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EPHB2 — SPRY2

Text-mined interactions from Literome

Tsavachidou et al., Cancer Res 2004 (MAP Kinase Signaling System...) : These data suggest that SPRY2 , an inhibitor of ERK signaling, may be bypassed in melanoma cells either by down-regulation of its expression in WT BRAF cells, or by the presence of the BRAF mutation
Nadeau et al., J Cell Biochem 2007 : Spry2 inhibits FGF dependent ERK activation and thus Spry acts as a feedback inhibitor of FGF mediated proliferation
Ishida et al., Cancer Sci 2007 (Neuroblastoma) : Expression of SPRY1, SPRY2, SPRY3 and SPRY4 in HEK293T cells transfected with RET and GDNF receptor family alpha1 ( GFRalpha1 ) genes significantly reduced sustained ERK activation as well as ELK-1 activation
Lito et al., J Biol Chem 2008 (Cell Transformation, Neoplastic...) : In the parental, non-H-Ras transformed fibroblasts, expression of Spry2 resulted in the inhibition of H-Ras and ERK activation, suggesting that the positive effect of Spry2 in tumor formation is specific to H-Ras transformation
Burgess et al., BMC developmental biology 2010 : Phospho-Erk1 and Erk2 levels were elevated in the lens but not in the cornea and Spry 1 and Spry 2 , negative regulators of Ras-Raf-Erk signaling, were upregulated more in the corneal than in the lens epithelial cells
Lee et al., Hepatology 2010 (Carcinoma, Hepatocellular...) : In HCC cell lines, Spry2 overexpression inhibits c-Met induced cell proliferation as well as ERK and AKT activation, whereas loss of Spry2 potentiates c-Met signaling
Chen et al., Carcinogenesis 2010 (Bronchial Neoplasms) : Repression of Spry2 potentiated the nickel induced ERK phosphorylation, and forced expression of Spry2 in BEAS-2B cells decreased the nickel induced ERK phosphorylation and significantly suppressed nickel induced anchorage independent growth
Anderson et al., J Biol Chem 2011 (Anoxia) : Silencing of pVHL increased levels of Spry2 by decreasing its ubiquitylation and degradation and thereby augmented the ability of Spry2 to inhibit FGF elicited activation of ERK1/2
Patel et al., J Clin Invest 2013 (Cell Transformation, Neoplastic...) : Here, we show that SPRY2 deficiency alone triggers activation of AKT and ERK , but this is insufficient to drive tumorigenesis