IDO inhibits a tryptophan sufficiency signal that stimulates mTOR

@inproceedings{Metz2012IDOIA,
  title={IDO inhibits a tryptophan sufficiency signal that stimulates mTOR},
  author={Richard Metz and Sonja Rust and James B DuHadaway and Mario R. Mautino and David H. Munn and Nicholas N. Vahanian and Charles J. Link and George C Prendergast},
  booktitle={Oncoimmunology},
  year={2012}
}
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, is recognized as an important effector of the IDO pathway. However, in a mouse model of inflammatory carcinogenesis, ablation of Gcn2 did not promote resistance against tumor development like the… CONTINUE READING

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