EC Number   |
General Information |
Reference |
|---|
    1.4.3.3 | malfunction |
a total loss of enzymatic activity is associated with the adult onset of familial amyotrophic lateral sclerosis. Altered enzyme expression levels and activity have been reported in schizophrenia |
723920 |
| 1.4.3.3 | malfunction |
an increase in DAO expression in parts of the brain is involved in aberrant D-amino acid metabolism |
699644 |
| 1.4.3.3 | malfunction |
increased level of D-serine resulting from decreased catalysis correct the performance of mice with deficient NMDAR glycine site activation in behavioral tasks relevant to the negative and cognitive symptoms of schizophrenia |
698099 |
| 1.4.3.3 | malfunction |
the DAAO risk gene is associated with schizophrenia, linkage between DAAO and schizophrenia in a severely affected subpopulation of schizophrenia patients, genotyping, expression analysis, and detailed overview |
699646 |
| 1.4.3.3 | metabolism |
D-serine is synthesized from L-serine by serine racemase and degraded by D-amino acid oxidase in neurons, overview |
711720 |
| 1.4.3.3 | metabolism |
the oxidative half-reaction starts with a single electron transfer from FAD to O2, followed by triplet-singlet transition. FAD oxidation is completed by a proton coupled electron transfer to the oxygen species and the reaction terminates with H2O2 formation by proton transfer from the oxidized substrate to the oxygen species via a chain of water molecules. The substrate plays a double role by facilitating the first electron transfer and by providing a proton in the last step |
763534 |
| 1.4.3.3 | more |
metabolism of extracellular D-serine and effects of D-serine metabolites with pathophysiological role of DAO, overexpression of DAO in astroglial cells induces the enhanced cytotoxicity, reaction product beta-hydroxypyruvate also induces cell death, comprising apoptosis, in the astroglial cell, but not in the other cells derived from liver and kidney, overview |
712324 |
| 1.4.3.3 | more |
mutation R199W in the D-amino acid oxidase gene, DAO is associated with classical adult onset familial amyotrophic lateral sclerosis, FALS in a three generational FALS kindred, the 14.52 cMregiononchromosome 12q22-23 is linked to disease. Lentiviral-mediated expression of R199WDAO in primary motor neuron cultures causes increased TUNEL labeling. This effect also occurs in motor neurons cocultured on transduced astrocytes expressing R199W, indicating that the motor neuron cell death induced by this mutation is mediated by both cell autonomous and noncell autonomous processes |
713430 |
| 1.4.3.3 | more |
phenotypes of mutant mice resulting from enhanced N-methyl-D-aspartate receptor function, accumulation of D-amino acids in the organs and body fluids of mutant mice, overview. Mutant mice lacking DAO do not show great abnormalities, but responses to the nociceptive stimuli are different between the mutant and wild-type mice. The function of NMDA receptors is enhanced in the mutant mice, with long-term potentiation in the CA1 area of hippocampus being augmented. Mutant mice display an anxiety-like behavior and have aminoaciduria |
711720 |
| 1.4.3.3 | physiological function |
D-amino acid oxidase functions in metamorphosis |
724793 |
