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Literature summary extracted from

  • Lassiter, R.; Merchen, T.D.; Fang, X.; Wang, Y.
    Protective role of kynurenine 3-monooxygenase in allograft rejection and tubular injury in kidney transplantation (2021), Front. Immunol., 12, 671025 .
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

EC Number Cloned (Comment) Organism
1.14.13.9 gene kmo, quantitative RT-PCR enzyme expression analysis Sus scrofa
1.14.13.9 gene kmo, quantitative RT-PCR enzyme expression analysis Homo sapiens

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
1.14.13.9 mitochondrial outer membrane
-
 Sus scrofa 5741
-
1.14.13.9 mitochondrial outer membrane
-
 Homo sapiens 5741
-

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
1.14.13.9 L-kynurenine + NADPH + H+ + O2 Sus scrofa
-
 3-hydroxy-L-kynurenine + NADP+ + H2O
-
 ?
1.14.13.9 L-kynurenine + NADPH + H+ + O2 Homo sapiens
-
 3-hydroxy-L-kynurenine + NADP+ + H2O
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
1.14.13.9 Homo sapiens O15229
-
-
1.14.13.9 Sus scrofa Q9MZS9
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
1.14.13.9 kidney high enzyme expression level Sus scrofa
-
1.14.13.9 kidney high enzyme expression level Homo sapiens
-
1.14.13.9 Pan-T cell peripheral blood Pan-T cells Homo sapiens
-
1.14.13.9 tubular epithelial cell cortical renal TEC Sus scrofa
-
1.14.13.9 tubular epithelial cell cortical renal TEC Homo sapiens
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
1.14.13.9 L-kynurenine + NADPH + H+ + O2
-
 Sus scrofa 3-hydroxy-L-kynurenine + NADP+ + H2O
-
 ?
1.14.13.9 L-kynurenine + NADPH + H+ + O2
-
 Homo sapiens 3-hydroxy-L-kynurenine + NADP+ + H2O
-
 ?

Synonyms

EC Number Synonyms Comment Organism
1.14.13.9 KMO
-
 Sus scrofa
1.14.13.9 KMO
-
 Homo sapiens

Cofactor

EC Number Cofactor Comment Organism Structure
1.14.13.9 FAD
-
 Sus scrofa
1.14.13.9 FAD
-
 Homo sapiens
1.14.13.9 NADPH
-
 Sus scrofa
1.14.13.9 NADPH
-
 Homo sapiens

Expression

EC Number Organism Comment Expression
1.14.13.9 Sus scrofa KMO is downregulated in autografts and is almost completely silenced in allograft rejection down
1.14.13.9 Homo sapiens KMO is downregulated in autografts and is almost completely silenced in allograft rejection down

General Information

EC Number General Information Comment Organism
1.14.13.9 malfunction KMO is downregulated in autografts and is almost completely silenced in allograft rejection Sus scrofa
1.14.13.9 malfunction KMO is downregulated in autografts and is almost completely silenced in allograft rejection Homo sapiens
1.14.13.9 physiological function kynurenine 3-monooxygenase (KMO) and kynureninase are reduced in ischemia-reperfusion procedure and further decreased in rejection allografts among mismatched pig KTx, molecular mechanism, overview. TEC injury in acutely rejection allografts is associated with alterations of Bcl2 family proteins, reduction of tight junction protein 1 (TJP1), and TEC-specific KMO. Three cytokines, IFNgamma, TNFalpha, and IL1beta, are identified as triggers of TEC injury by altering the expression of Bcl2, BID, and TJP1. Allograft rejection and TEC injury are always associated with a dramatic reduction of KMO. 3-Hydroxy-L-kynurenine (3HK) and hydroxyl-3 anthranilic acid (3HAA) as direct and downstream products of KMO, effectively protect TEC from injury via increasing expression of Bcl-xL and TJP1. 3HK and 3HAA effectively inhibit T cell proliferation Sus scrofa
1.14.13.9 physiological function renal tubular epithelial cells (TECs) are the primary targets of ischemia-reperfusion injury (IRI) and rejection by the recipient's immune response in kidney transplantation (KTx). Kynurenine 3-monooxygenase (KMO) and kynureninase are reduced in ischemia-reperfusion procedure, molecular mechanism, overview. TEC injury in acutely rejection allografts is associated with alterations of Bcl2 family proteins, reduction of tight junction protein 1 (TJP1), and TEC-specific KMO. Three cytokines, IFNgamma, TNFalpha, and IL1beta, aere identified as triggers of TEC injury by altering the expression of Bcl2, BID, and TJP1. Allograft rejection and TEC injury are always associated with a dramatic reduction of KMO. 3-Hydroxy-L-kynurenine (3HK) and hydroxyl-3 anthranilic acid (3HAA) as direct and downstream products of KMO, effectively protect TEC from injury via increasing expression of Bcl-xL and TJP1. 3HK and 3HAA effectively inhibit T cell proliferation Homo sapiens