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MET — PIK3R1
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
Complex of ERBB3-PIK3R1
→
MET
(directlyIncreases, ERBB3/PIK3R1 Activity)
Evidence: To investigate how MET activates ERBB3 tyrosine phosphorylation, we first expressed ERBB3 alone or in combination with MET in Chinese hamster ovary (CHO) cells, which normally do not express detectable levels of EGFR, ERBB2, or ERBB3. Coexpression of MET and ERBB3 resulted in marked phosphorylation of ERBB3 (Fig. 3D). This phosphorylation could be blocked with PHA-665752 but not with high concentrations of gefitinib (3 mM), lapatinib (3 mM) or the SRC family kinase inhibitor PP2 (10 mM). In addi...
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KEGG Focal adhesion:
EGFR/ERBB2/FLT1/FLT4/IGF1R/KDR/MET/PDGFRA/PDGFRB
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
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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
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Petrelli et al., Nature 2002
:
Cbl, in turn, binds and ubiquitinates activated
HGF receptor , and by recruiting the
endophilin-CIN85 complex , it
regulates receptor internalization
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