The structure of the mammalian target of rapamycin complex 2 (mTORC2) reveals the architecture of the complex and explains the structural basis of rapamycin insensitivity.

High PI3K-Akt-mTORC1 activity inhibits Schwann cell differentiation, while after onset of myelination, residual PI3K-Akt-mTORC1 activity promotes myelin growth.

Structural and functional analysis reveals the mechanistic basis for mammalian target of rapamycin (mTOR)-dependent roles of DEP domain-containing mTOR interacting protein (DEPTOR) in cancer and metabolic regulation.

Transcription profiling of activated cells using Phospho-Trap, a new method for identifying activated cells, reveals a critical role for mTOR signaling in red blood cell development and the pathogenesis of anemia

ATF4 is a metabolic effector of mTORC1 signaling, co-opted to induce gene targets involved in amino acid synthesis, uptake, and tRNA charging, contributing to mTORC1-driven protein and glutathione synthesis.

The inhibitory protein DEPTOR make two widely separated interactions with mTOR that are both necessary for its unique partial mTOR inhibition, and DEPTOR is a more potent inhibitor of mutation- or RHEB-activated mTORC1 than basal mTORC1.

LARP1 turns off and on the translation of an essential class of mRNAs by acting as a key effecter and regulator for mTORC1.

Chronic engagement of Natural killer cell inhibitory receptors by MHC-I molecules maintains a high activity of the mTOR pathway allowing subsequent amplification of signaling through activating receptors upon acute stimulation.

Epilepsy caused by focal Pten deletion is only prevented when both mTOR complexes are simultaneously inhibited, but not alone, suggesting they play independent roles in the development of epilepsy.

The crucial regulator of brain function, mTOR, signals through distinct macromolecular complexes to control how synaptic vesicles are released from the presynaptic terminal.