IDO inhibits a tryptophan sufficiency signal that stimulates mTOR: A novel IDO effector pathway targeted by D-1-methyl-tryptophan

Tryptophan catabolism by indoleamine 2,3-dioxygenase (IDO) alters inflammation and favors T-cell tolerance in cancer, but the underlying molecular mechanisms remain poorly understood. The integrated stress response kinase GCN2, a sensor of uncharged tRNA that is activated by amino acid deprivation,...

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Veröffentlicht in:	Oncoimmunology 2012-12, Vol.1 (9), p.1460-1468
Hauptverfasser:	Metz, Richard, Rust, Sonja, DuHadaway, James B., Mautino, Mario R., Munn, David H., Vahanian, Nicholas N., Link, Charles J., Prendergast, George C.
Format:	Artikel
Sprache:	eng
Schlagworte:	amino acid starvation autophagy Binding Biology Bioscience Calcium Cancer Cell Cycle IDO IDO2 immunomodulation Landes mTOR Organogenesis PKC-θ Proteins Research Paper S6K stress signaling TDO
Online-Zugang:	Volltext
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