Gene interactions and pathways from curated databases and text-mining

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CCL20 — MAPK3

Text-mined interactions from Literome

Sullivan et al., J Leukoc Biol 1999 : These results suggest that MIP-3alpha can regulate multiple, parallel signal transduction pathways in eosinophils, and suggest that MAPK activation by MIP-3alpha in eosinophils is a significant signaling pathway for migration induction
Brand et al., J Cell Biochem 2006 (Colorectal Neoplasms...) : CCL20 activated Akt, ERK-1/2 , and SAPK/JNK MAP kinases and increased IL-8 protein expression
Hosokawa et al., Clin Exp Immunol 2005 : On the other hand, we found that not only NF-kappaB, p38 MAPK and ERK but also c-Jun NH2-terminal kinase (JNK) are involved in CCL20 production induced by E. coli LPS
Keates et al., J Immunol 2007 : Macrophage-inflammatory protein-3alpha mediates epidermal growth factor receptor transactivation and ERK1/2 MAPK signaling in Caco-2 colonic epithelial cells via metalloproteinase dependent release of amphiregulin ... We show that nonstimulated Caco-2 and HT-29 colonic epithelial cells express CCR6, and that stimulation of Caco-2 cells by MIP-3alpha can dose dependently increase cell proliferation as well as activate the epidermal growth factor receptor (EGFR) and ERK1/2 MAPK
Kim et al., J Clin Immunol 2009 (Asthma...) : To investigate the underlying mechanism, the activation of MAPK and intracellular reactive oxygen species ( ROS ) in these C. pneumoniae infected BECs was measured, as well as the effects of inhibitors of MAPK and ROS on CCL20 and VEGF expression
Ghosh et al., Infect Immun 2011 : By focusing on mitogen activated protein kinases, we show that both extracellular signal regulated kinase 1/2 and p38, but not JNK, are required for hBD-, TNF-a-, and IL-1ß induced secretion of CCL20 by HOECs
Hosokawa et al., Hum Immunol 2012 (Periodontal Diseases) : Inhibitors of p38 mitogen activated protein kinase , extracellular signal regulated kinase ( ERK ), protein kinase B ( Akt ), and nuclear factor ?B ( NF-?B ) significantly inhibited CCL20 production in TWEAK and IL-1ß stimulated HGFs. Western blot analysis revealed that phosphorylations of ERK, Akt, and inhibitor of NF-?B were enhanced in TWEAK and IL-1ß treated HGFs