The phosphoinositide 3-kinase pathway
What this study shows
Review establishing PI3K as a central signaling hub controlling cell survival, metabolism, and growth downstream of growth-factor receptors and upstream of Akt and mTOR.
At a glance
| Evidence type | R Review — secondary literature, not a new result Marked R because it is a review or synthesis of existing evidence rather than a new primary result; that is a different form of writing, not a weaker one. |
| Study type | Narrative Review |
| Model system | Review article |
| Journal | Science |
| Year | 2002 |
| Peer reviewed | Yes |
| Record last updated | 2026-08-22 |
| Source | DOI 10.1126/science.296.5573.1655 · PMID 12040186 |
Extracted findings
| Intervention | Not applicable (review) |
| Target | PI3K / PIP3 (upstream of Akt-mTOR) |
| Model | Review |
| Effect | Reviews the PI3K pathway in cell survival, metabolism, gene expression and cytoskeletal control |
In the Atlas
Related topics
More studies on this topic
- TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling (2002)
- mTOR inhibition augments antitumor immune effector response by reprogramming the TP53-mutant, immune-cold HNSCC tumor microenvironment (2026)
- Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways (2001)
- Decoding the PI3K/Akt/mTOR-JAK/STAT signaling axis in multiple sclerosis: mechanistic crosstalk and therapeutic opportunities. (2026)
Learn the biology
Want to understand the biology behind this study? → Growth Factor Signalling