Signaling pathway mTOR can sense its principal activator amino acid arginine via a different mechanism than that previously described for other amino acids.

A major Th1 cytokine IFN-γ mediates mitochondrial damage that leads to mTORC1 inhibition and Paneth cells death.

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

Alterations in mTOR signaling drive similar dysregulations in the critical mid-fetal neurodevelopmental processes of neurite outgrowth and cell migration in two distinct subsets of autism, idiopathic and 16p11.2 deletion.

Enhanced metabolic efficiency associated with the tumor-predisposing African-centric p53 variant.

Tsc2 inactivation in mouse mesenchymal progenitors produced tumors with vascular anomalies reminiscent of human angiomyolipomas, and a gene expression signature in Tsc2-deficient tissues which included Lgals3, as a novel potential biomarker for TSC1/2 loss.

Protein kinase A (PKA) phosphorylates Raptor and inhibits mammalian target of rapamycin complex 1 (mTORC1) activity.

Expression of mTORC1 pathway gene variants in mouse medial prefrontal cortex leads to shared alterations in pyramidal neuron morphology, positioning, and membrane excitability but different changes in excitatory synaptic transmission.

The ZNRF2 enzyme helps the mTOR protein complex to sense amino acid levels and regulate mammalian cell growth.