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. Author manuscript; available in PMC: 2009 Sep 14.
Published in final edited form as: Cell Cycle. 2009 Apr 2;8(7):1003–1006. doi: 10.4161/cc.8.7.8045

Figrure 1. mTORC1-mediated cell growth machinery in the regulation of hematopoietic stem cell quiescence.

Figrure 1

mTORC1 functions to integrates various upstream signaling pathways to regulate protein synthesis and cell growth. mTORC1 hyper-activation resulting from inactivation of PTEN, TSC1, PML and potentially Fbxw7 (all highlighted in box), drives HSC from quiescent state and leads to subsequent HSC exhaustion. Akt promotes mTORC1 activation and inhibits FoxO transcriptional factors. FoxOs (highlighted in box) function to maintain HSC quiescence through suppression of reactive oxygen species (ROS). For simplicity and for the focus of this review, several components of mTORC1 pathway, such as AMPK, REDD1, are not shown in this figure.