Oliver's mTOR Atlas Evidence Platform
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Pathway link PI3K-AKT

PI3K Akt/PKB

PI3K activates Akt/PKB.

That lipid pulls Akt to the cell membrane, where it gets switched on.

PIP3 pulls Akt to the membrane, where it gets phosphorylated and activated.

The conditions it holds under

Mammalian cell study (LIU2015) plus a review (CAN2002). Cell biochemistry; not tested in whole animals or in people by the cited sources.

PIP3 recruits Akt; recruitment alone does not activate it. Full activation additionally needs PDK1 (T308) and mTORC2 (S473), so the strength of this link depends on the activity of both of those.

Time it takes
seconds
Step
indirect (through steps not drawn here)
Measured in
mammalian cells
Where in the cell
plasma membrane
Reaches people?
plausible in people, not shown directly
How settled
settled in the literature

Studies behind it

YearEvidenceStudy
2002 R The phosphoinositide 3-kinase pathwayCAN2002 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.
2015 M PtdIns(3,4,5)P3-Dependent Activation of the mTORC2 Kinase ComplexLIU2015 PIP3 relieves SIN1 PH-domain autoinhibition to activate the mTORC2 kinase complex.

Points the other way

No study in the Atlas contradicts this link. That means none in this curated set, not none in the literature.

Who has checked this

Checked by
No researcher outside the project has checked this link yet.
Curator sign-off
Not signed off yet. This link was drafted with AI help and has not been reviewed link by link; treat it as a proposal until it is.
Curated by
Oliver Barton, with AI help for drafting; see how links are checked.

“How settled” describes how far researchers in the field agree. It is not the same as the sign-off above, which only says whether a named curator has checked this page.

If this link rests on your own work: a click on “This looks right” below, or a short note through “Report an error”, helps us more than anything else on this page.

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