Gene interactions and pathways from curated databases and text-mining

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EPHB2 — TYR

Text-mined interactions from Literome

Hermanns et al., J Biol Chem 2000 : Moreover, Tyr ( 861 ) is essential for activation of ERK1/2 and for full activation of the alpha(2)-macroglobulin promoter, but not for an exclusively STAT-responsive promoter
Cunnick et al., J Biol Chem 2001 : We found that both Tyr-627 and Tyr-659 of Gab1 were required for SHP2 binding to Gab1 and for ERK2 activation by EGF
Dorsey et al., Blood 2002 (Leukemia, Myeloid) : Analysis of these cell lines indicated that induction of Gab2WT expression, but not Gab2Tyr604Phe expression, led to Erk activation, growth arrest, cell spreading, and enlargement ; expression of megakaryocyte/platelet lineage-specific integrins alphaIIb/beta3 ( CD41/CD61 ) ; and upregulation of RNA for megakaryocyte/platelet proteins
Kim et al., J Cell Sci 2003 : In contrast, a specific extracellular signal regulated protein kinase ( ERK ) pathway inhibitor, PD98059, increased tyrosinase activity and melanin production, and PD98059 also restored the S1P induced reduction of tyrosinase activity and pigmentation
Fu et al., Nutr Cancer 2003 (Neoplasm Invasiveness...) : Tyr/Phe deprivation inhibits expression and phosphorylation of focal adhesion kinase ( FAK ) and extracellular regulated kinase (ERK) in DU145 but not PC3 or normal cells
Arnaud et al., Biochem J 2004 (Leukemia, Prolymphocytic, T-Cell) : Expression of the Gab2 Tyr-614 -- > Phe ( Y614F ) mutant, defective in SHP-2 association, prevents ERK ( extracellular-signal regulated kinase ) activation and expression of a luciferase reporter plasmid driven by the c-fos SRE ( serum response element ), indicating that interaction of SHP-2 with Gab2 is required for ERK activation in response to IL-2
Huang et al., J Biol Chem 2004 : Full activation of ERK2 requires dual phosphorylation of Thr183 and Tyr185 in the activation loop
Choi et al., J Dermatol Sci 2006 (Hypopigmentation) : These results suggest that hinokitiol induced ERK phosphorylation reduces MITF and TYR transcription, and mediates the action of hinokitiol on melanogenesis
Jin et al., Arch Dermatol Res 2008 : Furthermore, ERK functionally regulated the MbetaCD induced melanin formation in melanocytes ; a ERK inhibitor, PD98059, almost completely attenuated the MbetaCD mediated inhibition of melanin synthesis and down-regulation of MITF and tyrosinase expression
Son et al., J Pharm Pharmacol 2011 (Melanoma, Experimental) : The ERK inhibitor increased tyrosinase activity and melanin production and reversed the acteoside induced decrease in tyrosinase activity and melanin content
Li et al., FEBS J 2013 : With stimuli, ERK activity is significantly increased by the phosphorylation of Thr202 and Tyr204 at its activation loop
Chiluiza et al., J Biol Chem 2013 (Glomerulosclerosis, Focal Segmental) : Phosphorylation of Thr-70, Ser-282, and Tyr-31/285 were not necessary for ERK activation by mutant TRPC6, although a phosphomimetic TRPC6 S282E mutant was capable of ERK activation
Kim et al., Life Sci 2013 : Furthermore, a specific ERK pathway inhibitor, PD98059, blocked GGA induced melanin reduction and then prevented downregulation of MITF and tyrosinase by GGA
Van der Zon et al., Biochemistry 1996 : We have examined whether this specific Tyr residue contributes to the generation of TK-specific responses, such as Tyr phosphorylation of Shc, activation of Ras and Erk1,2 , and stimulation of DNA synthesis