Function
Processes
Ligand-activated receptor tyrosine kinase at the head of the pathway.
A compact insulin receptor signaling module. Insulin binding activates the receptor tyrosine kinase INSR, which autophosphorylates and phosphorylates IRS adaptors. IRS phosphotyrosines recruit PI3K and route the signal into PIP3-AKT signaling, controlling FOXO-dependent transcription, glucose uptake, glycogen metabolism, growth, and survival. The module is grounded in GO:0008286 and uses PAINT PTN anchors for the insulin receptor and AKT-family signaling roles where local IBD seed rows support them.
All recommended fields populated.
✗ none found
No MODULE:insulin_receptor_signaling deep-research report alongside the module YAML.
✓ every leaf node grounds to a representative protein.
✓ every declared conforms_to bundle matches its template motif.
0 complete review(s) · 1 with deep research · 4 missing review · 0 reviewed but lacking deep research
| Gene | Review | Complete | Deep research |
|---|---|---|---|
| FOXO1 Q12778 | ✓ | 145/148 | ✓ |
| INSR P06213 | ✗ | — | — |
| PIK3R1 P27986 | ✗ | — | — |
| AKT2 P31751 | ✗ | — | — |
| IRS1 P35568 | ✗ | — | — |
Insulin binding stabilizes the active receptor dimer, enabling activation-loop autophosphorylation and phosphorylation of adaptor substrates.
Ligand-activated receptor tyrosine kinase at the head of the pathway.
IRS proteins are phosphorylated by INSR and provide SH2 docking sites for PI3K regulatory subunits, routing the signal into the PI3K-AKT arm.
Receptor-phosphorylated adaptor that recruits SH2-domain effectors.
SH2-domain regulatory subunit that links IRS phosphotyrosines to PI3K activation.
PI3K-generated PIP3 activates AKT, which phosphorylates FOXO transcription factors and other metabolic/growth substrates.
Major kinase output linking insulin receptor activation to metabolism and growth.
AKT-regulated transcription factor family controlling fasting and stress-response genes.