◀ Back to IRF6
IRF6 — PLA2G1B
Text-mined interactions from Literome
Chen et al., Br J Pharmacol 2000
:
In addition to COX-2 induction, arachidonic acid ( AA ) release and steady-state mRNA levels of type V secretory phospholipase A ( 2 ) ( sPLA ( 2 ) ) and Ca ( 2+ ) -independent
PLA(2) ( iPLA ( 2 ) ) were also increased in the
presence of
LPS and UTP ; the LPS induced increase in iPLA ( 2 ) activity was also potentiated by UTP
Rozenfeld et al., Am J Physiol Gastrointest Liver Physiol 2001
(Shock, Septic) :
PAF and
LPS caused an increase in
PLA2-II activity, which was abrogated in GF and ABX rats ... We conclude that PAF- and
LPS induced increases in
PLA2-II activity are dependent on gut bacteria, and ABX and GF rats are less susceptible to LPS induced injury than CN rats
Won et al., Glia 2005
:
In glial cells,
lipopolysaccharide (LPS) induced the activities of
PLA2 ( calcium independent PLA2 ; iPLA2 and cytosolic PLA2 ; cPLA2 ) as well as gene expression of iNOS
Assogba et al., Eur J Med Chem 2005
:
It is also able to block the
PLA2-II activities
induced by
LPS and IL-6 in HepG2 cell line and no cytotoxicity is observed when PMS1062 is tested up to a concentration of 100 microM in two different cell lines ( A549 and LLC-PK1 )
Kessen et al., J Lipid Res 2005
:
LPS stimulation also
results in increased expression and secretion of a secretory
PLA2 , specifically GV PLA2 ... Experiments employing pyrrophenone suggested that GIVA PLA2 is the dominant player involved in AA release, but it appears not to be involved in the regulation of
LPS induced expression of GV
PLA2 or cyclooxygenase-2
Nakano et al., FEBS Lett 1990
(Vasculitis) :
Two potent inflammatory mediators, interleukin 1 (IL-1) and tumor necrosis factor (TNF) as well as
lipopolysaccharide (LPS) increased group II
phospholipase A2 (PLA2) mRNA levels, which resulted in enhanced secretion of the PLA2 enzyme from rat smooth muscle cells ... cAMP elevating agents also stimulated the release of
PLA2 and increased the mRNA, but IL-1, TNF and
LPS did not
affect cAMP levels
Oka et al., J Biol Chem 1991
:
The potent antiinflammatory agent dexamethasone suppressed the
PLA2-II expression
induced by
LPS ... H-7, a protein kinase C inhibitor, inhibited the
LPS induced
PLA2-II expression, but did not inhibit the TNF induced one
Bickford et al., J Cyst Fibros 2013
(Aspergillosis, Allergic Bronchopulmonary...) :
Interestingly,
PLA2G2D was
induced by
LPS , IL-2, IL-6, IL-13, and Af only in CFTR-deficient human IB3.1 cells
Tong et al., Mol Chem Neuropathol 1995
(Pheochromocytoma) :
However, neither antibody was able to inhibit the
PLA2 release
induced by
LPS , suggesting that the effect of LPS was not complicated by the release of IL-1 beta or TNF alpha
Roshak et al., J Biol Chem 1994
:
In contrast, there was no effect on the type II 14-kDa-like
PLA2 activity measured in the 100,000 x g particulate fraction nor did
LPS induce the release of type II 14-kDa PLA2 into the medium
Forehand et al., J Immunol 1993
:
We examined this possibility by studying the
effect of
LPS on neutrophil
PLA2 activity
Tan et al., J Immunol 1996
:
The purpose of this study is to examine the
regulation of intestinal
PLA2-II by PAF and
LPS ... In contrast, PMN depletion prevented
LPS induced
PLA2-II enzyme activity but enhanced the gene expression ... We conclude that : 1 ) both PAF and
LPS induce gene transcription and enzyme activation of
PLA2-II in the small intestine ; 2 ) PAF up-regulates PLA2-II via PMN activation ; 3 ) LPS effect is independent of endogenous PAF formation ; and 4 ) different pathways exist for PAF and LPS in the regulation of intestinal PLA2-II gene expression in vivo
Laine et al., Gut 1996
:
These data show that
LPS causes release of pancreatic
PLA2 into blood plasma, activation of PLA2 in pancreatic tissue, and apoptosis of acinar cells
Balsinde et al., Biochem J 1997
(Leukemia P388) :
PAF also activated
phospholipase A2 (PLA2) and enhanced arachidonic acid ( AA ) release in P388D1 macrophages, and bacterial
lipopolysaccharide (LPS) increased the responsiveness of these cells to PAF
Vial et al., Biochem J 1998
:
Surprisingly, incubation of AM with PGE2, dibutyryl-cAMP, cholera toxin or rolipram ( an inhibitor of specific cAMP-phosphodiesterase ) inhibited both basal and
LPS stimulated
PLA2-II expression ... Hence, in contrast to other cell systems, we report that : ( i ) agents elevating intracellular cAMP levels down-regulate both basal and
LPS induced
PLA2-II synthesis, ( ii ) prostaglandins exert a negative feedback effect on this synthesis, probably through an elevation of intracellular cAMP levels, and ( iii ) inhibition of TNF-alpha release may account, at least in part, for the down-regulation of PLA2-II expression by endogenously produced prostaglandins and cAMP elevating agents
Cannon et al., Br J Pharmacol 1998
:
In addition,
phospholipase A2 (PLA2) is
activated by
LPS resulting in the release of platelet activating factor (PAF) and lipoxygenase but not cyclo-oxygenase products
Barbour et al., Mol Immunol 1998
:
Enzyme assays indicate that
LPS treatment
induces the activation of cytosolic
PLA2 in RAW264.7, but not in P388D1 cells