1.14.13.9: kynurenine 3-monooxygenase
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For detailed information about kynurenine 3-monooxygenase, go to the full flat file.
Word Map on EC 1.14.13.9
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1.14.13.9
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mercury
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hg
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kynurenic
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3-hydroxykynurenine
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quinolinic
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2,3-dioxygenase
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kynureninase
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indoleamine
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cronbach
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huntington
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bartlett
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paint
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3-hydroxyanthranilic
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quin
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neuroactive
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ochre
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realgar
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psychometric
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calcite
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methylmercury
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xanthurenic
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eigenvalue
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vermilion
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hematite
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test-retest
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excitotoxins
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ommochrome
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artwork
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geochemical
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indoleamine-2,3-dioxygenase
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archaeological
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varimax
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roman
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mineralogical
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slovenia
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micro-raman
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molecular biology
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medicine
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analysis
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pharmacology
- 1.14.13.9
- mercury
- hg
-
kynurenic
- 3-hydroxykynurenine
-
quinolinic
-
2,3-dioxygenase
- kynureninase
- indoleamine
-
cronbach
- huntington
-
bartlett
-
paint
-
3-hydroxyanthranilic
-
quin
-
neuroactive
-
ochre
-
realgar
-
psychometric
-
calcite
- methylmercury
-
xanthurenic
-
eigenvalue
-
vermilion
-
hematite
-
test-retest
-
excitotoxins
-
ommochrome
-
artwork
-
geochemical
- indoleamine-2,3-dioxygenase
-
archaeological
-
varimax
-
roman
-
mineralogical
-
slovenia
-
micro-raman
- molecular biology
- medicine
- analysis
- pharmacology
Reaction
Synonyms
BcKMO, Bna4, cinnabar, EC 1.14.1.2, EC 1.99.1.5, FAD dependent kynurenine 3-monooxygenase, flavin adenine dinucleotide dependent kynurenine 3-monooxygenase, hKMO, Hs-KMO, K3H, KMO, KYN-OHase, kynurenine 3-hydroxylase, kynurenine 3-monooxygenase, kynurenine hydroxylase, kynurenine monooxygenase, kynurenine-3-monooxygenase, L-kynurenine 3-monooxygenase, L-kynurenine,NADPH2:oxygen oxidoreductase (3-hydroxylating), L-kynurenine-3-hydroxylase, More, NADPH-dependent flavin monooxygenase, oxygenase, kynurenine 3-mono-, pfKMO, Rat-KMO, scKMO
ECTree
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Application on EC 1.14.13.9 - kynurenine 3-monooxygenase
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APPLICATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
analysis
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comprehensive panel of biochemical and cell-based assays that use liquid chromatography/tandem mass spectrometry to quantify unlabeled kynurenine and 3-hydroxykynurenine and application to measure kynurenine monooxygenase inhibition in cell and tissue extracts, as well as cellular assays
diagnostics
the upregulation of KMO currently serves as an independent prognostic biomarker to identify certain liver malignancies, particularly hepatocellular carcinoma (HCC). HCC patients who express increased KMO activity are known to have unfavorable clinical outcomes compared to those who do not. The upregulation of KMO also plays a critical role in triple-negative breast cancer progression and metastasis. The pharmacological inhibition of KMO with GSK180 granted therapeutic protection in acute pancreatitis rodent models preventing multiple organ failures
drug development
medicine
molecular biology
pharmacology
drug development
enzyme KMO is an important drug target due to its role in regulating the levels of bioactive substances with contrasting effects. For treatment of central nervous related diseases, it is required that enzyme inhibitors should be both blood brain barrier permeable and should not cause hydrogen peroxide as a harmful side product. Molecular dynamics simulations and MM/GBSA calculations, overview
drug development
enzyme KMO is an important drug target due to its role in regulating the levels of bioactive substances with contrasting effects. For treatment of central nervous related diseases, it is required that enzyme inhibitors should be both blood brain barrier permeable and should not cause hydrogen peroxide as a harmful side product. Molecular dynamics simulations and MM/GBSA calculations, overview
drug development
enzyme KMO is an important drug target due to its role in regulating the levels of bioactive substances with contrasting effects. For treatment of central nervous related diseases, it is required that enzyme inhibitors should be both blood brain barrier permeable and should not cause hydrogen peroxide as a harmful side product. Molecular dynamics simulations and MM/GBSA calculations, overview
drug development
importance of KMO as a drug target in neurological disease, benefits of brain permeable inhibitors in modulating kynurenine pathway metabolites in the central nervous system teeating brain neurological diseases
drug development
importance of KMO as a drug target in neurological disease, benefits of brain permeable inhibitors in modulating kynurenine pathway metabolites in the central nervous system teeating brain neurological diseases
drug development
importance of KMO as a drug target in neurological disease, benefits of brain permeable inhibitors in modulating kynurenine pathway metabolites in the central nervous system teeating brain neurological diseases
drug development
KMO has been identified as a therapeutic target for limiting neuronal damage from ischemia and specific diseases. The inhibition of KMO in vivo has synergistic neuroprotective effects that include elevation of the concentration of kynurenate, that both slows glutamate release and antagonizes NMDA receptors, reducing aberrant excitation. Inhibition of KMO also has the added benefit of halting the accumulation of specific neurotoxic and/or apoptotic metabolites, such as 3-hydroxy-L-kynurenine and quinolinic acid
drug development
the enzyme is a target for drug development in neurological, but also other, diseases, pharmacophore development with receptor-based pharmacophore modeling, detailed overview
medicine
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the enzyme is an attractive target for the treatment of ischemic stroke
medicine
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T helper 17 cells preferentially express kynurenine 3-monooxygenase. Enzyme inhibition, either with a specific inhibitor or via siRNA-mediated silencing, markedly increases IL-17 productionin vitro, whereas IFN-gamma production by T helper 1 cells is unaffected. Inhibition of kynurenine 3-monooxygenase significantly exacerbates disease in a Th17-driven model of autoimmune gastritis
medicine
inhibition of the enzyme shows benefit in neurodegenerative diseases such as Huntington's and Alzheimer's. It is a target for acute pancreatitis multiple organ dysfunction syndrome
medicine
inhibition of the enzyme shows benefit in neurodegenerative diseases such as Huntington's and Alzheimer's. It is a target for acute pancreatitis multiple organ dysfunction syndrome (AP-MODS)
medicine
the enzyme is a potential drug target for treatment of neurodegenerative disorders such as Huntington's and Alzheimer's diseases
medicine
the enzyme is a potential therapeutic target for neurodegenerative and neurologic disorders
medicine
importance of KMO as a drug target in neurological disease, benefits of brain permeable inhibitors in modulating kynurenine pathway metabolites in the central nervous system teeating brain neurological diseases. KMO inhibitors with brain permeability would be predicted to be more efficacious for treating neurodegenerative diseases than peripheral treatment, as inhibition of KMO in the CNS leads to increased neuroprotective KYNA levels as well as decreased levels of neurotoxic metabolites
medicine
importance of KMO as a drug target in neurological disease, benefits of brain permeable inhibitors in modulating kynurenine pathway metabolites in the central nervous system teeating brain neurological diseases. KMO inhibitors with brain permeability would be predicted to be more efficacious for treating neurodegenerative diseases than peripheral treatment, as inhibition of KMO in the CNS leads to increased neuroprotective KYNA levels as well as decreased levels of neurotoxic metabolites
medicine
importance of KMO as a drug target in neurological disease, benefits of brain permeable inhibitors in modulating kynurenine pathway metabolites in the central nervous system teeating brain neurological diseases. KMO inhibitors with brain permeability would be predicted to be more efficacious for treating neurodegenerative diseases than peripheral treatment, as inhibition of KMO in the CNS leads to increased neuroprotective KYNA levels as well as decreased levels of neurotoxic metabolites
medicine
KMO and its enzymatic product QUIN are potential broad-spectrum antiviral factor therapeutics against emerging pathogenic viruses
medicine
rationale for enzyme KMO inhibition as a therapeutic strategy to protect against acute kidney injury (AKI) during critical illness. Renal ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI)
medicine
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the enzyme is an attractive target for the treatment of ischemic stroke
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medicine
Mus musculus C57BL/6N x C57BL/6J
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rationale for enzyme KMO inhibition as a therapeutic strategy to protect against acute kidney injury (AKI) during critical illness. Renal ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI)
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molecular biology
development of a transformant selection system for Tribolium castaneum on the basis of mutant rescue
molecular biology
wild-type KMO gene can be used as a marker gene for visually screening transgenic silkworms
molecular biology
the wild-type enzyme gene can be used as a marker gene for visually screening transgenic silkworms
molecular biology
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wild-type KMO gene can be used as a marker gene for visually screening transgenic silkworms
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pharmacology
kynurenine represents a branch point of the kynurenine pathway, being converted into the neurotoxin 3-hydroxykynurenine via kynurenine monooxygenase, neuroprotectant kynurenic acid, and anthranilic acid. As a result of this branch point, kynurenine monooxygenase is an attractive drug target for several neurodegenerative and/or neuroinflammatory diseases, especially Huntington's, Alzheimer's, and Parkinson's diseases
pharmacology
the enzyme is a potential drug target for treatment of neurodegenerative disorders such as Huntington's and Alzheimer's diseases
