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CRK — IL18

Text-mined interactions from Literome

Wyman et al., J Leukoc Biol 2002 (Calcium Signaling...) : IL-18 activation of PMNs was blocked by inhibition of p38 MAP kinase activity ( SB203580 ) or by inhibition of p38 MAP kinase activation by chelation of cytosolic Ca2+
Garcia-Cao et al., EMBO Rep 2003 (MAP Kinase Signaling System) : Consistent with recent reports demonstrating the antagonistic actions of NF-kappaB and c-Jun amino-terminal kinase (JNK) signalling, we have found that Par4 ( -/- ) cells show a reduced activation of the sustained phase of JNK and p38 stimulation by TNF-alpha and interleukin 1
Zvalova et al., Glia 2004 : Therefore, interleukin-1beta (IL-1beta), which contributes to stroke induced brain injury and activates p38/SAPK2 , and hyperosmolarity induced by sorbitol, a potent stimulus of p38/SAPK2 in non-neuronal cells, were used to investigate a possible involvement of p38/SAPK2 in GJC modulation in mouse cultured astrocytes
Sahar et al., Circ Res 2005 (Arteriosclerosis...) : We observed that IL-18 activated Src kinase, protein kinase C, p38 and JNK MAPKs, Akt kinase, transcription factors NF-kB and AP-1, and induced expression of pro-inflammatory cytokines in VSMC
Iikura et al., Lab Invest 2007 : However, IL-1beta, IL-18 or IL-33 induced phosphorylation of Erk, p38 and JNK in naïve HUCBMCs, and IL-33 or IL-1beta, but not IL-18 , enhanced the survival of naive HUCBMCs and promoted their adhesion to fibronectin
Zabalgoitia et al., Free Radic Biol Med 2008 : IL-18 induced p38alpha MAPK activation, and suppressed p38beta isoform expression
Wijagkanalan et al., Mol Pharmacol 2008 (Pneumonia) : DPML significantly inhibited tumor necrosis factor alpha, interleukin-1beta , and cytokine induced neutrophil chemoattractant-1 levels, suppressed neutrophil infiltration and myeloperoxidase activity, and inhibited NFkappaB and p38 mitogen activated protein kinase activation in the lung
Cuong et al., Life Sci 2009 (Inflammation...) : Pre-treatment with C-K significantly inhibited zymosan mediated secretion of tumor necrosis factor-alpha, interleukin (IL)-6 , and IL-12 p40, and the activation of ERK1/2 and p38
Byun et al., Biochem Biophys Res Commun 2012 (Inflammation) : In addition, EGCG treated DCs inhibited lipopolysaccharide (LPS) induced production of pro-inflammatory cytokines ( tumor necrosis factor [TNF ] -a, interleukin [ IL]-1ß, and IL-6 ) and activation of mitogen activated protein kinases ( MAPKs ), e.g., extracellular signal regulated kinase 1/2 ( ERK1/2 ), p38 , c-Jun N-terminal kinase (JNK), and nuclear factor ?B ( NF-?B ) p65 translocation through 67LR