A novel population of hematopoietic cells unmasked by mTORC1 inactivation reveals a new mechanism of innate immune tolerance and a new consequence of defective hematopoiesis.

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

IQ domain phosphorylation regulates calmodulin binding and myosin-1 function.

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

Non-specific sodium entry inhibits T cell receptor induced gene expression and differentiation of T cells by depleting intracellular ATP and disrupting mTORC2 dependent signalling axis.

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.

The Mtgr1 protein promotes the maintenance of pluripotency and germ cell formation via its interaction with the stem cell regulator Prdm14.

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.

The key Target of Rapamycin Complex (TORC1) component Kog1 moves into bodies during glucose starvation to limit reactivation of the complex.

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