◀ Back to MET
MET — PIK3CA
Pathways - manually collected, often from reviews:
-
KEGG Focal adhesion:
EGFR/ERBB2/FLT1/FLT4/IGF1R/KDR/MET/PDGFRA/PDGFRB
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
HGF(dimer)/MET(dimer)/GAB1 complex (MET-GAB1-HGF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Yu et al., J Biol Chem 2001, Yu et al., J Biol Chem 2002*, Graziani et al., J Biol Chem 1991*, Schaeper et al., Proc Natl Acad Sci U S A 2007, Ponzetto et al., Cell 1994
Evidence: assay, physical interaction
Text-mined interactions from Literome
Taher et al., Biochem Biophys Res Commun 2002
(Arteriosclerosis...) :
Stimulation with HGF led to activation of
Met as well as to
activation of
PI3-K , PKB/Akt, MEK, and the MAP kinases Erk1 and -2
Maulik et al., J Cell Mol Med 2002
(Carcinoma, Small Cell...) :
We show that association of c-Met with
PI3K and GAB2 is
diminished by inhibiting
c-Met
Watson et al., Neoplasia (New York, N.Y.) 2006
(Adenocarcinoma...) :
We conclude that inhibition of c-Met may be a useful therapeutic strategy for EA. Factors other than receptor overexpression, such as
c-Met dependent
PI3K/Akt signaling, may be predictive of an individual tumor 's response to c-Met inhibition
Martínez-Palacián et al., PloS one 2013
:
Altogether, results presented here provide solid evidences that both paracrine and autocrine
HGF/Met signaling
requires PI3K to promote mouse hepatic oval cell survival against TGF-ß induced oxidative stress and apoptosis