Gene interactions and pathways from curated databases and text-mining

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EPHB2 — RET

Text-mined interactions from Literome

Hennige et al., Endocrinology 2001 : Suppression of the Ret-9bp tyrosine kinase activity by SHP1 caused a decrease in activation of Erk2 ( extracellular signal regulated kinase ) and abolished PKB/Akt ( protein kinase B ) phosphorylation
Mitsutake et al., Endocrinology 2006 (Carcinoma, Papillary...) : To determine the key RAF isoform mediating RET/PTC induced ERK phosphorylation, we stably transfected doxycycline-inducible RET/PTC3 expressing thyroid PCCL3 cells with small interfering RNA vectors to induce selective knockdown of BRAF or CRAF ... Conditional RET/PTC3 expression induced comparable ERK phosphorylation in CRAF knockdown and control cells but negligible ERK phosphorylation in BRAF knockdown cells
Iavarone et al., J Biol Chem 2006 (MAP Kinase Signaling System...) : By using RET/PTC3 molecules mutated in specific tyrosine autophosphorylation sites, we characterized Tyr ( 981 ), a known binding site for c-Src, as a major determinant of RET/PTC3 induced Erk8 activation , although, surprisingly, the underlying mechanism did not strictly depend on the activity of Src ... In contrast, we present evidence that RET/PTC3 acts on Erk8 through Tyr ( 981 ) -mediated activation of c-Abl
Knostman et al., Thyroid 2007 (Carcinoma, Papillary...) : Only one line had thyroid targeted, doxycycline regulated RET/PTC1 and luciferase coexpression, in which doxycycline induction of RET/PTC1 led to Erk phosphorylation and reduced expression of the sodium/iodide symporter ( NIS )
van Weering et al., Oncogene 1995 : These results suggest that Ret can induce ERK2 activation in a p21ras dependent manner in cells derived from tissue where Ret is endogenously expressed
van Puijenbroek et al., Oncogene 1997 (Neuroectodermal Tumors, Primitive, Peripheral) : Analysis of the kinetics of ERK2 activation and downstream events revealed that Ret and FGF receptor activation led to sustained ERK2 activation and SRE transactivation, while PDGF treatment led to transient ERK2 activation and failed to induce SRE transactivation