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CSRP1 — EPHB2

Text-mined interactions from Literome

Senis et al., Journal of thrombosis and haemostasis : JTH 2003 : There were no detectable perturbations in CRP induced activation of Syk, PLCgamma2, cortactin, Erk , Jnk, Akt or p38 in platelets from mice lacking Fps/Fes, Fer, or both kinases
Singh et al., Arterioscler Thromb Vasc Biol 2007 (Atherosclerosis) : This increased CRP expression was attenuated in the presence of anti-leptin receptor antibodies and also by inhibition of ERK1/2 by PD98059 ( 20 to 40 micromol/L )
Wang et al., Arterioscler Thromb Vasc Biol 2008 (Atherosclerosis) : Furthermore, CRP substantially activated ERK1/2 in THP-1 derived foam-like cells
Kawahara et al., Cardiovasc Pathol 2008 (Inflammation) : CRP triggered the activation of p38MAPK and ERK1/2 , but not Jun N-terminal kinase
Chen et al., FEBS Lett 2009 (MAP Kinase Signaling System) : CRP could also increase protein expression of phosphorylated nuclear factor-kappaB (NF-kappaB), IkappaB-alpha and ERK1/2 in dose- and time dependent manner
Schneeweis et al., J Atheroscler Thromb 2010 (Inflammation) : Immunoblotting with phosphospecific antibodies revealed rapid and transient activation/phosphorylation of the protein kinase Akt within 20 minutes after stimulation with VEGF, which was inhibited by 86 % in EC pretreated with CRP ( 10 microg/mL, 24 h, p < 0.05 ). Subsequent VEGF induced phosphorylation of eNOS downstream of Akt was completely inhibited in CRP treated EC. In contrast, CRP-pretreatment did not affect VEGF induced phosphorylation of ERK1/2. Interestingly, stimulation of EC with CRP for 16-24 h induced marked expression of the phosphatase and tensin homolog (PTEN), which functions as a negative regulator of phosphatidylinositol 3 kinase (PI3K) -- > Akt signalling
Choi et al., Biochem Biophys Res Commun 2011 : In addition, increased phosphorylation of p53 and ERK induced by CRP was considerably reversed by Fc gamma receptor IIIa ( Fc?RIIIa ) knock-down using siRNA
Cui et al., Cell Signal 2012 : Our results showed that CRP markedly activated c-Raf/MEK/ERK and JAK1/ERK signaling pathways but not JAK1/STAT3 signaling pathway by using the phosphor-specific antibodies against these pathways, and blockages of c-Raf/MEK/ERK and JAK1/ERK signaling pathways by the specific ERK1/2 inhibitor U0126 and JAK1 inhibitor piceatannol could significantly decrease CRP induced MMP-10 expression