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MAPK10 — MET

Text-mined interactions from Literome

Moriuchi et al., Biochem Biophys Res Commun 2001 (MAP Kinase Signaling System) : Treatment with a combination of HGF and EGF, in comparison with that of either HGF or EGF, induced tyrosine phosphorylation of both c-Met and EGF receptor (EGFR) independently and additively stimulated MAPK activity and cyclin D1 expression, resulting in additive stimulation of DNA synthesis
Copp et al., J Biol Chem 2003 (MAP Kinase Signaling System) : Binding of InlB to the HGF receptor results in mitogen activated protein ( MAP ) kinase and phosphoinositide 3-kinase activation, followed by changes in the organization of the actin cytoskeleton
Mood et al., J Cell Physiol 2006 : We show that cell-cycle progression and activation of MAPK and JNK mediated by the oncogenic Met receptor, Tpr-Met, are dependent on its kinase activity and the presence of the twin phosphotyrosine ( Y482 & Y489 ) residues in its C-terminus, but that the recruitment of Grb2 and Shc adaptor proteins is dispensable, implicating other signaling molecules
Tan et al., FEBS Lett 2011 (Carcinoma, Hepatocellular...) : Forced expression of miR-198 decreased c-MET expression at both mRNA and protein levels and consequently diminished HGF induced phosphorylation of p44/42 MAPK in HCC cells
Fabian et al., J Cell Biol 1993 : Injection of Mos-specific antisense oligodeoxyribonucleotides inhibited MAPK activation in response to progesterone and Tpr-Met , but failed to inhibit these events in oocytes expressing an oncogenic deletion mutant of Raf-1 ( delta N'Raf )