Phosphoinositide 3-kinase; produces signaling lipids downstream of growth-factor receptors; activates Akt and sits upstream of the entire mTOR pathway.
| Tier | What it means | Studies |
|---|---|---|
| D | Mechanistic / in vitro / review | 5 |
No direct human evidence in the Atlas for this entity yet — everything below rests on animal or mechanistic work.
| Study | Year | Tier | Finding |
|---|---|---|---|
| BANERJEE2026 | 2026 | D | Review mapping the mechanistic crosstalk between PI3K/Akt/mTOR and JAK/STAT pathways in MS neuroinflammation, identifying dual-pathway mTOR targeting as a therapeutic opportunity to reduce immune dysr |
| DIB2015 | 2015 | D | Review of mTORC1 regulation by PI3K signalling. |
| CAN2002 | 2002 | D | 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. |
| INO2002 | 2002 | D | Akt directly phosphorylates and inactivates TSC2, disrupting the TSC1-TSC2 complex and releasing its inhibition of mTOR - the link between growth-factor/insulin signaling and mTORC1 activation. |
| ROM2001 | 2001 | D | Shows IGF-1 drives muscle fiber hypertrophy specifically through the Akt-mTOR pathway, establishing mTORC1 as a central node for muscle growth signaling. |