Falcon deep research attempt timed out on 2026-05-04 while running
just deep-research-falcon mouse Akt1; no Akt1-deep-research-falcon.md file
was produced. Review decisions used the cached UniProt record, cached
publications, and BioReason research.
Core function judgment: AKT1 is a PH-domain AGC serine/threonine protein kinase
activated downstream of PI3K and growth factor/insulin signaling. UniProt
describes AKT1 as one of three closely related AKT serine/threonine kinases that
regulate metabolism, proliferation, survival, growth, and angiogenesis through
serine/threonine phosphorylation of downstream substrates [UniProt:P31750
"This is mediated through serine and/or threonine phosphorylation"]. The
BioReason report supports the same architecture-based conclusion:
PH-domain membrane recruitment plus an AGC kinase domain explains
ATP-dependent serine/threonine kinase activity
[file:mouse/Akt1/Akt1-bioreason-rl-predictions.md "A cytoplasmic AGC-type
serine/threonine kinase"].
Key local evidence for process calls includes insulin-stimulated GLUT4
translocation PMID:9415393, GSK3/CRMP2 signaling PMID:22057101, direct regulation of mTORC2
[PMID:23684622 "Akt directly regulates mTORC2"; PMID:26235620 "positive
feedback loop between Akt and mTORC2"], and MICU1/mitochondrial calcium control
PMID:30504268.
Curation stance: protein serine/threonine kinase activity and protein
phosphorylation are core. PI3K/AKT, insulin, mTORC1/2, growth factor, survival,
metabolic, migration, and development terms are valid pathway contexts but are
kept as non-core unless the term directly describes AKT1 catalytic activity.
Generic protein binding, broad kinase/transferase labels, and very broad
cellular responses are marked as over-annotated when a more informative term is
already present.