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 | 2026-10-01 |
| Source | DOI 10.1126/science.296.5573.1655 · PMID 12040186 |
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 | 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
Links in the pathway map
- Supports Growth hormone / IGF-1 axis activates PI3K
- Supports IRS-1 / IRS-2 activates PI3K
- Supports PI3K activates Akt/PKB
More studies on this topic
- IGF2BP3-Mediated m6A Modification of OLR1 mRNA Promotes Immune Evasion in CRC via the PI3K/AKT/mTOR Pathway (2026)
- A dynamic network model of mTOR signaling reveals TSC-independent mTORC2 regulation (2012)
- Evidence for direct activation of mTORC2 kinase activity by phosphatidylinositol 3,4,5-trisphosphate (2011)
- The PI3K-AKT network at the interface of oncogenic signalling and cancer metabolism (2019)
Learn the biology
Want to understand the biology behind this study? → Growth Factor Signalling
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