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

In the orbitofrontal cortex, mTORC1, a multiprotein complex centered around the kinase mTOR, contributes to the development and/or maintenance of habitual alcohol seeking.

Modulating the nutrient sensor TORC1 only in neurons in C. elegans is sufficient to regulate systemic longevity via inter-tissue signals that remodel mitochondria networks in non neuronal cells.

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

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

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.