Gene interactions and pathways from curated databases and text-mining

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CRK — IL5

Text-mined interactions from Literome

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
Ip et al., Immunopharmacol Immunotoxicol 2005 : We investigated the roles of p38 mitogen activated protein kinase ( MAPK ) and nuclear factor kappa-B (NF-kappaB) in IL-3, IL-5 , and GM-CSF induced adhesion, morphological changes, and subsequence transmigration of human eosinophils
Munitz et al., Blood 2006 (Calcium Signaling...) : Cross linking of IRp60 inhibited IL-5 mediated JAK2 phosphorylation as well as eotaxin- and IL-5/GM-CSF mediated ERK1/2 and p38 phosphorylation
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