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- W2598111690 endingPage "117864691769193" @default.
- W2598111690 startingPage "117864691769193" @default.
- W2598111690 abstract "Regulatory and functional aspects of the kynurenine (K) pathway (KP) of tryptophan (Trp) degradation are reviewed. The KP accounts for ~95% of dietary Trp degradation, of which 90% is attributed to the hepatic KP. During immune activation, the minor extrahepatic KP plays a more active role. The KP is rate-limited by its first enzyme, Trp 2,3-dioxygenase (TDO), in liver and indoleamine 2,3-dioxygenase (IDO) elsewhere. TDO is regulated by glucocorticoid induction, substrate activation and stabilization by Trp, cofactor activation by heme, and end-product inhibition by reduced nicotinamide adenine dinucleotide (phosphate). IDO is regulated by IFN-γ and other cytokines and by nitric oxide. The KP disposes of excess Trp, controls hepatic heme synthesis and Trp availability for cerebral serotonin synthesis, and produces immunoregulatory and neuroactive metabolites, the B 3 “vitamin” nicotinic acid, and oxidized nicotinamide adenine dinucleotide. Various KP enzymes are undermined in disease and are targeted for therapy of conditions ranging from immunological, neurological, and neurodegenerative conditions to cancer." @default.
- W2598111690 created "2017-04-07" @default.
- W2598111690 creator A5039449961 @default.
- W2598111690 date "2017-01-01" @default.
- W2598111690 modified "2023-10-18" @default.
- W2598111690 title "Kynurenine Pathway of Tryptophan Metabolism: Regulatory and Functional Aspects" @default.
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