1.13.11.6: 3-hydroxyanthranilate 3,4-dioxygenase
This is an abbreviated version!
For detailed information about 3-hydroxyanthranilate 3,4-dioxygenase, go to the full flat file.
Word Map on EC 1.13.11.6
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1.13.11.6
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quinolinic
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kynureninase
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quin
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2,3-dioxygenase
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3-monooxygenase
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excitotoxin
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phosphoribosyltransferase
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kynurenine-oxoglutarate
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aminocarboxymuconate-semialdehyde
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kynurenic
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3-hydroxykynurenine
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ibotenic
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epilepsy-prone
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picolinic
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drug development
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medicine
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pharmacology
- 1.13.11.6
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quinolinic
- kynureninase
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quin
-
2,3-dioxygenase
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3-monooxygenase
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excitotoxin
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phosphoribosyltransferase
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kynurenine-oxoglutarate
- aminocarboxymuconate-semialdehyde
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kynurenic
- 3-hydroxykynurenine
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ibotenic
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epilepsy-prone
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picolinic
- drug development
- medicine
- pharmacology
Reaction
Synonyms
3-HAD, 3-HAO, 3-hydroxyanthranilate 3,4-dioxygenase, 3-hydroxyanthranilate oxygenase, 3-hydroxyanthranilic acid oxidase, 3-hydroxyanthranilic acid oxygenase, 3-hydroxyanthranilic oxygenase, 3HAO, EC 1.13.1.6, HAD, HAO, oxygenase, 3-hydroxyanthranilate 3,4-di-
ECTree
1.13.11.6 3-hydroxyanthranilate 3,4-dioxygenaseAdvanced search results
results (
results (Inhibitors
Inhibitors on EC 1.13.11.6 - 3-hydroxyanthranilate 3,4-dioxygenase
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INHIBITOR 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
IMAGE
1-ethyl-3-(3-dimethylaminopropyl)carbodiimide methiodide
carboxyl-directed reagent, 1 mM, 26% inhibition
4,6-dibromo-3-hydroxyanthranilic acid
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NCR-631, characterization of in vivo effects, reversible inhibition with short half-life following systematic administration
6-chloro-3-hydroxyanthranilic acid
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5-20 mM, loss of enzymatic activity as a function of the inhibitor concentration
diethyl dicarbonate
modifies histidine residues of catechol dioxygenases, 1 mM, 70% inhibition
Dithionitrobenzoic acid
cysteine-directed reagent, 1 mM, complete inhibition
o-methoxybenzoylalanine
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in whole-liver homogenates, but in purified enzyme preparations only in the presence of mitochondria
4-Chloro-3-hydroxyanthranilate
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it is possible that inhibition of 3-HAD may improve neurologic status through an increased production of kynurenic acid, a non-specific inhibitor of excitatory amino acid receptors and an inhibitor of quinolinic acid neurotoxicity
4-Chloro-3-hydroxyanthranilate
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the inactivation results in the consumption of 2 equivalents of oxygen and the production of superoxide. The inhibitor stimulates the oxidation of the active site Fe(II) to the catalytically inactive Fe(III) oxidation state. The inactivated enzyme can be reactivated by treatment with DTT and FeI(II). The nhibitor does not form an adduct with the enzyme. Four conserved cysteines are oxidized to two disulfides (Cys125-Cys128 and Cys162-Cys165) during the inactivation reaction. These results are consistent with a mechanism in which the enzyme, complexed to the inhibitor and O2, generates superoxide which subsequently dissociates, leaving the inhibitor and the oxidized iron center at the active site
additional information
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not at a concentration of 0.5 mM: L-tryptophan, quinolinic acid, kynurenic acid, nicotinic acid mononucleotide, picolinic acid, phthalic acid, glutaric acid, L-aspartic acid, L-glutamic acid, N-methyl-D-aspartic acid, kainic acid
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additional information
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both geometrical end electronic structural feature of 4,5- and 4,6-disubstituted and 4,5,6-trisubstituted 3-hydroxyanthranilic derivates play an important role in the inhibitory potency
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