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EPHB2 — SFTPC

Text-mined interactions from Literome

Bektas et al., Biochemistry 2003 : In addition, neither SPC nor LPC stimulated the binding of GTPgammaS to membranes prepared from GPR4 expressing cells and did not activate ERK1/2 ... Collectively, our results suggest that SPC and LPC are not the ligands for GPR4 and that this receptor may constitutively inhibit ERK1/2 activation
Mathieson et al., Br J Pharmacol 2006 : In contrast, SPC increased p38MAPK phosphorylation ( 3.0+/-0.3-fold increase ) but did not stimulate ERK1/2 ... CREB activation by SPC required both p38MAPK and CaMK activation, but not ERK1/2
Kim et al., Pigment Cell Res 2006 (MAP Kinase Signaling System) : These results suggest that the ERK pathway is involved in the melanogenic signaling cascade, and that ERK activation by SPC reduces melanin synthesis via MITF downregulation
Jeon et al., J Cell Biochem 2007 : SPC treatment induced sustained activation of an extracellular signal regulated kinase ( ERK ), in contrast to transient activation of ERK in response to platelet derived growth factor (PDGF)-BB, which stimulated proliferation of MS1 cells ... Both the SPC induced cell death and ERK activation were abolished by pretreatment of the cells with the MEK inhibitor U0126 or by overexpression of a dominant negative mutant of MEK1 ( DN-MEK1 ) ... Pretreatment of the cells with N-acetylcysteine, an antioxidant, completely prevented the SPC induced ROS generation, apoptosis, and ERK activation, whereas the ROS generation was not abrogated by treatment with U0126 ... Consistent with these results, SPC induced cell death of human umbilical vein endothelial cells ( HUVECs ) through ROS mediated activation of ERK
Kwon et al., J Dermatol Sci 2007 (MAP Kinase Signaling System) : Protein kinase C ( PKC ) activation by phorbol myristate acetate ( PMA ) potentiated IL-6 mRNA expression, whereas PKC inhibition by bisindolylmaleimide blocked SPC induced p42/44 ERK phosphorylation and IL-6 expression
Moon et al., Int J Biochem Cell Biol 2007 : Pretreatment of the cells with U0126, an MEK inhibitor, markedly attenuated the SPC induced expression of FN and delayed phosphorylation of Smad2, suggesting that ERK is involved in the SPC induction of FN expression through activation of Smad2
Jeong et al., Mol Cell Biochem 2012 (Hypopigmentation...) : In the present study, we confirmed that SPC activated ERK and that a specific inhibitor of the ERK pathway ( PD98059 ) recovered SPC induced hypopigmentation