◀ Back to MAPK1
GAB1 — MAPK1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
Erk1-2 (MAPK3/MAPK1)
→
HGF(dimer)/MET(dimer)/GRB2/GAB1/SHP2 complex (MET-GRB2-GAB1-PTPN11-HGF)
(modification, collaborate)
Schaeper et al., J Cell Biol 2000, Maroun et al., Mol Cell Biol 2000
Evidence: mutant phenotype
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
Erk1-2 (MAPK3/MAPK1)
→
HGF(dimer)/MET(dimer)/GAB1/SHP2 complex (MET-GAB1-PTPN11-HGF)
(modification, collaborate)
Schaeper et al., J Cell Biol 2000, Maroun et al., Mol Cell Biol 2000
Evidence: mutant phenotype
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
Erk1-2-active (MAPK3/MAPK1)
→
HGF(dimer)/MET(dimer)/GAB1 complex (MET-GAB1-HGF)
(modification, activates)
Yu et al., J Biol Chem 2001
Evidence: mutant phenotype
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Cunnick et al., J Biol Chem 2000
:
Expression of
Gab1Y627F blocked the
extracellular signal regulated kinase-2 ( ERK2 ) activation by lysophosphatidic acid (LPA) and EGF
Cunnick et al., J Biol Chem 2001
:
Thus, physical association of activated SHP2 with
Gab1 is necessary and
sufficient to mediate the ERK
mitogen activated protein kinase activation
Cai et al., J Cell Biol 2002
(MAP Kinase Signaling System) :
Gab1 and SHP-2
promote Ras/MAPK regulation of epidermal growth and differentiation
Chen et al., J Biol Chem 2002
:
Incubation of cells with the specific EGFR inhibitor AG4178 blocked MbetaCD induced phosphorylation of EGFR, SHC, phospholipase C-gamma, and
Gab-1 as well as
MAPK activation
Fragale et al., Hum Mutat 2004
(MAP Kinase Signaling System...) :
Coexpression of
Grb2 associated binder-1-FF , which lacks SHP2 binding motifs, blocked the epidermal growth factor mediated increase in SHP2 's phosphatase activity and
resulted in a dramatic reduction of
extracellular signal regulated kinase 2 activation
Lamothe et al., Mol Cell Biol 2004
:
We demonstrate that Gab1 is essential for FGF1 stimulation of both PI 3-kinase and the antiapoptotic protein kinase Akt, while FGF1 induced
mitogen activated protein kinase ( MAPK ) stimulation is not
affected by
Gab1 deficiency
Eulenfeld et al., J Cell Sci 2009
:
Instead, additional
MAPK dependent phosphorylation of Ser551 in
Gab1 is crucial for the recruitment of Gab1 to the plasma membrane