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1 he activation of group IVA phospholipase A2 (cPLA2).
2 tion of group IV cytosolic phospholipase A2 (cPLA2).
3 gs of the 85-kDa cytosolic phospholipase A2 (cPLA2).
4 n also activated cytosolic phospholipase A2 (cPLA2).
5 phospholipids by cytosolic phospholipase A2 (cPLA2).
6 sphatidylcholine vesicle binding affinity of cPLA2.
7 e cells with fluorescent protein chimeras of cPLA2.
8 on of other annexins as well as of COX-2 and cPLA2.
9 th the dexamethasone-mediated suppression of cPLA2.
10 h accompanied enhanced catalytic activity of cPLA2.
11 ynthesis, but not for the phosphorylation of cPLA2.
12  mediated by calcium-triggered activation of cPLA2.
13 e believe is a novel inherited deficiency of cPLA2.
14 terfering with the intracellular movement of cPLA2.
15 tes and this is necessary for stimulation of cPLA2.
16          When compared to the C2 domain from cPLA2, a similar orientation for the beta-sandwich regio
17 ation (herbimycin) inhibited the increase in cPLA2 activation and AA release.
18 98059) significantly inhibited sPLA2-induced cPLA2 activation and AA release.
19                        Our data suggest that cPLA2 activation and its catalytic product platelet-acti
20 FB mediate hypoxia-induced Src-PLD1-PKCgamma-cPLA2 activation and retinal neovascularization via acti
21 t1 blocked hypoxia-induced Src-PLD1-PKCgamma-cPLA2 activation and retinal neovascularization.
22 attenuated hypoxia-induced Src-PLD1-PKCgamma-cPLA2 activation and retinal neovascularization.
23 of these results, we propose a mechanism for cPLA2 activation by calcium and phosphorylation.
24               We also studied the results of cPLA2 activation by epidermal growth factor (EGF) and ca
25 derstand the mechanisms of Src-PLD1-PKCgamma-cPLA2 activation by vascular endothelial growth factor A
26 rosine phosphorylation and Src-PLD1-PKCgamma-cPLA2 activation in HRMVECs.
27 sessments were used to test whether blocking cPLA2 activation pharmacologically or genetically reduce
28 ctively, the results suggest a model whereby cPLA2 activation regulates Group V sPLA2 expression, whi
29                     Notably, the SCI-induced cPLA2 activation was mediated by the extracellular signa
30 so inhibited VEGFA-induced Src-PLD1-PKCgamma-cPLA2 activation, but only modestly.
31 a2+ availability is a dispensable signal for cPLA2 activation, which suggests the existence of altern
32 nflammatory cells, completely independent of cPLA2 activation.
33 cing signal transduction events that lead to cPLA2 activation.
34 s are involved in the regulation of group IV cPLA2 activation.
35 505 phosphorylation partially contributes to cPLA2 activation.
36 r attenuated VEGFA-induced Src-PLD1-PKCgamma-cPLA2 activation.
37  with FcepsilonRI-mediated events leading to cPLA2 activation.
38                     Deactivating MYC lowered cPLA2 activity along with COX2 and 5-LOX mRNA levels.
39  partially purified sPLA2 from BMMC enhanced cPLA2 activity and AA release.
40  PLA2 to BMMC caused a transient increase in cPLA2 activity and translocation of this activity to mem
41 opyranoside BSA, also induced an increase in cPLA2 activity in BMMC.
42 of the 16:4(n-3)-GPR120 axis led to enhanced cPLA2 activity in these splenic macrophages and secretio
43                                    Embryonic cPLA2 activity remained constant from the 1-cell stage u
44                            The inhibition of cPLA2 activity resulted in the blockade of the chlamydia
45 ion nor cPLA2 phosphorylation; consequently, cPLA2 activity was not affected by hVPLA2.
46                                Inhibition of cPLA2 activity with AACOCF3 increased DNA synthesis in R
47  residence is important in the regulation of cPLA2 activity, we explored the contributions of the C2
48 del membranes and hence in the regulation of cPLA2 activity.
49 eneration, via the regulation of the Src and cPLA2 activity.
50 d an increase in cytosolic phospholipase A2 (cPLA2) activity with a preferential release of membrane-
51 ibited tumor cell growth, phosphorylation of cPLA2 alpha promoted growth and counteracted Smad-mediat
52  expression of cPLA2alpha, but inhibition of cPLA2 alpha, cyclooxygenase-2 (COX-2), or EP1 receptor r
53 ies the action of cytosolic phospholipase A2(cPLA2) alpha in regulating eicosanoid biosynthesis by mo
54 pase A2, and the cytosolic phospholipase A2 (cPLA2)alpha isoform has been specifically shown to direc
55 ntained transcripts and protein for group IV cPLA2-alpha and cPLA2-gamma.
56 ective for cleavage at sn-2 as compared with cPLA2-alpha and cPLA2-gamma.
57 rs at micromolar Ca2+ concentrations for the cPLA2-alpha C2 domain, but requires 3- and 10-fold highe
58          The greater Ca2+ sensitivity of the cPLA2-alpha domain results from its higher intrinsic Ca2
59                               Docking of the cPLA2-alpha domain to zwitterionic lipids is triggered b
60 ctively, require greater than 400 ms for the cPLA2-alpha domain, compared to 13 ms for the PKC-beta d
61        Finally, the recombinant C2 domain of cPLA2-alpha exhibited calcium-independent membrane bindi
62 LA2-beta, that has significant homology with cPLA2-alpha in both the calcium-dependent lipid binding
63 e, thrombin or the calcium ionophore A23187, cPLA2-alpha relocated to intracellular membranes.
64 A-AM demonstrated that a substantial pool of cPLA2-alpha remained associated with membrane fractions
65 timulation with calcium-mobilizing agonists, cPLA2-alpha translocates to intracellular phospholipid m
66  Calcium-independent membrane association of cPLA2-alpha was not due to hydrophobic or cytoskeletal i
67 is study, the calcium-induced association of cPLA2-alpha with EA.hy.926 endothelial cell membranes wa
68            Cytosolic phospholipase A2-alpha (cPLA2-alpha) is a calcium-activated enzyme involved in a
69  proteins: cytosolic phospholipase A2-alpha (cPLA2-alpha), protein kinase C-beta (PKC-beta), and syna
70 s the generation of free arachidonic acid by cPLA2-alpha, this enzyme has become an attractive pharma
71 n of calcium-independent membrane-associated cPLA2-alpha.
72 et membrane play a role in the regulation of cPLA2-alpha.
73 estigate whether cytosolic phospholipase A2 (cPLA2 ), an important isoform of PLA2 that mediates the
74 inated regulation of two metabolic pathways (cPLA2 and 5-lipoxygenase), which results in the generati
75 e pathway by up-regulating expression of the cPLA2 and 5-LOX genes.
76                             Up-regulation of cPLA2 and 5-LOX in middle ear epithelial cells was accom
77  genes that govern the lipoxygenase pathway, cPLA2 and 5-LOX, was observed in rats following inoculat
78 fferent human PLA2s: the cytosolic Group IVA cPLA2 and calcium-independent Group VIA iPLA2.
79 JAK3 activity reduced the phosphorylation of cPLA2 and COX-2 protein levels.
80  for 18 h, i.e., a lag in phosphorylation of cPLA2 and ERK1/2 lasting 30 s before its eventual rise.
81                              The kinetics of cPLA2 and ERK1/2 phosphorylation following stimulation w
82 te a change in the intracellular position of cPLA2 and found that cPLA2 did not translocate normally
83  two human cytosolic PLA2 enzymes: group IVA cPLA2 and group VIA iPLA2.
84 ExoU interacts in vitro with an inhibitor of cPLA2 and iPLA2 enzymes and contains a putative serine-a
85  catalytic dyad homologous to those found in cPLA2 and iPLA2 enzymes.
86 cytosolic and the calcium-independent PLA2s (cPLA2 and iPLA2), are key enzymes mediating oligomeric a
87 ds and putative membrane-binding residues of cPLA2 and measured the effects of mutations on its enzym
88           When HEK293 cells transfected with cPLA2 and mutants were stimulated with ionomycin, the wi
89  this study we investigated the influence of cPLA2 and secreted phospholipase A2 (sPLA2) Group IIA, G
90 d5 is accompanied by the rapid activation of cPLA2 and the cPLA2-dependent release of [3H]arachidonic
91                Pharmacological inhibition of cPLA2 and the hVPLA2-induced activation of eosinophils d
92 on of both chlamydial activation of the host cPLA2 and uptake of glycerophospholipids from the host c
93  blocked by various inhibitors of cytosolic (cPLA2) and Ca2+ -independent (iPLA2) phospholipase A2 en
94 osphorylation of cytosolic phospholipase A2 (cPLA2) and consequent thromboxane A2 (TXA2) production.
95 gh expression of cytosolic phospholipase A2 (cPLA2) and cyclooxygenase (COX) 2.
96  the kinetics of cytosolic phospholipase A2 (cPLA2) and extracellular signal-regulated kinase (ERK1/2
97  the function of cytosolic phospholipase A2 (cPLA2) and its role in membrane regulation at the Golgi
98 osphorylation of cytosolic phospholipase A2 (cPLA2), and arachidonic acid (AA) and LTC4 release follo
99 holipase A2 (PLA2), Group IV cytosolic PLA2 (cPLA2), and cyclooxygenase-2 (COX-2).
100 itor of cPLA2, short interfering RNA against cPLA2, and several calcium signaling blockers, indicatin
101 ted in increased interaction between p11 and cPLA2, anti-cPLA2 antibodies were used to immunoprecipit
102 ased interaction between p11 and cPLA2, anti-cPLA2 antibodies were used to immunoprecipitate p11.cPLA
103 ere activated by an autocrine loop involving cPLA2, arachidonic acid release, COX-2-dependent PGI(2)
104 ines, IL-1beta and IL-6, thereby identifying cPLA2 as an important regulator of the inflammatory prog
105  It was over 70 times more selective for the cPLA2 as compared with the human nonpancreatic secreted
106 atic activity of cytosolic phospholipase A2 (cPLA2) as at-tested to by arachidonic acid release withi
107  thiol antioxidant NAC reduces activation of cPLA2 (assessed by isoform gel-shift and membrane transl
108                                              cPLA2 association with Golgi was slower than the isolate
109  report the X-ray crystal structure of human cPLA2 at 2.5 A. cPLA2 consists of an N-terminal calcium-
110 ms of cPLA2, we show that phosphorylation of cPLA2 at both Ser-505 and Ser-727 and elevation of Ca(2+
111  blocked collagen-induced phosphorylation of cPLA2 at its two phosphorylation sites in vivo, Ser505 a
112 shift of cPLA2 induced by phosphorylation of cPLA2 at various sites.
113           Since inhibition of iPLA2, but not cPLA2, attenuated IgM binding to apoptotic cells, these
114 al SAPK cascades and that phosphorylation of cPLA2 augments arachidonic acid release.
115                      Transient expression of cPLA2-beta cDNA in COS cells results in an increase in c
116                                              cPLA2-beta is markedly less selective for cleavage at sn
117                  Northern analysis reveals a cPLA2-beta transcript of 8 kilobase pairs that is expres
118  cDNA encoding a 1012-amino acid polypeptide cPLA2-beta, that has significant homology with cPLA2-alp
119                   With the identification of cPLA2-beta, the newly defined cPLA2 family now comprises
120 eading to LTC4 generation by phosphorylating cPLA2, but not histamine release or IL-4 production, in
121                      In vitro, activation of cPLA2 by ceramide-1-phosphate or A23187 induced spinal n
122 g surface on the Ca2+-activated C2 domain of cPLA2 by engineering a single cysteine substitution at 1
123       The current paradigm for activation of cPLA2 by stimuli proposes that both an increase in intra
124 swelling of cells and their nuclei activates cPla2 by translocating it from the nucleoplasm to the nu
125                                 The isolated cPLA2 C2 domain associated with Golgi membranes rapidly
126  beta-sandwich region is found; however, the cPLA2 C2 domain is translocated 5-7 A deeper into the me
127 ing the high-resolution crystal structure of cPLA2-C2 as a starting point, we embedded two copies of
128 the C2 domain of cytosolic phospholipase A2 (cPLA2-C2) in a 1-palmitoyl-2-oleoyl-phosphatidylcholine
129     These results demonstrate a role for the cPLA2 catalytic domain in regulating membrane associatio
130                  Cytosolic phospholipase A2 (cPLA2) catalyzes release of arachidonic acid from membra
131           Activated cytosolic phospholipase (cPLA2) catalyzes the production of arachidonic acid, whi
132 ntibodies were used to immunoprecipitate p11.cPLA2 complexes and Western blots of the immunoprecipita
133 y crystal structure of human cPLA2 at 2.5 A. cPLA2 consists of an N-terminal calcium-dependent lipid-
134 s that host cell cytosolic phospholipase A2 (cPLA2) contributes to E. coli K1 invasion of BMECs but n
135                  Cytosolic phospholipase A2 (cPLA2) controls AA generation.
136                                     The GIVD cPLA2 (cPLA2delta) is a potential drug target for develo
137  and activity of cytosolic phospholipase A2 (cPLA2), cyclooxygenase-2 (COX-2), and production of PGs.
138 eover small inhibitory RNAs directed against cPLA2 decreased the effect of A23187 and EGF on IL-8 and
139 d activation of eosinophils derived from the cPLA2-deficient mouse corroborated that hVPLA2 mediates
140 rachidonic acid release and translocation of cPLA2, demonstrating the requirement for a functional C2
141 lecithin induces susceptibility through both cPLA2-dependent and -independent pathways.
142 ied by the rapid activation of cPLA2 and the cPLA2-dependent release of [3H]arachidonic acid ([3H]AA)
143 tracellular position of cPLA2 and found that cPLA2 did not translocate normally in infected cells, ra
144 ined the role of cytosolic phospholipase A2 (cPLA2) during human eosinophil adherence to ICAM-1- or V
145                         Blocking activity of cPLA2 efficiently suppressed expression of inflammatory
146 icating the presence of one or more group IV cPLA2 enzymes.
147 dentify protein residues in the C2 domain of cPLA2 essential for its Ca2+ and membrane binding, we se
148 ound to be the most potent inhibitor of GIVA cPLA2, exhibiting an XI(50) value of 0.011 mole fraction
149                  SCI significantly increased cPLA2 expression and activation.
150 ntification of cPLA2-beta, the newly defined cPLA2 family now comprises three members that may have d
151 pts and protein for group IV cPLA2-alpha and cPLA2-gamma.
152 age at sn-2 as compared with cPLA2-alpha and cPLA2-gamma.
153 kedly altering basal and cytokine-stimulated cPLA2 gene expression in intestinal epithelial cells, le
154 uation were used to access expression of the cPLA2 gene in rat small intestinal epithelial and mouse
155 occurs through a direct reduction of de novo cPLA2 gene transcription.
156               These results demonstrate that cPLA2 has an influence on IL-8 and COX 2 gene and protei
157 ich the gene for cytosolic phospholipase A2 (cPLA2) has been disrupted to demonstrate the absolute re
158        Group IVA cytosolic phospholipase A2 (cPLA2) has been shown to play a critical role in the ago
159 ression of a previously identified zebrafish cPLA2 homologue.
160 ly IL-3 priming results from preconditioning cPLA2, i.e., causing its phosphorylation, while late pri
161 c Abeta(1-42) to increase phosphorylation of cPLA2 in astrocytes through the NADPH oxidase and mitoge
162  to demonstrate the absolute requirement for cPLA2 in both the immediate and the delayed phases of ei
163 0 minutes postinjury or genetically deleting cPLA2 in mice ameliorated motor deficits, and reduced ce
164  allow the sustained membrane interaction of cPLA2 in response to transient calcium increases.
165    However, no studies addressed the role of cPLA2 in the regulation of cholesterol-rich membranes th
166 fluorophosphonate suggest a key role for the cPLA2 in the response as well.
167  kinases MNK1, MSK1, and PRAK1 phosphorylate cPLA2 in vitro uniquely on Ser-727 as shown by mass spec
168 s were able to phosphorylate wild-type human cPLA2 in vitro, although to different extents, but not c
169 er expression of cytosolic phospholipase A2 (cPLA2) in H596 cells than that of A549 cells.
170 nd activation of cytosolic phospholipase A2 (cPLA2) in intact cells remain to be fully characterized.
171 donyl-selective, cytosolic phospholipase A2 (cPLA2) in intestinal cells.
172 iates the release of AA and leukotriene in a cPLA2-independent manner.
173                                         This cPLA2-independent pathway involved changes in cell membr
174 oth pathways, it was sufficient only for the cPLA2-independent pathway.
175 ts on the membrane binding and activation of cPLA2, indicating that two calcium ions bound to the C2
176 accompanied by a time-dependent gel shift of cPLA2 induced by phosphorylation of cPLA2 at various sit
177                                     However, cPLA2 inhibition neither prevented CBRM1/5 expression no
178 ion of arachidonic acid to eosinophils after cPLA2 inhibition with arachidonyl trifluoromethylketone
179 nship of 2-oxoamide-based compounds and GIVA cPLA2 inhibition.
180 eatment with the most potent 2-oxoester GIVA cPLA2 inhibitor resulted in over 50% decrease in KLA-eli
181 chidonyl trifluoromethyl ketone, a selective cPLA2 inhibitor, and was confirmed with BMEC derived fro
182        Methyl arachidonyl fluorophosphate, a cPLA2 inhibitor, inhibited the effect of A23187 and of E
183 sed by arachidonyl trifluoromethyl ketone, a cPLA2 inhibitor.
184 s suppressed by AACOCF3, a phospholipase A2 (cPLA2) inhibitor.
185 donic acid release are abrogated by group IV cPLA2 inhibitors (methyl arachidonyl fluorophosphate and
186 up leads to highly potent and selective GIVA cPLA2 inhibitors (X I(50) values 0.00007-0.00008) and do
187 roup IV cPLA2, to infected MPhi treated with cPLA2 inhibitors completely restored the antimycobacteri
188 ion of GV sPLA2, and none of the potent GIVA cPLA2 inhibitors inhibited either GV sPLA2 or GVIA iPLA2
189 the development of potent and selective GIVA cPLA2 inhibitors is of great importance.
190  The novel, highly potent and selective GIVA cPLA2 inhibitors provide excellent tools for the study o
191                        Importantly, group IV cPLA2 inhibitors significantly reduced MPhi antimycobact
192                   Two of these specific GIVA cPLA2 inhibitors were also found to have potent therapeu
193                   The structurally unrelated cPLA2 inhibitors, arachidonyl trifluoromethylketone and
194                        Our data suggest that cPLA2 is a substrate for several SAPK cascades and that
195                                      Whereas cPLA2 is essential for immediate eicosanoid generation b
196 ding loops show that the membrane binding of cPLA2 is largely driven by hydrophobic interactions resu
197 y, while the FMLP-induced phosphorylation of cPLA2 is not affected by the inhibitors of the p38 MAP k
198                                              cPLA2 is phosphorylated on multiple sites in Sf9 cells;
199                                              cPLA2 is regulated by phosphorylation and by calcium, wh
200 iPLA2 is the dominant PLA2 in rat brain, and cPLA2 is the most abundant PLA2 in P388D1 macrophages an
201  both NIH3T3 and MC3T3E1 cells suggests that cPLA2 is the most likely enzyme that catalyzes the relea
202      How tissue damage is sensed to activate cPLA2 is unknown.
203                  Cytosolic phospholipase A2 (cPLA2) is a Ca2+-dependent enzyme that mediates agonist-
204 e Group IVA cytosolic phospholipase A2 (GIVA cPLA2) is a key provider of substrates for the productio
205         Cytosolic group IV phospholipase A2 (cPLA2) is a ubiquitously expressed enzyme with key roles
206  previously that cytosolic phospholipase A2 (cPLA2) is able to activate gene expression through PPAR-
207 The C2 domain of cytosolic phospholipase A2 (cPLA2) is involved in the Ca2+-dependent membrane bindin
208 man platelets, cytosolic phospholipase A(2) (cPLA2) is phosphorylated on Ser-505 by p38 protein kinas
209 riments show that cytosolic phospholipase 2 (cPLA2) is the key enzyme mediating the p25-induced LPC p
210             Cytosolic phospholipase A2 (GIVA cPLA2) is the only PLA2 that exhibits a marked preferenc
211   Group IVA cytosolic phospholipase A2 (GIVA cPLA2) is the rate-limiting provider of pro-inflammatory
212  that sPLA2 isoforms (pla2g5, 12a, and 12b), cPLA2 isoform (pla2g4a), iPLA2 isoform (pla2g6), and PLA
213 l migration in vitro Genetic ablation of the cPLA2 isoform cPLA2alpha dramatically reduced lung infla
214  gamma interferon, or their combination, and cPLA2-IVA mediated the release of arachidonic acid, whic
215                            The expression of cPLA2-IVA was increased in response to M. tuberculosis,
216 marrow-derived macrophages (BMDMs) expressed cPLA2-IVA, cPLA2-IVB, iPLA2-VI, sPLA2-IIE, and sPLA2-XII
217 r survival of M. tuberculosis was similar in cPLA2-IVA-deficient and wild-type macrophages.
218 ved macrophages (BMDMs) expressed cPLA2-IVA, cPLA2-IVB, iPLA2-VI, sPLA2-IIE, and sPLA2-XIIA.
219 or, and was confirmed with BMEC derived from cPLA2 knockout mice.
220                                Activation of cPLA2 leads to generation of intracellular arachidonic a
221                             The C2 domain of cPLA2 linked to GFP translocates to the nuclear envelope
222                                              cPLA2 may play a key role in the pathogenesis of SCI, at
223 293 cells leads to significant inhibition of cPLA2-mediated arachidonate release.
224 rophages to UV radiation results in a rapid, cPLA2-mediated arachidonic acid mobilization, without in
225 vation conditions leads to inhibition of the cPLA2-mediated arachidonic acid mobilization.
226                  Cytosolic phospholipase A2 (cPLA2) mediates agonist-induced arachidonic acid release
227                                        Basal cPLA2 messenger RNA (mRNA) expression was repressed 75%
228                        Induced expression of cPLA2 mRNA by several proinflammatory cytokines was bloc
229 COX-2 of its substrate by the suppression of cPLA2 mRNA expression is an additional mechanism used by
230 e COX-2 of its substrate, AA, by suppressing cPLA2 mRNA expression.
231 y suppress the production of cytosolic PLA2 (cPLA2) mRNA.
232 itro, although to different extents, but not cPLA2 mutants that had Ser505 replaced by alanine.
233 l pretreatment with AACOCF3 (an inhibitor of cPLA2), nifedipine (a Ca(2+) channel blocker), or 3'-met
234               In Sf9 insect cells expressing cPLA2, okadaic acid, and the calcium-mobilizing agonists
235 s responsible for in vivo phosphorylation of cPLA2 on Ser-727.
236 jor effects on the expression or activity of cPLA2 or COX-2.
237 ntigen, it had no effect on translocation of cPLA2 or ERK1/2 activation, suggesting that it does not
238  in the level of cytosolic phospholipase A2 (cPLA2) or COX-1 were observed, and Group IIA sPLA2 was n
239 ands' cycle by knockdown of phospholipase 2 (cPLA2) or overexpression of lysophosphatidycholine acylt
240                                              cPLA2 overexpression and activation increased both IL-8
241                  In this study, we show that cPLA2, p38 mitogen-activated protein kinase (MAPK), and
242                         Remarkably, blocking cPLA2 pharmacologically at 30 minutes postinjury or gene
243                      Finally, FMLP increases cPLA2 phosphorylation and arachidonic acid release.
244                                LPS increases cPLA2 phosphorylation and arachidonic acid release.
245 H, caused complete inhibition of ADP-induced cPLA2 phosphorylation and TXA2 generation, without affec
246 ective inhibitors abolished 2MeSADP-mediated cPLA2 phosphorylation and TXA2 generation.
247 cal inhibition of p38 leads to inhibition of cPLA2 phosphorylation at both Ser-505 and Ser-727 sugges
248                  In addition, JAK3 regulates cPLA2 phosphorylation independent of transcription.
249 embrane via a C2 domain, whereas the role of cPLA2 phosphorylation is less clearly defined.
250 dhesion to VCAM-1 corresponded temporally to cPLA2 phosphorylation, which accompanied enhanced cataly
251           Stimulation by TNF-alpha increases cPLA2 phosphorylation, which is inhibited by SB 203580,
252 r stimulation of human neutrophils increases cPLA2 phosphorylation.
253 e in intracellular calcium concentration nor cPLA2 phosphorylation; consequently, cPLA2 activity was
254 enase pathway showed that gene disruption of cPLA2 prevented the provision of arachidonic acid substr
255            It had little effect on levels of cPLA2 protein.
256 ncorporated similar levels of phosphate into cPLA2 relative to the ability of each kinase to stimulat
257 damage activates cytosolic phospholipase A2 (cPLA2), releasing arachidonic acid (AA), which is oxidiz
258                      After [Ca2+]i decrease, cPLA2 remained associated with membrane in a Ca(2+)-inde
259  action of iPLA2 is immediate, the action of cPLA2 requires a lag time of approximately 12-15 min, pr
260 ACOCF3) and ShRNA mediated downregulation of cPLA2 resulted in reduced LDs, and increased autophagy.
261 ff assays showed a marked decline in de novo cPLA2 RNA synthesis, implicating a transcriptional mecha
262 ghts into the molecular mechanisms governing cPLA2's function in signal transduction.
263 s was associated with increased ERK mediated cPLA2(S505) phosphorylation.
264 l fluorophosphonate, a specific inhibitor of cPLA2, short interfering RNA against cPLA2, and several
265 port that activation of the host Raf-MEK-ERK-cPLA2 signaling cascade is required for the chlamydial u
266  be the major modulator of Src-PLD1-PKCgamma-cPLA2 signaling in HRMVECs, facilitating their angiogeni
267 sting an active manipulation of the host ERK-cPLA2 signaling pathway by chlamydiae.
268 ceptors 1 and 4, cytosolic phospholipase A2 (cPLA2), Src tyrosine kinases, p38 MAPK, phospholipase C,
269 ristic of the Ca2+-dependent cytosolic PLA2 (cPLA2) subtype.
270            There is an initial activation of cPLA2 that induces expression of Group V PLA2, which in
271 ible for the subsequent induction of type IV cPLA2 that mediates the release of arachidonic acid for
272 nts a novel structural class of inhibitor of cPLA2 that partitions into the phospholipid bilayer and
273 for the phosphorylation and translocation of cPLA2 to mitochondria.
274 isphosphate (PtdInsP2) in the association of cPLA2 to model membranes and hence in the regulation of
275 hought to be needed for translocation of the cPLA2 to the membrane via a C2 domain, whereas the role
276          FMLP/CB-stimulated translocation of cPLA2 to the nuclear envelope assessed by specific immun
277 ecessary and sufficient for translocation of cPLA2 to the nuclear envelope when calcium is increased;
278 slocation of green fluorescent protein (GFP)-cPLA2 to the nuclear envelope.
279 est and negligible effects on the binding of cPLA2 to zwitterionic and anionic membranes, respectivel
280 Translocation of cytosolic phospholipase A2 (cPLA2) to Golgi and ER in response to intracellular calc
281 chidonic acid, the major product of group IV cPLA2, to infected MPhi treated with cPLA2 inhibitors co
282                                              cPla2 translocation upon nuclear swelling was reconstitu
283  Ca(2+) was necessary but not sufficient for cPla2 translocation, and nuclear swelling was required i
284           The major enzymes in this pathway, cPLA2 type IVA, COX-2, and mPGES-1, were dramatically up
285 mediating the p25-induced LPC production and cPLA2 upregulation is critical in triggering the p25-med
286          When assaying the human recombinant cPLA2 using membranes isolated from [3H]arachidonate-lab
287 b and SAPK4 incorporated less phosphate, and cPLA2 was a poor substrate for SAPK3.
288     The chlamydia-induced phosphorylation of cPLA2 was also blocked by a dominant negative ERK2.
289   Furthermore, activation of both ERK1/2 and cPLA2 was dependent on chlamydial growth and restricted
290                                    Activated cPLA2 was localized mainly in neurons and oligodendrocyt
291                                Expression of cPLA2 was low, and 5-LOX gene expression was not detecte
292 sPLA2 involved activation of cytosolic PLA2 (cPLA2) was next tested.
293 ype and phosphorylation site mutant forms of cPLA2, we show that phosphorylation of cPLA2 at both Ser
294 osphorylation of Ser505 and Ser727 activates cPLA2, we systematically analyzed the effects of S505A,
295 tern analyses revealed that these changes in cPLA2 were accompanied by a time-dependent gel shift of
296 f phosphorylation sites and the C2 domain of cPLA2 were investigated.
297 Ca(2+)-dependent cytosolic phospholipase A2 (cPLA2) were activated in chlamydia-infected cells.
298 through at least two pathways, TNF-alpha and cPLA2, which are both also critical for antimycobacteria
299                           AA is generated by cPLA2, which may be stimulated through an AGE-activated
300 r) inhibited the phosphorylation of ERKs and cPLA2 without inhibition of several other tyrosine phosp

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