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ABL1 — EGFR

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: EGFR → ABL1 (directlyIncreases, EGFR Activity) Tanos et al., J Biol Chem 2006*
  Evidence: Moreover, we show that activated Abl phosphorylates the EGFR primarily on tyrosine 1173, and that mutation of this site to phenylalanine restores ligand-dependent endocytosis of the EGFR in the presence of activated Abl.

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: EGFR — ABL1 (direct interaction, unspecified method) Jones et al., Nature 2006
• IRef Intact Interaction: EGFR — ABL1 (direct interaction, protein array) Jones et al., Nature 2006
• IRef Ophid Interaction: EGFR — ABL1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Okuda et al., Blood 2001 (Cell Transformation, Neoplastic) : In addition to BCR/ABL, STI571 also inhibits v-Abl , TEL/ABL, the native platelet derived growth factor ( PDGF ) beta receptor, and c-KIT, but it does not inhibit SRC family kinases, c-FMS, FLT3, the epidermal growth factor receptor , or multiple other tyrosine kinases
Tanos et al., J Biol Chem 2006 : The Abl nonreceptor tyrosine kinase is activated by ligand stimulated EGFR, but the role of Abl in EGFR signaling has not been defined ... These findings reveal a novel role for Abl in promoting increased cell-surface expression of the EGFR and suggest that Abl/EGFR signaling may cooperate in human tumors
Balaji et al., J Cell Sci 2012 : We report that RIN1-RAB5 signaling favors EGFR downregulation over EGFR recycling, whereas RIN1-ABL signaling stabilizes EGFR and inhibits macropinocytosis