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1 ived leukocytes were Lp-PLA2-deficient (bmLp-PLA2 (-/-)).
2 A2alpha (cPLA2alpha) or calcium-independent PLA2.
3 five percent of participants had abnormal Lp-PLA2.
4 future challenge with a near-lethal dose of PLA2.
5 y response in part by effects elicited by Lp-PLA2.
6 3) complexes with a wide range of mutants of PLA2.
7 allosteric states of the interface activated PLA2.
8 ng of the sulfate head group in contact with PLA2.
9 s is characterized by local production of Lp-PLA2.
10 branes on the activation of human pancreatic PLA2.
11 inhibitors for group VIA calcium-independent PLA2.
12 d substantially long dissociation rates from PLA2.
13 (20-30 min post-P4) rely on group X secreted PLA2.
14 intracellular PLA2, the calcium-independent PLA2.
15 ciation and subsequent enzymatic reaction of PLA2.
16 responses are dependent on CD1a protein and PLA2.
17 na benthamiana via recombinant expression of PLA2.
18 apoB, only prava40 led to a reduction in Lp-PLA2 (-15%, p = 0.008) and atorva10 to a decrease in OxL
19 g/dL) below the cut-off value of circulating PLA2 (2.07 nM, equivalent to 290 ng/dL) present in serum
20 BI)-induced neuroinflammation via activating PLA2/5-LOX/LTB4 cascade using a partial frontal lobe res
22 spholipase A2/5-lipoxygenase/leukotriene-B4 (PLA2/5-LOX/LTB4) axis is an important inflammatory signa
24 Lipoprotein-associated phospholipase A2 (Lp-PLA2), a member of the phospholipase A2 family of enzyme
25 rapy significantly decreased the level of Lp-PLA2, a vascular-specific, inflammatory enzyme that pred
26 ing that bee venom-derived phospholipase A2 (PLA2) activates T cells through generation of small neoa
30 LA2G7 single-nucleotide polymorphisms and Lp-PLA2 activity (3 prospective, 2 case-control, 2 cross-se
32 /d was associated with a 20% reduction in Lp-PLA2 activity (P<0.001), whereas Lp-PLA2 rose 3.6% with
33 nd PI use were positively associated with Lp-PLA2 activity and mass after adjusting for age, race, se
34 Here, we used pressure modulation of the PLA2 activity and of the membrane's physical-chemical pr
35 rction volume, sPLA2 IIA protein expression, PLA2 activity and significantly restored phosphatidylcho
36 e to develop a versatile assay that monitors PLA2 activity based on interactions with natural phospho
40 lly be used as nanosensors for monitoring of PLA2 activity in biological samples with minimal sample
41 s that the previously reported difference in PLA2 activity in CSF samples from healthy and AD individ
42 ma (iPLA2gamma) accounts for the majority of PLA2 activity in rabbit ventricular myocytes and is resp
47 ine the association of the following: (1) Lp-PLA2 activity versus cardiovascular biomarkers and risk
48 nts for the top versus bottom quartile of Lp-PLA2 activity were 1.61 (95% confidence interval, 1.31 t
49 ariants associated with modest effects on Lp-PLA2 activity were not associated with cardiovascular ri
50 phox) binds to phosphoPrdx6 and inhibits its PLA2 activity, an interaction that could function to ter
51 IIA) mRNA and protein expression, increased PLA2 activity, and loss of phosphatidylcholine after 1-h
52 ER stress, and NOXA, but not the increase in PLA2 activity, indicating that PLA2 is upstream of these
54 tic effects of the lipid phase transition on PLA2 activity, the membrane insertion depth of PLA2 incr
55 f lysophosphatidylcholine, the product of Lp-PLA2 activity, was documented on the mineralization of v
56 9V) showed the strongest association with Lp-PLA2 activity, with VV subjects having 7.2% higher activ
63 lipoprotein-associated phospholipase A(2)(Lp-PLA2) activity is associated with increased risk of coro
64 psids and maintained their phospholipase A2 (PLA2) activity, as determined by native dot blot Western
65 patatin-like proteins have phospholipase A2 (PLA2) activity, recombinant TgPL1 purified from Escheric
66 sitively characterised for phospholipase A2 (PLA2) activity, suggesting their plausible involvement i
70 tivity of Ca(2+)-dependent phospholipase A2 (PLA2), an inflammatory protein that (i) plays a role in
72 tically inert stoichiometric complex between PLA2 and any bile salts in which it forms a stable compl
76 Lp-PLA2 decrease included higher baseline Lp-PLA2 and IL-6 levels, smaller increases in total cholest
80 The strongest inhibitory activities toward PLA2 and TG were found in the hydrolysates obtained by h
81 we propose that 2 enzymes-phospholipase A2 (PLA2) and ectonucleotide pyrophophatase/phosphodiesteras
82 e investigated the role of phospholipase A2 (PLA2) and the effects of PLA2 products (polyunsaturated
84 ost similar to mammalian calcium-independent PLA2, and additionally contains leucine-rich repeats and
86 57-72 loop and the H(48)DNCY(52) segment of PLA2 are involved in transmitting the effect of the coop
88 lipoprotein-associated phospholipase A2 (Lp-PLA2) are associated with cardiovascular disease and dem
89 ues to build supporting the usefulness of Lp PLA2 as a predictor of coronary events in the general po
91 ts, an elicitor-responsive phospholipase A2 (PLA2) at the plasma membrane generates signal molecules
94 sight into the regulatory role that specific PLA2-bile salt interactions are likely to play in fat me
95 previous measurements of the equilibrium for PLA2 binding to lipid membranes, the average number of e
97 e by preferentially inducing the activity of PLA2 but not LPCAT in human and mouse SCD erythrocytes.
98 ivated protein kinase) and phospholipase A2 (PLA2), but its action is independent of phosphoinositide
99 when HDL was destabilized in the presence of PLA2 by the action of cholesteryl ester transfer protein
100 enhanced binding and activation of the bound PLA2 by the bile salt induced anionic charge in a zwitte
101 mplex of pig pancreatic IB phospholipase A2 (PLA2) can be considered a proxy for interface-activated
102 We evaluated the association between Lp-PLA2, cardiac allograft vasculopathy (CAV) assessed by 3
103 lts and to determine associations between Lp-PLA2, cardiometabolic risk factors, and subclinical athe
105 ions of a biphasic dependence of the rate of PLA2 catalyzed hydrolysis of zwitterionic glycerophospho
106 that lipid enzymes such as phospholipase A2 (PLA2) contain allosteric activator sites for specific ph
107 her work is necessary to document whether Lp-PLA2 could be considered as a novel target in CAVD.
108 disulfide linkages of several cytotoxins and PLA2 could be solved, including more than 20 disulfide b
109 thermore, we showed that the IgE response to PLA2 could protect mice from future challenge with a nea
112 the inflammatory process: phospholipase A2 (PLA2), cyclooxygenase 2 (COX-2), thrombin, and transglut
113 aglandin synthesis through the activation of PLA2, cyclooxygenases (COX-1 and -2) and prostaglandins
115 levels; factors associated with a larger Lp-PLA2 decrease included higher baseline Lp-PLA2 and IL-6
121 dltA S. aureus are equally resistant to gV/X PLA2 during phagocytosis and when exposed to the purifie
122 in the liposomal membrane were hydrolyzed by PLA2, encapsulated Gd was released into bulk solution, r
126 s showing distinct roles of several of these PLA2 enzymes in inflammatory metabolic diseases such as
127 cific drugs that target one or more of these PLA2 enzymes may be novel strategies for treatment of th
131 dividuals originates from differences in the PLA2 expression level rather than from the enzyme activi
133 PURPOSE OF REVIEW: The phospholipase A2 (PLA2) family of proteins includes lipolytic enzymes that
136 in and evolution of PLA2 toxins by examining PLA2 gene number, organization, and expression in both n
138 been tested with the human Group V secreted PLA2 (GV sPLA2) and the human Group VIA calcium-independ
142 Lipoprotein-associated phospholipase A2 (Lp-PLA2) has been hypothesized to be involved in atherogene
143 Lipoprotein-associated phospholipase A2 (Lp-PLA2) hydrolyses oxidized low-density lipoproteins into
144 conducted to describe the distribution of Lp-PLA2 in a cohort of human immunodeficiency virus (HIV)-i
146 have data emerged demonstrating a role of Lp-PLA2 in development of advanced coronary artery disease.
147 a (cPLA2alpha) is thought to be the dominant PLA2 in eosinophils; however, eosinophils also have secr
149 furthering our understanding of the role of PLA2 in health and disease and in detecting the pharmaco
150 e release of AA, we investigated the role of PLA2 in local and systemic disease during S. pneumoniae
159 LA2 and melittin, an activator of endogenous PLA2, induced spinal neuronal death in vitro, which was
160 en together, this study demonstrates that Lp-PLA2 inhibition can effectively prevent diabetes-mediate
161 definitive proof, of a potential role for Lp PLA2 inhibition in coronary heart disease prevention.
166 on the efficacy of darapladib, a specific Lp PLA2 inhibitor, show beneficial changes in plaque morpho
168 (i.c.v) with mepacrine [a phospholipase A2 (PLA2) inhibitor], ibuprofen [a nonselective COX inhibito
169 X in eicosanoid formation was examined using PLA2 inhibitors and murine tracheal epithelial cells wit
170 effects, or randomized trials of specific Lp-PLA2 inhibitors are needed to confirm or refute a contri
171 lipoprotein-associated phospholipase A2 (Lp-PLA2) inhibitors may play a role in reducing progression
175 othesis that local coronary production of Lp-PLA2 is enhanced in patients with early coronary atheros
178 Together, these results demonstrated that Lp-PLA2 is highly expressed in CAVD, and it plays a role in
185 Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a novel marker and participant in vascular infl
186 Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a risk factor for coronary artery disease (CAD)
187 Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an emerging biomarker of cardiovascular disease
189 elopment of inhibitors for phospholipase A2 (PLA2) is important in elucidating the enzymes implicatio
190 Lipoprotein-associated phospholipase A2 (Lp PLA2) is postulated to occupy a key position in the path
194 scular regulators, but the phospholipase A2 (PLA2) isoforms supporting their production within the ca
200 lipoprotein-associated phospholipase A2 (Lp-PLA2) level was seen in the statin group, compared with
210 Lipoprotein-associated phospholipase A2 (Lp-PLA2) levels predict incident coronary heart disease (CH
213 n, incubating cells with the two products of PLA2 (lysophosphatidic acid and arachidonic acid) mimick
214 ery and coronary sinus for measurement of Lp-PLA2, lysophosphatidylcholine (a product of Lp-PLA2), an
215 -based treatment had significantly higher Lp-PLA2 mass and activity than those who were treatment-nai
217 CAC) scores >100 had significantly higher Lp-PLA2 mass than those with lower or nondetectable calcium
219 lipoprotein-associated phospholipase A2 (Lp-PLA2) mass or activity is associated with an increased r
224 notherapy, the therapeutic administration of PLA2-MB treatment to mice that already had established a
228 lipoprotein-associated phospholipase A2 (Lp-PLA2), Mercodia oxidized LDL (OxLDL) with antibody 4E6,
229 he later, reparative phase, infarcts of bmLp-PLA2 (-/-) mice contained Ly-6C(low) macrophages with a
233 Cs required Prdx6-PLA2 We propose that Prdx6-PLA2 modulates NOX2 activation by generation of LPC that
235 lly trapped vesicle is quite small, only two PLA2 molecules at the lowest enzyme concentration studie
236 rattlesnakes ( approximately 6 mya), while a PLA2 myotoxin gene retained in C. atrox was deleted from
238 is hence markedly affected by HHP, rendering PLA2, next to being a primary osmosensor, a good candida
240 ice that lack the phospholipase A2 activity (PLA2) of Prdx6; addition of either lysophosphatidylcholi
243 optimized NP showed selectivity for venomous PLA2 over abundant serum proteins, was not cytotoxic, an
245 dependence of the initial catalytic rate of PLA2 peaks around the lipid phase transition temperature
246 in establishing drug tolerance by regulating PLA2/PKCalpha activity and reactive oxygen species.
247 udy, we observed expression of a cytoplasmic PLA2 (PLA2G4D) in psoriatic mast cells but, unexpectedly
250 f phospholipase A2 (PLA2) and the effects of PLA2 products (polyunsaturated fatty acids and lysophosp
251 enge with S. pneumoniae As phospholipase A2 (PLA2) promotes the release of AA, we investigated the ro
254 oform (pla2g4a), iPLA2 isoform (pla2g6), and PLA2-receptor (pla2r1) were present in all tissues of bo
255 studies, hydrolysis of HDL phospholipids by PLA2 reduced the particle size without changing its prot
257 containing signaling molecules; for example, PLA2 regulates the generation of precursors for the bios
259 mentation maps to a genomic region (pla1 and pla2, respectively) containing adjacent, apparently rece
262 nges were SAA (serum amyloid protein A), NPS-PLA2 (secreted phospholipase A2), and CA6 (carbonic anhy
263 e (NMR) and other complementary results with PLA2 show that decylsulfate molecules in E 2 (#) and E 3
264 tophagy gene ATG5 Accordingly, inhibition of PLA2 significantly decreased lipid droplets, decreased o
266 containing 20% palmitic acid and PEG induced PLA2-specific IgA and increased Foxp3(+) Treg frequencie
267 ils; however, eosinophils also have secreted PLA2 (sPLA2) activity that has not been fully defined.
268 limit of detection (LOD) of human secretory PLA2 (sPLA2) in up to 1000-fold-diluted cerebrospinal fl
269 nd human studies suggest that both secretory PLA2 (sPLA2)-V and sPLA2-IIA (encoded, respectively, by
271 f these methods require the use of unnatural PLA2 substrates that may alter enzyme kinetics, and prob
274 ic phospholipase A2 (GIVA cPLA2) is the only PLA2 that exhibits a marked preference for hydrolysis of
275 a previously unknown proteolytic activity of PLA2 that is specific to apoA-I and may contribute to th
276 olipase A2 (cPLA2 ), an important isoform of PLA2 that mediates the release of arachidonic acid, play
280 as critically dependent on phospholipase A2 (PLA2) to mobilize lysophospholipids and free fatty acids
281 e traced the genomic origin and evolution of PLA2 toxins by examining PLA2 gene number, organization,
286 onmineralized aortic valves revealed that Lp-PLA2 was increased by 4.2-fold in mineralized aortic val
288 e generation of LPC by PMVECs required Prdx6-PLA2 We propose that Prdx6-PLA2 modulates NOX2 activatio
289 and neutralizing venomous phospholipase A2 (PLA2), we demonstrate that broad-spectrum neutralization
290 To test the functional importance of Lp-PLA2, we generated chimeric mice whose bone marrow-deriv
292 idly increased activity of phospholipase A2 (PLA2), which led to an increase in cytoplasmic calcium,
293 subsequent inactivation of phospholipase A2 (PLA2), whose metabolites are known to modulate ion chann
295 ienced an ACS event, direct inhibition of Lp-PLA2 with darapladib added to optimal medical therapy an
297 used to examine the association of serum Lp-PLA2 with incident CHD (myocardial infarction, angina, o
299 al structures of the complexes of pancreatic PLA2 with the naturally occurring bile salts: cholate, g
300 The amphipathic bile salts are bound to PLA2 with their polar hydroxyl and sulfate/carboxy group
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