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CRK — GAB1
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
Complex of CRK-GAB1
→
MET
(increases, CRK/GAB1 Activity)
Evidence: Page 54 - "Crk appears to bind Gab1 in response to Met but not other receptor tyrosine kinases."
-
KEGG Bacterial invasion of epithelial cells:
GAB1
→
CRK/CRKL
(protein-protein, activation)
-
KEGG Renal cell carcinoma:
GAB1
→
CRK/CRKL
(protein-protein, activation)
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
CRK (CRK)
→
HGF(dimer)/MET(dimer)/GAB1 complex (MET-GAB1-HGF)
(modification, collaborate)
Lamorte et al., Oncogene 2000, Lamorte et al., J Biol Chem 2002*, Chan et al., Oncogene 2010
Evidence: physical interaction
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
CRK (CRK)
→
HGF(dimer)/MET(dimer)/GAB1/CRK complex (MET-GAB1-CRK-HGF)
(modification, collaborate)
Lamorte et al., Oncogene 2000, Lamorte et al., J Biol Chem 2002*, Chan et al., Oncogene 2010
Evidence: physical interaction
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
HGF(dimer)/MET(dimer)/GAB1 complex (MET-GAB1-HGF)
→
HGF(dimer)/MET(dimer)/GAB1/CRK complex (MET-GAB1-CRK-HGF)
(modification, collaborate)
Lamorte et al., Oncogene 2000, Lamorte et al., J Biol Chem 2002*, Chan et al., Oncogene 2010
Evidence: physical interaction
-
WikiPathways Signaling of Hepatocyte Growth Factor Receptor:
GAB1
→
CRK
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Watanabe et al., Mol Cancer Res 2006
(Sarcoma, Synovial) :
Adaptor molecule
Crk is
required for sustained phosphorylation of
Grb2 associated binder 1 and hepatocyte growth factor induced cell motility of human synovial sarcoma cell lines
Watanabe et al., Cell Res 2009
:
We have previously shown that
Crk overexpression, which is detectable in various human cancers,
induces tyrosine phosphorylation of
Gab1 without extracellular stimuli