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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