Recently, the protein complex, mammalian target of rapamycin complex 1 (mTORC1), has been identified to facilitate the expression of nuclear genes encoding mitochondrial proteins (NUGEMPs) in resting muscle cells via the interaction of the mTORC1 components, mTOR and raptor, the transcription factor Yin Yang 1, and peroxisome proliferator-activated receptor-γ coactivator-1α.

 Down-regulated microRNA-223 or elevated ZIC1 inhibits the development of pancreatic cancer via inhibiting PI3K/Akt/mTOR signaling pathway activation.

 This 2-step licensing of monocytes requires activation of the AKT/mTOR/mTORC1 signaling cascade by GM-CSF followed by signaling through the interferon-γ receptor (IFN-γR)/interferon regulatory factor-1 (IRF-1) pathway.

 Suppression of the GTPase-activating protein RGS10 increases Rheb-GTP and mTOR signaling in ovarian cancer cells.

 These results suggest that mTOR regulate EMT at least in part by down regulation of RhoA and Rac1 signaling pathways.

 Our results demonstrated that KU-0063794 blocked mTOR complex 1/2 (mTORC1/2) activation, and downregulated mTOR-regulated genes (Cyclin D1 and hypoxia-inducible factor 1α) in HepG2 cells.

 The signalling cascade dependent on the MT1-MMP-VEGFR-2-Src complex activated Akt and mTOR, ultimately leading to increased VEGF-A transcription.

 However, insulin induction of mTOR activity was maintained in IL-6-treated myotubes.

 Mechanistically, α-SMA overexpression activated the mammalian target of rapamycin (mTOR) signaling pathway.

 Mechanistic studies revealed that TGM2 promotes C2C12 myoblast differentiation via enhancing GPR56 mediated activation of the mTOR signaling.