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CCL20 — MAPK11
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
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
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