Identification of Sin1 as an essential TORC2 component required for complex formation and kinase activity
What this study shows
Identified Sin1 as an essential TORC2 component required for Akt phosphorylation.
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 | Genes & development |
| Year | 2006 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1101/gad.1461206 · PMID 17043309 · Free full text (PMC1619946) |
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 (Sin1) |
| Target | TORC2 / Sin1 / Akt |
| Model | Mammalian cells |
| Effect | Sin1 is an essential TORC2 component required for complex formation and kinase activity toward Akt |
In the Atlas
Related topics
Links in the pathway map
- Supports mTORC2 activates Akt/PKB
- Supports SIN1 / MAPKAP1 required-for mTORC2
More studies on this topic
- The mammalian target of rapamycin complex 2 controls folding and stability of Akt and protein kinase C (2008)
- mSin1 is necessary for Akt/PKB phosphorylation, and its isoforms define three distinct mTORC2s (2006)
- SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity (2006)
- Architecture of the human mTORC2 core complex (2018)
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