Rictor, a novel binding partner of mTOR, defines a rapamycin-insensitive and raptor-independent pathway that regulates the cytoskeleton
What this study shows
Discovery of Rictor and the SECOND mTOR complex, mTORC2. Crucially showed this complex is NOT blocked by rapamycin and does not use Raptor - it controls the cytoskeleton via PKC. This is the paper that split mTOR biology into 'two faces' at the molecular level.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Human cells + Drosophila) 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 + Drosophila |
| Journal | Current Biology |
| Year | 2004 |
| Peer reviewed | Yes |
| Record last updated | 2026-08-22 |
| Source | DOI 10.1016/j.cub.2004.06.054 · PMID 15268862 |
Extracted findings
| Intervention | Biochemical/genetic (rictor) |
| Target | mTORC2 (rictor) / actin cytoskeleton |
| Model | Human cells + Drosophila |
| Effect | Defines rictor-mTOR (mTORC2) as a rapamycin-insensitive, raptor-independent pathway regulating the cytoskeleton |
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)
- Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB (2006)
- Mammalian TOR complex 2 controls the actin cytoskeleton and is rapamycin insensitive (2004)
- Two TOR complexes, only one of which is rapamycin sensitive, have distinct roles in cell growth control (2002)
Learn the biology
Want to understand the biology behind this study? → What is mTOR?