Unsurprisingly, improper activation of TOR signaling has been implicated in the development of cancers and hamartoma syndromes and in metabolic diseases such as diabetes and obesity ( Manning, 2004). In response to these signals, TOR effects changes in a diverse number of downstream processes, including transcription, translation, nutrient import, and autophagy, to achieve the alignment of cellular energy utilization with available resources.

TOR activity is stimulated by insulin-responsive phosphatidylinositol-3 kinase (PI3K)/Akt signaling, by nutrients such as amino acids, and by high cellular energy levels (for reviews see Martin and Hall, 2005 Sarbassov et al., 2005a). The regulatory kinase target of rapamycin (TOR) has emerged as a convergence point for the transduction of these signals into appropriate changes in cell metabolism and growth.

Multicellular organisms must modulate cellular growth and proliferation in response to available nutrients, energy, and growth factor signaling.

Tor books reorganization