Increased mTORC1 Signaling UPRegulates Stress
Copyright policy )Increased mTORC1 Signaling UPRegulates Stress
In this issue of Molecular Cell, Ozcan et al. (2008) show that the loss of the tuberous sclerosis tumor suppressor complex induces endoplasmic reticulum stress, leading to attenuation of insulin receptor signaling activity via the unfolded protein response.
- Whitehead Institute for Biomedical Research United States
- Massachusetts Institute of Technology United States
- Broad Institute United States
TOR Serine-Threonine Kinases, Tumor Suppressor Proteins, Proteins, Cell Biology, Mechanistic Target of Rapamycin Complex 1, Endoplasmic Reticulum, Receptor, Insulin, Mice, Oxidative Stress, Multiprotein Complexes, Neoplasms, Animals, Humans, Molecular Biology, Signal Transduction, Transcription Factors
TOR Serine-Threonine Kinases, Tumor Suppressor Proteins, Proteins, Cell Biology, Mechanistic Target of Rapamycin Complex 1, Endoplasmic Reticulum, Receptor, Insulin, Mice, Oxidative Stress, Multiprotein Complexes, Neoplasms, Animals, Humans, Molecular Biology, Signal Transduction, Transcription Factors
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