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CD40 — PTGS2
Text-mined interactions from Literome
Garlichs et al., Atherosclerosis 2002
(Inflammation) :
Induction of
cyclooxygenase-2 and enhanced release of prostaglandin E ( 2 ) and I ( 2 ) in human endothelial cells by engagement of
CD40 ... The hypothesis was tested that
CD40-CD154 interaction is
involved in the induction of
cyclooxygenase-2 and the release of prostanoids in human endothelial cells
Dongari-Bagtzoglou et al., Inflamm Res 2003
:
CD40 ligation
triggers COX-2 expression in endothelial cells : evidence that CD40 mediated IL-6 synthesis is COX-2 dependent ... To investigate whether
CD40-CD154 interactions on HUVEC can
trigger COX-2 synthesis as well as PGE2 and PGI2 secretion in vitro and explore whether the CD40 triggered prostanoids provide costimulatory signals for IL-6 secretion in this cell type ... These studies demonstrate that
CD40 ligation
upregulates HUVEC
COX-2 expression and function
Inoue et al., J Immunol 2004
(MAP Kinase Signaling System) :
Using specific inhibitors for extracellular signal related kinase ( ERK ) and p38 mitogen activated protein kinase ( MAPK ), we found that both kinase pathways are involved in
CD40 induced
COX-2 expression
Okuno et al., J Neurosci Res 2005
(Parkinson Disease) :
We showed that both iNOS and
COX-2 were
up-regulated in microglia and astrocytes by
CD 40 stimulation in association with a low dose of interferon-gamma (IFN-gamma) in vitro
Futagami et al., Prostaglandins Leukot Essent Fatty Acids 2008
(Stomach Neoplasms) :
The aim of this study was to examine the
effect of MCP-1/CCR2 and
CD40-CD40L interaction on
COX-2 and VEGF expression in endothelial cells ...
CD40-CD40L interaction
induced COX-2 production and subsequently, upregulated COX-2 production contributed to elevated VEGF and CCR2 levels in CD40L stimulated HUVECs
Cao et al., J Biol Chem 1998
(Graves Disease) :
PGHS-2 is also
induced by
CD40 engagement in a time dependent manner, and this is mediated through increases in levels of steady-state mRNA ...
CD40 cross linking enhances mitogen activated protein kinase activation, and interrupting this pathway
attenuates the
PGHS-2 induction