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
What this study shows
The foundational genetic 'dissection' of the two complexes in living mice. Deleting Raptor was lethal early (mTORC1 essential); deleting Rictor or mLST8 selectively knocked out mTORC2 signaling to Akt and PKCalpha but spared S6K1. This cleanly assigned jobs to each complex and showed mLST8 is an mTORC2-specific requirement in mice.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Knockout mice (raptor/rictor/mLST8)) 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 | Knockout mice (raptor/rictor/mLST8) |
| Journal | Developmental Cell |
| Year | 2006 |
| Peer reviewed | Yes |
| Record last updated | 2026-07-29 |
| Source | DOI 10.1016/j.devcel.2006.10.007 · PMID 17141160 |
Extracted findings
| Intervention | Genetic (raptor / rictor / mLST8 knockout mice) |
| Target | mTORC1 vs mTORC2 / Akt-FOXO / PKCα |
| Model | Knockout mice |
| Effect | mTORC2 (rictor/mLST8) is required for Akt-FOXO and PKCα signaling but not S6K1; raptor/mTOR-null mice die early |
In the Atlas
Related topics
More studies on this topic
- GbetaL, a positive regulator of the rapamycin-sensitive pathway required for the nutrient-sensitive interaction between raptor and mTOR (2003)
- Rictor, a novel binding partner of mTOR, defines a rapamycin-insensitive and raptor-independent pathway that regulates the cytoskeleton (2004)
- Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB (2006)
- PRAS40 is an insulin-regulated inhibitor of the mTORC1 protein kinase (2007)
Learn the biology
Want to understand the biology behind this study? → What is mTOR?