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CXCL9 — EPHB2

Text-mined interactions from Literome

Wang et al., Biochemistry 2002 : Moreover, CXCL1 activation of PAK1 is independent of ERK1/2 activation, a conclusion based on the observations that the inhibition of MEK-ERK activation by expression of dominant negative ERK or by the MEK inhibitor, PD98059, has no effect on CXCL1 induced PAK1 activation or CXCL1 induced chemotaxis
Wang et al., Biochemistry 2003 : Moreover, CXCL10 can inhibit CXCL1 induced PAK1 and ERK activation as well as the CXCL1 induced chemotaxis through decreasing CXCL1 binding to cell surface heparan sulfate
Ottaiano et al., Cancer Immunol Immunother 2005 (Carcinoma...) : Further, CXCL12 activated ERK1/2 in SW480 cells
Granata et al., Eur J Immunol 2006 : sPLA ( 2 ) induced the phosphorylation of the MAPK p38 and ERK1/2 , and inhibition of these kinases by SB203580 and PD98059, respectively, reduced TNF-alpha and CXCL8 release
Sai et al., J Biol Chem 2006 : Although both mutant and wild-type receptors could mediate Akt and Erk activation in response to CXCL8 , the level of activation of these two kinases was much lower in the cell line expressing the mutant receptors
Petrai et al., Int J Biochem Cell Biol 2008 : In cells expressing CXCR3-A, CXCL10 ( IP-10 ) at nanomolar concentrations induced activation of ERK , Akt, and Src, as previously described in human vascular pericytes
Sambandam et al., Oncogene 2013 (Carcinoma, Squamous Cell...) : Also, CXCL13 significantly increased p-ERK1/2 in SAKA-T and MC3T3-E1 cells
Rigo et al., PloS one 2012 : In contrast, the structural variant [ N33A ] CXCL12 triggered no ß-arrestin dependent phosphorylation of ERK1/2 , and signaled via G protein dependent pathways alone ... We conclude that both recombinant CXCL12 and its structural variant [ N33A ] CXCL12 may transinhibit HER1 via G-proteins/calmodulin/calcineurin, but [ N33A ] CXCL12 does not activate ß-arrestin dependent ERK1/2 phosphorylation and retains a stronger inhibitory effect
Nawaz et al., Exp Eye Res 2013 (Diabetic Retinopathy...) : On the other hand, phosphorylation of ERK induced by VEGF and MCP-1 was inhibited by PF-4, Mig and IP-10
Colvin et al., Endocrinology 2013 (MAP Kinase Signaling System) : We demonstrated that both Dex and overexpression of Mig6 attenuated the phosphorylation of ERK1/2 and blocked the G ( 1 ) /S transition of the cell cycle
Purkerson et al., J Immunol 1998 (Lymphoma, B-Cell) : Cross linking mIg induces ERK activation in both WEHI-231 and normal B cells ... Finally, agents that elevate cAMP, causing protein kinase A-mediated inhibition of Raf-1, inhibited activation of ERK in response to mIg cross linking, but had no affect on ERK activation in response to anti-CD40 or Jun N-terminal kinase activation by signals through either receptor