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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 *
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