Lysosomal recruitment of TSC2 is a universal response to cellular stress
What this study shows
Lysosomal recruitment of TSC2 is a universal response to cellular stress that inhibits mTORC1.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Mammalian cells) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Mammalian cells |
| Journal | Nature communications |
| Year | 2016 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1038/ncomms10662 · PMID 26868506 · Free full text (PMC4754342) |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Various cellular stresses (amino-acid/growth-factor withdrawal, etc.) – mechanistic |
| Target | TSC2 / mTORC1 |
| Model | Mammalian cells |
| Effect | Diverse stresses relocate TSC2 to the lysosome → inhibit mTORC1 (a universal response) |
In the Atlas
Related topics
Links in the pathway map
More studies on this topic
- Mammalian TOR: a homeostatic ATP sensor (2001)
- AMPK phosphorylation of raptor mediates a metabolic checkpoint (2008)
- AMP-activated protein kinase induces a p53-dependent metabolic checkpoint (2005)
- Spatial control of the TSC complex integrates insulin and nutrient regulation of mTORC1 at the lysosome (2014)
Learn the biology
Want to understand the biology behind this study? → Rheb — The Critical Regulator
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