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EPHB2 — VCAM1

Text-mined interactions from Literome

Jiang et al., J Biol Chem 2004 (Inflammation) : The inhibitory effect of angiotensin II on iNOS expression was associated with a down-regulation of the sustained activation of extracellular signal regulated kinase ( ERK ) and NF-kappaB by interleukin-1beta, whereas the effect on VCAM-1 was independent of ERK activation
Cai et al., Arterioscler Thromb Vasc Biol 2004 (MAP Kinase Signaling System) : Contact dependent CD36 induction and ERK1/2 phosphorylation in monocytes were inhibited by blocking vascular cell adhesion molecule-1 on HVSMC, whereas soluble factor induced CD36 expression was attenuated by a monocyte chemoattractant protein-1 neutralizing antibody
Cuvelier et al., J Exp Med 2005 (Mechanotransduction, Cellular) : We found that ligation of either vascular cell adhesion molecule-1 or E-selectin, but not major histocompatibility complex class I, induced a shear dependent increase in ERK2 phosphorylation in cytokine stimulated endothelial cells
Fritz et al., J Immunol 2006 : Induction of VCAM-1 by OSM was diminished by pharmacological inhibitors of PI3K ( LY294002 ) but not inhibitors of ERK1/2 ( PD98059 ) or p38 MAPK ( SB203580 )
Chae et al., Cell Physiol Biochem 2007 : PD98059, an inhibitor of ERK1/2 inhibited the Ang II-induced increase of VCAM-1 but not of ICAM-1 in the plasma membranes
Ho et al., Immunobiology 2008 (Inflammation...) : Selective inhibitors of p38 MAPK ( SB203580 ), JNK ( SP600125 ) and ERK ( PD98059 ) could suppress TNF-alpha induced CCL2 and ICAM-1 expression, while only p38 MAPK and ERK inhibitors could suppress TNF-alpha induced VCAM-1 expression
Park et al., J Pharmacol Sci 2009 : The Cd-induced VCAM-1 expression was significantly suppressed by either a specific p38 mitogen activated protein kinase ( MAPK ) inhibitor ( SB202190 ) or a JNK inhibitor ( SP600125 ), but not by an ERK inhibitor ( U0126 )
Vitiello et al., Microbiol Immunol 2011 : Using two potent and selective inhibitors of MEK activation by Raf-1 ( PD-098059 ) and p38 ( SB-203580 ), it was also demonstrated that both ERK1/2 and p38 pathways play key roles in the production of IL-6 as well as in ICAM-1, VCAM-1 and E-selectin expression by Hib porin
Abdala-Valencia et al., PloS one 2011 : Mechanisms for vascular cell adhesion molecule-1 activation of ERK1/2 during leukocyte transendothelial migration ... Pharmacological inhibitors of ERK1/2 partially inhibit leukocyte transendothelial migration in a multi-receptor system but it is not known whether VCAM-1 activation of ERK1/2 is required for leukocyte transendothelial migration (TEM) on VCAM-1 ... In this study, we identified a mechanism for VCAM-1 activation of ERK1/2 in human and mouse endothelial cells ... VCAM-1 signaling, which occurs through endothelial cell NADPH oxidase, protein kinase Ca ( PKCa ), and protein tyrosine phosphatase 1B (PTP1B), activates endothelial cell ERK1/2 ... Inhibition of these signals blocked VCAM-1 activation of ERK1/2 , indicating that ERK1/2 is activated downstream of PTP1B during VCAM-1 signaling ... VCAM-1 activation of endothelial cell NADPH oxidase/PKCa/PTP1B induces transient ERK1/2 activation that is necessary for VCAM-1 dependent leukocyte TEM
Zhong et al., Biochem Biophys Res Commun 2012 (MAP Kinase Signaling System) : Omentin, NF-kB inhibitor ( BAY11-7082 ) and ERK inhibitor ( PD98059 ) reduced the up-regulation of ICAM-1 and VCAM-1 induced by TNF-a
Zhang et al., Scand J Immunol 2013 (MAP Kinase Signaling System) : In addition, IL-17 induced expression of VCAM-1 is partially dependent on activation of ERK1/2