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 | 2026-10-01 |
| Source | DOI 10.1016/j.molcel.2007.03.003 · PMID 17386266 |
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 | 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
Links in the pathway map
- Supports Akt/PKB inhibits PRAS40
- Supports PRAS40 inhibits mTORC1
- Supports Insulin activates PI3K
More studies on this topic
- The proline-rich Akt substrate of 40 kDa (PRAS40) is a physiological substrate of mammalian target of rapamycin complex 1 (2007)
- Insulin signalling to mTOR mediated by the Akt/PKB substrate PRAS40 (2007)
- Mechanisms of mTORC1 activation by RHEB and inhibition by PRAS40 (2017)
- Insulin activation of Rheb, a mediator of mTOR/S6K/4E-BP signaling, is inhibited by TSC1 and 2 (2003)
Learn the biology
Want to understand the biology behind this study? → Growth Factor Signalling
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