Falcon deep research attempt was not completed on 2026-05-04 after the provider
timed out during the batch run; no Src-deep-research-falcon.md file was
produced. Review decisions used the cached UniProt record, cached publications,
and BioReason research.
Core function judgment: SRC is a non-receptor protein tyrosine kinase with
SH3-SH2-kinase architecture. UniProt describes activation after engagement of
many receptor classes and phosphorylation of receptor/adaptor/cytoskeletal
substrates [UniProt:P05480 "Non-receptor protein tyrosine kinase... activated
following engagement of many different classes of cellular receptors"]. The
BioReason report independently supports the same domain-based call
[file:mouse/Src/Src-bioreason-rl-predictions.md "A cytoplasmic non-receptor
tyrosine kinase"].
Key local evidence for pathway and localization calls includes Src kinase
activation in growth factor-like signaling PMID:8910389, osteoclast function via
Src/Cbl/PI3K signaling PMID:14739300, Src-induced podosome formation PMID:21525037, inflammation-induced epithelial regeneration
through a gp130-Src-YAP module PMID:25731159, and
laminin-induced Rac/JNK activation by Src family kinases PMID:18044967.
Curation stance: protein tyrosine kinase activity, non-membrane spanning
protein tyrosine kinase activity, tyrosine phosphorylation, and major
cytoplasmic/plasma-membrane signaling localizations are core. Receptor-specific,
adhesion, osteoclast, podosome, epithelial, mitochondrial, and developmental
terms are kept as non-core pathway contexts. Generic protein-binding and broad
binding labels are marked over-annotated unless the term describes an
informative domain-mediated recognition mode.