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.

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

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

The H+ influx coupled to nutrient uptake and the plasma membrane H+-ATPase are central actors of the activation of target of rapamycin complex 1 (TORC1) in budding yeast Saccharomyces cerevisiae..

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.

Activation by amino acids causes mTORC1 to translocate transiently to the lysosomal surface.

A single point mutation in a Ras activator leads to aberrant constitutive mTOR signaling in peripheral T cells that consequently accumulate as abnormal T helper cells and stimulate the production of autoantibodies by B cells.

Interleukin 4 signaling co-opts the Akt-mTORC1-Acly pathway to couple metabolic input to the control of energetically demanding processes during macrophage M2 activation.

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