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.
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.
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.
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