Gene interactions and pathways from curated databases and text-mining

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HGF — PI3

Text-mined interactions from Literome

Day et al., Oncogene 1999 : HGF stimulated DNA synthesis in 184B5 and 32D/c-Met cells, while HGF/NK2 was mitogenically inactive, despite the ability of HGF/NK2 to stimulate c-Met autophosphorylation, mitogen activated protein kinase ( MAPK ), and phosphatidylinositol 3-kinase (PI3K) in both cell systems
Zhang et al., J Neurosci Res 2000 : HGF stimulated both mitogen activated protein ( MAP ) kinase and phosphatidylinositol-3 (PI3)-kinase activity in cerebellar granule neurons
Qiao et al., Cell Growth Differ 2000 (Carcinoma, Intraductal, Noninfiltrating...) : PI 3-kinase activity is also required for the HGF- and fibronectin induced survival responses, as well as anchorage independent colony growth
Chandrasekher et al., Exp Eye Res 2001 (MAP Kinase Signaling System) : HGF induced three- to five-fold increase in PI-3K activity in 5-10 min, whereas KGF stimulation resulted in two- to three-fold increase in activity in 2-10 min
Nakamura et al., Oncogene 2001 (Carcinoma, Renal Cell...) : With respect to downstream signaling molecules of HGFR in ACHN or VMRC-RCW, the Ras-MAPK pathway was downregulated, whereas phosphoinositide 3-kinase ( PI3-kinase ) was not further activated by HGF-treatment in VMRC-RCW cells
Cho et al., Hepatology 2003 : In conclusion, HGF induces nuclear translocation of C/EBP beta via the PI3-kinase pathway and stimulates C/EBP DNA binding and gene transcription and that the PI3-kinase mediated C/EBP activation by HGF may contribute to cell replication
Bardelli et al., Biochem Biophys Res Commun 2005 (Neoplasm Invasiveness...) : Since Gab1, JNK and PI 3-kinase are activated with same intensity and kinetics by HGF and by the two agonist antibodies, it is concluded that level and duration of MAPK activation by Met receptor are crucial for the induction of a full HGF dependent mitogenic and invasive program in KS cells
Gong et al., Kidney Int 2006 (Acute Disease...) : HGF activated phosphatidylinositol 3-kinase (PI3K)-Akt that in turn inhibited its downstream transducer glycogen synthase kinase ( GSK ) 3
Yoshizawa et al., Oncol Rep 2011 (Endometrial Neoplasms) : Here, we report that i ) treatment of RL95-2 cells with HGF resulted in phosphorylation of the HGF receptor c-Met, activation of Akt and I?B, translocation of NF-?B into the nucleus, and up-regulation of COX-2 mRNA ; ii ) the I?B-a phosphorylation inhibitor BAY11-7082 and the selective COX-2 inhibitor CAY10452 blocked HGF mediated anoikis resistance in RL95-2 cells ; and iii ) HGF induced migration and invasion in RL95-2 cells, while the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 and CAY10452 blocked these effects of HGF stimulation
Kim et al., Exp Cell Res 2011 : These results suggest that a-syntrophin is required for HGF induced migration of myoblasts and for proper PI3-kinase/Akt signaling
Rahimi et al., J Biol Chem 1996 : In this study we have shown that hepatocyte growth factor (HGF) induces a rapid tyrosine phosphorylation of PI 3-kinase and association with HGF receptor/Met in Mv1Lu epithelial cells ... Wortmannin, a potent inhibitor of PI 3-kinase, inhibited HGF induced PI 3-kinase activity, proliferation of Mv1Lu cells, and spontaneous growth of SP1 cells in a dose-, and time dependent manner ... Transfection of a dominant negative mutant p85 ( Deltap85 ) subunit of PI 3-kinase into SP1 cells strongly inhibited HGF stimulated proliferation and PI 3-kinase activity ... Overall, these results suggest that HGF induced PI 3-kinase activity is important for the mitogenic action of HGF in epithelial cells and further demonstrate that expression of c-Jun is not influenced by inhibition of PI 3-kinase activity