Oliver's mTOR Atlas Evidence Platform
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Pathway link IGF1-PI3K

Growth hormone / IGF-1 axis PI3K

Growth hormone / IGF-1 axis activates PI3K.

IGF-1 latches onto its own receptor and switches on PI3K, which builds a signalling lipid. Growth hormone works one step further back: it does not land on this receptor itself, it makes the liver release IGF-1, which then does. Insulin takes a receptor of its own into the same arm.

IGF-1 docks on the IGF-1 receptor, which recruits IRS proteins and switches on PI3K to make the lipid messenger PIP3. Growth hormone does not use this receptor: it signals through its own receptor and JAK2/STAT5b, and reaches this arm mostly by inducing hepatic IGF-1. The node is drawn as one axis because the Atlas's lifespan evidence comes from interventions that lower the whole axis at once.

The conditions it holds under

Compressed on purpose: growth hormone and IGF-1 are one node here, but they are not one molecule and they do not share a receptor. GH signals GHR-JAK2-STAT5b and acts on this arm largely by inducing hepatic IGF-1; patients with a homozygous STAT5b mutation have GH insensitivity with low IGF-1 and low IGFBP-3 (Kofoed 2003, PMID 13679528, outside this corpus). The dwarf-mouse lifespan evidence on this axis lowers GH and IGF-1 together, so it does not tell the two apart. Insulin enters the same arm through its own receptor and is drawn separately (INS-PI3K).

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.
2001 M Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathwaysROM2001 Shows IGF-1 drives muscle fiber hypertrophy through Akt, via both the mTOR and GSK3 branches, in cultured myotubes, establishing mTOR as a central node for muscle growth signaling.

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.

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