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IGF1R — SRC

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: IGF1R → SRC (directlyIncreases, IGF1R Activity)
  Evidence: 8550552;8940173
• NCI Pathway Database Plasma membrane estrogen receptor signaling: E2/ER alpha (dimer)/PELP1/Src/p52 SHC complex (ESR1-PELP1-SRC-SHC1) → IGF-1R heterotetramer complex (IGF1R) (modification, activates)
  Kahlert et al., J Biol Chem 2000, Song et al., Proc Natl Acad Sci U S A 2004
  Evidence: mutant phenotype, assay, physical interaction
• NCI Pathway Database Plasma membrane estrogen receptor signaling: E2/ER alpha (dimer)/PELP1/Src/p52 SHC complex (ESR1-PELP1-SRC-SHC1) → IGF-1R heterotetramer/IGF1 complex (IGF1R-IGF1) (modification, activates)
  Kahlert et al., J Biol Chem 2000, Song et al., Proc Natl Acad Sci U S A 2004
  Evidence: mutant phenotype, assay, physical interaction
• WikiPathways Signaling Pathways in Glioblastoma: IGF1R/ERBB3/FGFR1/PDGFRA/PDGFRB/ERBB2/EGFR/FGFR2/MET → SRC (mim-stimulation)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: IGF1R — SRC (in vitro) Peterson et al., J Biol Chem 1996*
• IRef Hprd Interaction: IGF1R — SRC (in vivo) Peterson et al., J Biol Chem 1996*

Text-mined interactions from Literome

Sekharam et al., Anticancer Res 2003 (Adenocarcinoma...) : Insulin-like growth factor 1 receptor activates c-SRC and modifies transformation and motility of colon cancer in vitro
Song et al., J Steroid Biochem Mol Biol 2010 (Breast Neoplasms) : The Src inhibitor PP2 and IGF-1-R inhibitor AG1024 greatly blocked fulvestrant induced ERalpha/IGF-1-R interaction leading to a further depletion of total cellular ERalpha induced by fulvestrant and further enhanced fulvestrant induced cell growth arrest
Spartà et al., FEBS Lett 2010 (Neuroblastoma) : Furthermore, MOPr induced activation of IGF-I receptor requires the tyrosine kinase c-Src
Zhao et al., J Biol Chem 2011 (Colitis...) : NT also rapidly induces Src tyrosine phosphorylation, whereas pretreatment of cells with the Src inhibitor PP2 before NT exposure decreases NT-induced IGF-1R phosphorylation
Fujita et al., J Biol Chem 2013 : Inhibitors of IGF1R, Src , AKT, and ERK1/2 did not suppress avß3-IGF-IGF1R ternary complex formation, suggesting that activation of these kinases are not required for ternary complex formation
Peterson et al., J Biol Chem 1996 : The goal of the present study was to analyze the mechanistic basis and functional significance of the Src induced phosphorylation and activation of the IGF-I receptor ... 2 ) We determined that the sites of Src induced phosphorylation of the IGF-I receptor are the same as the ligand induced autophosphorylation sites and that the Src kinase can catalyze these phosphorylations directly