PRAS40 is an insulin-regulated inhibitor of the mTORC1 protein kinase
What this study shows
Identified PRAS40 as the missing insulin-controlled brake INSIDE mTORC1. When insulin is absent PRAS40 clamps the complex shut; insulin makes Akt phosphorylate PRAS40, releasing the brake so Rheb can fully switch mTORC1 on. Explained how hormone signals set the exact strength of mTORC1 activity.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Human cells (biochemistry)) 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 | Human cells (biochemistry) |
| Journal | Molecular Cell |
| Year | 2007 |
| Peer reviewed | Yes |
| Record last updated | 2026-08-22 |
| Source | DOI 10.1016/j.molcel.2007.03.003 · PMID 17386266 |
Extracted findings
| Intervention | Biochemical/genetic (PRAS40) |
| Target | mTORC1 / PRAS40 |
| Model | Human cells (biochemistry) |
| Effect | PRAS40 is an insulin-regulated inhibitor of the mTORC1 kinase (raptor-binding) |
In the Atlas
Related topics
More studies on this topic
- Ablation in mice of the mTORC components raptor, rictor, or mLST8 reveals that mTORC2 is required for signaling to Akt-FOXO and PKCalpha, but not S6K1 (2006)
- mTOR controls mitochondrial oxidative function through a YY1-PGC-1alpha transcriptional complex (2007)
- AMPK phosphorylation of raptor mediates a metabolic checkpoint (2008)
- Raptor, a binding partner of target of rapamycin (TOR), mediates TOR action (2002)
Learn the biology
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