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CRK — IL10

Text-mined interactions from Literome

Sato et al., J Immunol 1999 : TNF-alpha induced tyrosine phosphorylation and enzymatic activation of ERK2, SAPK/JNK, and p38mapk , whereas IL-10 did not induce these events
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
Maloney et al., J Biol Chem 2005 (MAP Kinase Signaling System) : Because interleukin 10 (IL-10) production is strongly p38 dependent , we examined the effect of A52R on IL-10 gene induction
Kim et al., J Microbiol Biotechnol 2008 (MAP Kinase Signaling System) : These results suggest that the synergistic effect of PGA1 on LPS induced IL-10 expression is NF-kappaB dependent and mediated by mitogen activated protein ( MAP ) kinases, p38 , and SAPK/ JNK signaling pathways, and also associated with the PPARgamma pathway
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
Dagvadorj et al., Innate Immun 2008 : IL-10 inhibited the activation of nuclear factor (NF)-kappaB, p38 and stress activated protein kinase ( SAPK ) in LPS stimulated RAW 264.7 cells
Sommer et al., Vet Immunol Immunopathol 2009 : In uninfected cells, inhibition of MAPK revealed that CD40L mediated increase in IL-6 gene expression was dependent on activation of ERK1/2, while increases in IL-12p40, iNOS, and IL-10 gene expression were dependent on activation of p38
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