Gene interactions and pathways from curated databases and text-mining

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Text-mined interactions from Literome

Takeishi et al., J Mol Cell Cardiol 2001 (MAP Kinase Signaling System...) : The activity and time course of ERK1/2 was not changed, but p90RSK activation by reperfusion was completely inhibited by preconditioning
Tada et al., J Invest Dermatol 2002 : The mitogen induced phosphorylation of p90rsk and CREB was dependent on ERK1/2 activation, and was mediated by intracellular calcium mobilization and by protein kinase C and tyrosine kinase activation, but not by activation of the cAMP dependent protein kinase A. Exposure of melanocytes to ultraviolet radiation B resulted in the phosphorylation of the stress induced mitogen- activated protein kinases p38 and JNK/SAPK, but not ERK1/2
Wang et al., J Cell Physiol 2006 : In late stage differentiating cells Raf-1 and p90RSK are found as a complex, and inhibition of Raf-1, but not MEK or ERK expression reduces the levels of phosphorylated p90 RSK
Li et al., Biochem Biophys Res Commun 2006 : Inhibition of ERK1/2 with PD98059 ( 10 ( -5 ) M ) completely inhibited the activation of p90 ( RSK ), but did not block CREB-S133 phosphorylation in TPA perfused heart, indicating that PKA, CaMKII, and p90 ( RSK ) do not phosphorylate CREB-S133 in the murine heart
Szokodi et al., Circulation 2008 (MAP Kinase Signaling System) : Suppression of ERK1/2 activation prevented p90RSK phosphorylation and attenuated the inotropic effect of ET-1
Le et al., Circ Res 2012 (Diabetes Mellitus, Experimental...) : Overexpression of either p90RSK or an ERK5 fragment ( aa571-807 ) inhibits ERK5/CHIP association, suggesting that p90RSK and CHIP competes for ERK5 binding and that p90RSK activation is critical for inhibiting ERK5/CHIP interaction ... These data suggest a role for p90RSK in inhibiting CHIP activity and promoting cardiac apoptosis through binding to and phosphorylation of ERK5-S496
Le et al., Circulation 2013 (Atherosclerosis...) : A crucial role for p90RSK mediated reduction of ERK5 transcriptional activity in endothelial dysfunction and atherosclerosis