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EPHB2 — PTK6

Text-mined interactions from Literome

Frank et al., Endocrinology 2000 : In this regard, H2O2 and a membrane permeable thiol oxidizing agent, diamide, stimulated protein tyrosine phosphorylation of p120 and p70, and ERK activation in VSMCs. H2O2 also enhanced PTK activity
Akhand et al., Free Radic Biol Med 2001 (MAP Kinase Signaling System) : These results demonstrated that GO and MGO triggered two distinct signal cascades, one for PTK dependent control of ERK and another for PTK independent redox linked activation of JNK/p38 MAPK and caspases in HUVECs, depending on the structure of the carbon skeleton of the chemicals
Duchemin et al., J Neurochem 2002 : Pertussis toxin, as well as Src protein tyrosine kinase and protein kinase C inhibitors, did not prevent the GM1 induced activation of Erk2 , apparently excluding the participation of Gi and Gq/11 protein coupled receptors
Yu et al., J Biol Chem 2003 : IL-6 increased phosphorylation of STAT3 ( at Tyr ( 705 ) ) and ERK1/2 ( at Tyr ( 204 ) ) within 5 min that peaked at 15-30 min and returned to basal levels at 2 h. Phosphorylation of STAT3 was blocked by genistein, a protein tyrosine kinase inhibitor, and AG490, a JAK2 inhibitor, but not PD98059, an ERK1/2 kinase inhibitor
Bian et al., Exp Eye Res 2003 (Translocation, Genetic) : These results suggest that activation of DEX-sensitive, CSA-resistant MEK/ERK and p38 pathways, and activation of NF-kappaB, PKC, and PTK are essential for IL-8 and MCP-1 expression by hRPE cells
Ogasawara et al., Int J Hematol 2003 (Leukemia, B-Cell...) : We found that Lyn protein tyrosine kinase was constitutively phosphorylated on tyrosine, and that ERK and p38 MAPK were constitutively active in all cases of the B-cell tumor
Kobayashi et al., Vet Immunol Immunopathol 2005 : Moreover, the ConA induced IFN-gamma mRNA expression was partly prevented by genistein, a global PTK inhibitor, and PD-98059, an ERK inhibitor , respectively
Hisaoka et al., J Pharmacol Exp Ther 2007 : Taken together, these findings indicate that ERK activation through PTK regulates antidepressant induced GDNF production and that the GDNF production in glial cells may be a novel action of the antidepressant, which is independent of monoamine
Ostrander et al., Cancer Res 2007 (Breast Neoplasms) : Breast tumor kinase ( protein tyrosine kinase 6 ) regulates heregulin induced activation of ERK5 and p38 MAP kinases in breast cancer cells
Chung et al., Arch Pharm Res 2008 : Whereas the PTK inhibitor, genistein, partially inhibited ERK1/2 activation, the EGFR tyrosine kinase inhibitor, tyrphostin 51, had no effect
Liu et al., Lab Invest 2009 (Liver Cirrhosis) : We provide evidence that PTK787/ZK222584 ( PTK/ZK ) , a potent tyrosine kinase inhibitor that blocks vascular endothelial growth factor receptor ( VEGFR ), significantly inhibits PDGF receptor expression, as well as PDGF simulated HSC proliferation, migration and phosphorylation of ERK1/2 , Akt and p70S6 kinase
Sánchez et al., Chem Biol Interact 2009 : On the other hand, the PTK inhibitors caused disparate effects on ERK phosphorylation, and co-treatment with the MEK/ERK inhibitor PD98059 enhanced the pro-apoptotic capacity of the PTK inhibitors
Agarwal et al., J Biol Chem 2010 : We also show that functionally active Src PTK is essential for activation of ERK1/2 upon pneumococcal infections
Schlaepfer et al., J Biol Chem 1997 : FN-stimulated c-Src PTK activity was enhanced by wild type FAK expression, whereas FN-stimulated activation of ERK2 was blocked by expression of the c-Src binding site Phe-397 mutant of FAK
Sieg et al., EMBO J 1998 : Significantly, repression of endogenous Src-family PTK activity by p50 ( csk ) overexpression inhibited FN-stimulated cell spreading, Pyk2 tyrosine phosphorylation, Grb2 binding to Shc, and ERK2 activation in the FAK- but not in FAK+ cells