate and D-alanine in central nervous system and serum in mutant mice lacking D-amino acid oxidase [12].
• Biochemical analyses of marker enzymes for peroxisomes (catalase and D-amino acid oxidase), mitochondria (cytochrome oxidase) and lysosomes (acid phosphatase) were performed on kidneys at ages from 17 days prenatal to adult [13].
• The amount and distribution of D-proline in the brains of ddY/DAO+ mice and ddY/DAO- mice are almost the same, and relatively high amounts of D-proline have been observed in the pituitary gland and in the pineal gland [11].
• We evaluated the role of D-amino-acid oxidase on spatial learning and long-term potentiation (LTP) in the hippocampus, since this enzyme metabolizes D-amino-acids, some of which enhance the N-methyl-D-aspartate receptor functions [3].

Associations of Dao1 with chemical compounds

• Determination of free D-proline and D-leucine in the brains of mutant mice lacking D-amino acid oxidase activity [11].
• In the brains of ddY/DAO- mice, D-leucine amounts are approximately 10 times higher than those obtained in ddY/DAO+ mice and regional difference has not been observed, while the amounts of L-proline and L-leucine are not significantly different between the two strains [11].
• Amino acid levels in D-alanine-administered mutant mice lacking D-amino acid oxidase [14].
• Urine from mutant mice lacking D-amino-acid oxidase contained a large amount of alanine compared with that from normal mice [15].
• The normal increase in activity or rate of synthesis of beta-glucuronidase following androgen administration requires pituitary hormones and/or products of these hormones, while the increase in activity of enzymes like alcohol dehydrogenase and D-amino acid oxidase does not require pituitary hormones [16].

Other interactions of Dao1

• The enzyme locus (Dao) was shown to segregate independently of Hao-1, encoding the peroxisomal enzyme hydroxyacid oxidase (liver on A4 isozyme) [8].
• On the contrary, the activity of acyl-CoA oxidase, a microperoxisomal H2O2-producing enzyme, in the cerebral cortex of SAMP8 was increased 1.6 fold in comparison with that in age-matched SAMR1 without change in the activity of D-amino acid oxidase [17].
• Mice lacking D-amino acid oxidase activity display marked attenuation of stereotypy and ataxia induced by MK-801 [18].
• 1. Activity of D-amino acid oxidase was detected in tissue extract of mouse liver by two sensitive spectrophotometric methods [19].
• D-aspartate oxidase activity and D-aspartate content in a mutant mouse strain lacking D-amino acid oxidase [20].

Analytical, diagnostic and therapeutic context of Dao1

• 2. Immunoblotting using an antibody against hog kidney D-amino-acid oxidase showed that kidney homogenates of the mutant mice as well as that of the normal mice had proteins reactive to the antibody [21].
• Unlike the effect of hypophysectomy on kidney glucuronidase, there was no reduction in the accumulation of alcohol dehydrogenase or D-amino acid oxidase in kidney of hypophysectomized mice after androgen treatment [16].
• This study was designed to examine the localization of DAO mRNA in the mouse kidney using in situ hybridization histochemistry (ISH) [22].
• Thin-layer chromatography and amino acid analysis showed that mutant (ddY/DAO-) mice lacking D-amino-acid oxidase activity excreted about 3.5 times more methionine in urine than did normal (ddY/DAO+) mice [23].
• High-performance liquid chromatography using a chiral column showed that approximately 82% of urinary methionine of the ddY/DAO- mice had the D-configuration [23].

References