Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 1.14.13.9 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
Search for more literature for 1.14.13.9

Cloned(Commentary)

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

Localization

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

Natural Substrates/ Products (Substrates)

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

Organism

Organism UniProt Comment Textmining
Homo sapiens O15229
-
-
Sus scrofa Q9MZS9
-
-

Source Tissue

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

Substrates and Products (Substrate)

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

Synonyms

Synonyms Comment Organism
KMO
-
 Sus scrofa
KMO
-
 Homo sapiens

Cofactor

Cofactor Comment Organism Structure
FAD
-
 Sus scrofa
FAD
-
 Homo sapiens
NADPH
-
 Sus scrofa
NADPH
-
 Homo sapiens

Expression

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

General Information

General Information Comment Organism
malfunction KMO is downregulated in autografts and is almost completely silenced in allograft rejection Sus scrofa
malfunction KMO is downregulated in autografts and is almost completely silenced in allograft rejection Homo sapiens
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
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