ライフサイエンスコーパス: sPLA2

1 he inhibition of secretary phospholipase A2 (sPLA2).

2 n/vesicle aggregation, as observed for hGIIA sPLA2.

3 xpression of group V sPLA2 but IIA not group sPLA2.

4 A2 and nonpancreatic human group IIA (hGIIA) sPLA2.

5 cles comparable to that of the human group V sPLA2.

6 the number of cells staining positively for sPLA2.

7 erably larger in hGX than in human group IIA sPLA2.

8 ade PIN showed positive immunoreactivity for sPLA2.

9 injury (MOF sPLA2, 2.4 +/- 0.97, vs. non-MOF sPLA2, 0.86 +/- 0.16 active units (AU); p < .05) and con

10 A2 activity beginning 36 hrs postinjury (MOF sPLA2, 2.4 +/- 0.97, vs. non-MOF sPLA2, 0.86 +/- 0.16 ac

11 We show that group IIA sPLA2, a known genetic modifier of mouse intestinal tumo

12 enables further studies of the mechanisms of sPLA2 action influencing the development and tumorigenes

13 vity, the protease(s) responsible for pro-GX sPLA2 activation have not been identified.

14 as no association of rs525380C>A with plasma sPLA2 activity (difference in geometric mean of sPLA2 ac

15 We tested the association of this SNP with sPLA2 activity and CHD events in 4 prospective and 14 ca

16 s show a strong association between elevated sPLA2 activity and CHD, no assay to measure sPLA2-V leve

17 he contribution of sPLA2-X to the measure of sPLA2 activity and coronary heart disease (CHD) risk tra

18 nate mucosal immunity by suppressing luminal sPLA2 activity and MUC2 density compared with chow.

19 non-MOF patients, MOF patients had elevated sPLA2 activity beginning 36 hrs postinjury (MOF sPLA2, 2

20 able to distinguish differences in levels of sPLA2 activity between neoplasia-resistant strains, whic

21 nal ensemble averaging methods used to probe sPLA2 activity do not allow one to obtain such informati

22 sPLA2 activity encompasses several sPLA2 isoenzymes, inc

23 ped a sensitive assay to directly quantitate sPLA2 activity in the murine intestinal tract utilizing

24 suppressed FLAG-pro-GX sPLA2 processing and sPLA2 activity in Y1 cells, and it significantly attenua

25 We conclude that increased sPLA2 activity is associated with the development of pos

26 tissue was harvested for analysis of tissue sPLA2 activity or immediate use in an ex-vivo intestinal

27 are not significantly associated with plasma sPLA2 activity or with CHD risk.

28 A2 activity (difference in geometric mean of sPLA2 activity per rs525380 A-allele 0.4% (95% confidenc

29 sPLA2 activity was sequentially measured and correlated

30 C-Norfolk subjects in the highest tertile of sPLA2 activity were older and had higher inflammatory ma

31 variant, were significantly associated with sPLA2 activity, intermediate CHD risk traits, or CHD ris

32 h fluid (SIWF) was collected for analysis of sPLA2 activity, MUC2 density, and luminal levels of IL-4

33 ompared with those in the lowest tertile for sPLA2 activity.

34 dies report that secretory phospholipase A2 (sPLA2) activity is a marker for coronary heart disease (

35 owever, eosinophils also have secreted PLA2 (sPLA2) activity that has not been fully defined.

36 ine if intestinal secreted phospholipase A2 (sPLA2) activity was also attenuated in susceptible strai

37 Likewise, SC secretory phospholipase A2 (sPLA2) activity, measured with a fluorometric assay, is

38 ted that group V secretory phospholipase A2 (sPLA2) amplifies the action of cytosolic phospholipase A

39 When sPLA2 and cPLA2alpha are both present, the effect of H2O

40 Interleukin-4 (IL-4) and IL-13 regulate sPLA2 and MUC2 production through the IL-13 receptor.

41 L-4 and IL-13 release and PN reduces luminal sPLA2 and MUC2, we hypothesized that adding IL-25 to PN

42 erses this dysfunction and increases luminal sPLA2 and MUC2.

43 cation by two endogenous mechanisms, namely, sPLA2 and NHE1, which are known to be important for acid

44 : Agkistrodon piscivorus piscivorus (AppD49) sPLA2 and nonpancreatic human group IIA (hGIIA) sPLA2.

45 nd PGE2 , plasma secretory phospholipase A2 (sPLA2 ), and 11beta prostaglandin F2alpha (11betaPGF2alp

46 crobial molecule secretory phospholipase A2 (sPLA2) and the goblet cell glycoprotein mucin2 (MUC2).

47 ted with the human Group V secreted PLA2 (GV sPLA2) and the human Group VIA calcium-independent PLA2

48 de compound had appreciable inhibition of GV sPLA2, and none of the potent GIVA cPLA2 inhibitors inhi

49 the putative membrane binding surface of the sPLA2 are modestly more important for bactericidal activ

50 the first 5 d after birth, and inhibition of sPLA2 between days 0 to 1 and days 5 to 6 delays postnat

51 These results suggest that preferred sPLA2 binding conformation of the natural product is sim

52 ase packing of DAPC and DMPE interferes with sPLA2 binding, irrespective of the phospholipid headgrou

53 restored by adenoviral expression of group V sPLA2 but IIA not group sPLA2.

54 Group IIa secretory PLA2 (sPLA2) can generate arachidonate from cellular phospholi

55 The inhibition is dependent on sPLA2 catalytic activity and primarily due to hydrolysis

56 he inflammatory-type human group IIA (hGIIA) sPLA2 circulates at high levels in the serum of malaria

57 f the products tested had elevated levels of sPLA2 compared with fresh plasma from healthy adult volu

58 g of sPLA2 was monitored using a fluorescein-sPLA2 conjugate.

59 These data demonstrate that group V sPLA2 contributes to the innate immune response both thr

60 Using the human group X sPLA2 crystal structure, we prepared a highly potent and

61 as measured in vivo in wild-type (WT) and GX sPLA2-deficient (GX KO) mice and ex vivo using pancreati

62 Y1 cells, and it significantly attenuated GX sPLA2-dependent inhibition of steroidogenic acute regula

63 omposition, all GUVs were reduced in size as sPLA2-dependent lipid hydrolysis proceeded.

64 of lateral packing of the lipids in C. atrox sPLA2 enzymatic hydrolysis of a membrane surface.

65 circulating sPLA2-IIA mass (38% to 44%) and sPLA2 enzyme activity (3% to 23%) per C allele.

66 analysis failed to show associations between sPLA2 enzyme activity and MVE.

67 gher circulating levels of sPLA2-IIA mass or sPLA2 enzyme activity have been associated with increase

68 ual members of the large family of mammalian sPLA2 enzymes.

69 Secretory phospholipase A2 (sPLA2) enzymes are considered to play a role in atherosc

70 molecular weight secretory phospholipase A2 (sPLA2) enzymes in eicosanoid generation have relied on d

71 e indicates that secretory phospholipase A2 (sPLA2) enzymes promote atherogenic processes.

72 is study, using a FLAG epitope-tagged pro-GX sPLA2 expression construct (FLAG-pro-GX sPLA2), we deter

73 We examined the group IIa sPLA2 expression in benign prostatic tissues, prostatic

74 We demonstrate that gV-sPLA2 expression in M is sufficient for the development

75 IN), and adenocarcinoma to determine whether sPLA2 expression is altered in the carcinogenesis of hum

76 onsistent with the contention that group IIA sPLA2 expression is elevated in neoplastic prostatic tis

77 Secretory phospholipase A2 (sPLA2) generates bioactive phospholipid products implica

78 ence of cPLA2 and secreted phospholipase A2 (sPLA2) Group IIA, Group V, and Group X on IL-8 and COX-2

79 ve previously showed the presence of Group V sPLA2 (GV sPLA2) in human and mouse atherosclerotic lesi

80 man group X (hGX) secreted phospholipase A2 (sPLA2) has been solved to a resolution of 1.97 A.

81 sPLA2 hydrolyzes the liquid domains in the binary lipid

82 Group X secretory phospholipase A2 (GX sPLA2) hydrolyzes mammalian cell membranes, liberating f

83 sPLA2 IB enhanced podocyte arachidonic acid (AA) content

84 These data indicate that sPLA2 IB has the potential to induce human podocyte apop

85 However, the roles of the PLA2R and sPLA2 IB in the pathogenesis of glomerular diseases are

86 After binding with the PLA2R, sPLA2 IB induced podocyte apoptosis in a time- and conce

87 neys of patients with higher PLA2R and serum sPLA2 IB levels.

88 Group IB secretory phospholipase A2 (sPLA2 IB), which is one of the ligands of the PLA2R, is

89 sPLA2 IB-induced podocyte PLA2R upregulation was not onl

90 The sPLA2 IB-PLA2R interaction stimulated podocyte apoptosis

91 significantly attenuated infarction volume, sPLA2 IIA protein expression, PLA2 activity and signific

92 uggests that cytokine induction up-regulates sPLA2 IIA protein expression, resulting in altered lipid

93 egulation of secretory phospholipase A2 IIA (sPLA2 IIA) mRNA and protein expression, increased PLA2 a

94 gate the role of secretory phospholipase A2 (sPLA2)-IIA in cardiovascular disease.

95 tly increased PLA2 activity, secretory PLA2 (sPLA2)-IIA mRNA and protein levels, PtdCho-PLC activity,

96 We identified amino acid residues in sPLA2-IIA (Arg-74 and Arg-100) that are critical for int

97 ggest that both secretory PLA2 (sPLA2)-V and sPLA2-IIA (encoded, respectively, by the neighbouring PL

98 n a previous study, a selective inhibitor of sPLA2-IIA (LY315920NA/S-5920) was well tolerated and app

99 s of intestinal tissues were consistent with sPLA2-IIA activity levels.

100 own by sequencing to carry variant wild-type sPLA2-IIA alleles.

101 sPLA2-IIA also bound to alpha4beta1.

102 in vitro CN and CNJ culturing confirmed that sPLA2-IIa amplifies ocular surface inflammation in CNJ b

103 found in neutrophils only in the presence of sPLA2-IIA and 12-LO in an in vivo model of autoimmune in

104 mice, we show that the coordinated action of sPLA2-IIA and 12-LO promotes inflammatory arthritis.

105 o determine whether the relationship between sPLA2-IIA and coronary heart disease is causal.

106 Treated mice exhibited upregulated sPLA2-IIa and cytokine gene transcription.

107 3 and alpha4beta1 may serve as receptors for sPLA2-IIA and mediate pro-inflammatory action of sPLA2-I

108 er, the M-type receptor is species-specific: sPLA2-IIA binds to the M-type receptor in rodents and ra

109 Here we demonstrated that sPLA2-IIA bound to integrin alphavbeta3 at a high affini

110 isolates are highly sensitive to killing by sPLA2-IIA but not by human antimicrobial peptides.

111 sive GBS disease contain increased levels of sPLA2-IIA compared with normal sera from healthy individ

112 We showed that sPLA2-IIA competed with VCAM-1 for binding to alpha4beta

113 S. aureus adsA strain induced sPLA2-IIA expression by alveolar macrophages after phago

114 adenosine production (adsA strain) increased sPLA2-IIA expression in guinea pig airways and was clear

115 Ocular surface inflammation and sPLA2-IIa expression were examined by immune-staining an

116 veolar macrophages, leading to inhibition of sPLA2-IIA expression.

117 sine-mediated inhibition of phagocytosis and sPLA2-IIA expression.

118 sPLA2-IIa function was confirmed via in vitro CN and CNJ

119 Consistent with predictions from the sPLA2-IIA gene sequence in inbred strains, we detected l

120 Continuous 7-day infusion of an inhibitor of sPLA2-IIA had no beneficial effect on 28-day all-cause m

121 Moreover, treated mice showed heavier sPLA2-IIa immune staining than the controls in the CNJ e

122 (DE) model was used to elucidate the role of sPLA2-IIa in ocular surface inflammation.

123 This is the first report regarding sPLA2-IIa in the regulation of ocular surface inflammati

124 nd the catalytically inactive H47Q mutant of sPLA2-IIA induced cell proliferation and ERK1/2 activati

125 Independent of its catalytic activity, sPLA2-IIA induces pro-inflammatory signals in a receptor

126 Furthermore, CNJ cultures treated with sPLA2-IIa inhibitor showed significantly reduced sPLA2-I

127 induced by sPLA2-IIa with various amount of sPLA2-IIa inhibitor, S-3319.

128 atory action of sPLA2-IIA, and that integrin-sPLA2-IIA interaction is a novel therapeutic target.

129 sPLA2-IIa is a biomarker for many inflammatory diseases

130 Because sPLA2-IIA is induced during inflammation, and 12-LO expr

131 s11573156, a variant in PLA2G2A encoding the sPLA2-IIA isoenzyme, as an instrumental variable.

132 previously associated with higher and lower sPLA2-IIA levels respectively.

133 6 C allele associated with lower circulating sPLA2-IIA mass (38% to 44%) and sPLA2 enzyme activity (3

134 ) levels yet lower oxLDL/LDL (P = 0.006) and sPLA2-IIA mass (P = 0.04), probably reflecting LD with P

135 Reducing sPLA2-IIA mass is unlikely to be a useful therapeutic go

136 Higher circulating levels of sPLA2-IIA mass or sPLA2 enzyme activity have been associ

137 able analysis for MVE for a 1-log unit lower sPLA2-IIA mass was 1.04 (95% CI: 0.96 to 1.13), and diff

138 ypes of PLA2G2A are strongly associated with sPLA2-IIA mass, but not lipid levels.

139 t is entirely due to sPLA2-IIA, showing that sPLA2-IIA might represent an important component of humo

140 ment significantly attenuated PLA2 activity, sPLA2-IIA mRNA and protein levels, and PtdCho-PLC activi

141 enzyme activity in inbred strains containing sPLA2-IIA mutations; these strains were also associated

142 Elevated plasma sPLA2-IIA predicts coronary heart disease (CHD) risk, bu

143 vide experimental and clinical evidence that sPLA2-IIA protects humans against GBS infections.

144 Thus sPLA2-IIA receptors in human have not been established.

145 individuals, indicating that GBS induces an sPLA2-IIA response in blood during human infection.

146 d for prostaglandin E2 production induced by sPLA2-IIa with various amount of sPLA2-IIa inhibitor, S-

147 hydrolysis of the mitochondrial membrane by sPLA2-IIA yields inflammatory mediators (ie, lysophospho

148 Secretory phospholipase A2 group IIA (sPLA2-IIA) has been identified as a biomarker of atheros

149 The type IIA secretory phospholipase A2 (sPLA2-IIA) is a host protein endowed with antibacterial

150 Secretory phospholipase A2 group IIA (sPLA2-IIA) plays an important role in the pathogenesis o

151 f human group IIA secreted phospholipase A2 (sPLA2-IIA), a bactericidal enzyme induced during acute i

152 substrate of secreted phospholipase A2 IIA (sPLA2-IIA), a phospholipase otherwise specific for bacte

153 d activity of secreted phospholipase A2 IIA (sPLA2-IIA), present in inflammatory fluids, and platelet

154 Group IIA secretory phospholipase A2 (sPLA2-IIA), released during inflammation, is increased i

155 IFA of sPLA2-IIa, -V, and -X in DE CNJ confirmed the upregulati

156 Immunofluorescence assay (IFA) of the sPLA2-IIa, -V, and -X isoforms were used to confirm qRT(

157 ought to represent the composite activity of sPLA2-IIA, -V, and -X.

158 2-IIA and mediate pro-inflammatory action of sPLA2-IIA, and that integrin-sPLA2-IIA interaction is a

159 phase response in which serum amyloid A and sPLA2-IIa, present at sites of inflammation and tissue d

160 s Ptd-Cho levels by differentially affecting sPLA2-IIA, PtdCho-PLC, and CCTalpha after transient foca

161 t the bactericidal effect is entirely due to sPLA2-IIA, showing that sPLA2-IIA might represent an imp

162 Using transgenic mice that express human sPLA2-IIA, we demonstrate that this enzyme is crucial fo

163 2-IIa inhibitor showed significantly reduced sPLA2-IIa-induced inflammation.

164 but catalytic activity is not required, for sPLA2-IIA-induced proliferative signaling.

165 ggest that, in the airway, S. aureus escapes sPLA2-IIA-mediated killing through adenosine-mediated in

166 However, the role of adenosine in sPLA2-IIA-mediated S. aureus killing by host is still un

167 s) expressed cPLA2-IVA, cPLA2-IVB, iPLA2-VI, sPLA2-IIE, and sPLA2-XIIA.

168 The intensity of sPLA2 immunoreactivity was also different among benign p

169 r studies identified a unique function of gV-sPLA2 in activation of M and in their capacity to recrui

170 relative concentration variations of active sPLA2 in CSF and the specific enzymatic activity can be

171 Adoptive transfer studies suggested that gV-sPLA2 in dendritic cells was necessary for sensitization

172 provide clear evidence of a role for group V sPLA2 in regulating eicosanoid generation in response to

173 Overexpression of human sPLA2 in transgenic mice reduces both HDL cholesterol an

174 sly showed the presence of Group V sPLA2 (GV sPLA2) in human and mouse atherosclerotic lesions, its h

175 of detection (LOD) of human secretory PLA2 (sPLA2) in up to 1000-fold-diluted cerebrospinal fluid (C

176 The sPLA2 inhibition with varespladib may be harmful and is

177 A recent phase III clinical trial of an sPLA2 inhibitor (varespladib) was stopped prematurely fo

178 The sPLA2 inhibitor varespladib has favorable effects on lip

179 ved from LY315920, a well-known indole-based sPLA2 inhibitor.

180 chemically unrelated secretory phospholipase sPLA2 inhibitors, bromphenacylbromide and 1-hexadecyl-3-

181 on is replaced with a Z-olefin or an alkyne, sPLA2 inhibitory activity suffered relative to the natur

182 findings provide strong evidence that pro-GX sPLA2 is a substrate for furin and PCSK6 proteolytic pro

183 cells in the small intestine, while group X sPLA2 is expressed by Paneth/goblet-like cells in the co

184 In this study, we determined that GX sPLA2 is expressed in insulin-producing cells of mouse p

185 In this study, we demonstrate that gV-sPLA2 is inducibly expressed in mouse and human macropha

186 We report that group V sPLA2 is present in the Golgi apparatus and recycling en

187 GX sPLA2 is produced as a pro-enzyme (pro-GX sPLA2) that co

188 san by mouse peritoneal macrophages, group V sPLA2 is recruited to the phagosome.

189 that: 1) the overall positive charge of the sPLA2 is the dominant factor in dictating bactericidal p

190 Group IIA secreted phospholipase A(2) (sPLA2) is known to display potent Gram-positive bacteric

191 sPLA2 activity encompasses several sPLA2 isoenzymes, including sPLA2-V.

192 sent in all tissues of both strains, whereas sPLA2 isoforms (pla2g1b, 2e, and 3) were absent.

193 sPLA2 isoforms (pla2g2a, 2d, 2f, and 10) showed tissue-

194 qRT(2)-PCR revealed that sPLA2 isoforms (pla2g5, 12a, and 12b), cPLA2 isoform (pl

195 sPLA2 isoforms exhibit differential expression patterns

196 These findings suggest that at least some sPLA2 isoforms must have significant roles in ocular sur

197 Gene expression of select sPLA2 isoforms was quantified via real-time reverse-tran

198 whereas IL-25 significantly increased tissue sPLA2 levels compared with PN alone.

199 have identified a secreted phospholipase A2 (sPLA2)-like protein, BomoTx, from the Brazilian lancehea

200 ession levels of secretory phospholipase A2 (sPLA2), lysophospholipid acyltransferase (LPEAT), lysoph

201 support the hypothesis that dysregulation of sPLA2 may play a role in prostatic carcinogenesis.

202 IS was lower in MIN6 cells overexpressing GX sPLA2 (MIN6-GX) compared with control (MIN6-C) cells.

203 otein (LDL) particles, and the ability of GV sPLA2-modified LDL (GV-LDL) to induce macrophage foam ce

204 We previously reported that GX sPLA2 negatively regulates adrenal glucocorticoid produc

205 y 50% in peritoneal macrophages from group V sPLA2-null mice compared with macrophages from wild-type

206 otrienes were markedly attenuated in group V sPLA2-null mice compared with wild-type controls.

207 hermore, peritoneal macrophages from group V sPLA2-null mice demonstrated a >50% attenuation in phago

208 The effect of GX sPLA2 on GSIS was abolished when cells were treated with

209 ect of deletion of the gene encoding group V sPLA2 on phagocytosis of zymosan.

210 nt GIVA cPLA2 inhibitors inhibited either GV sPLA2 or GVIA iPLA2.

211 IN6 pancreatic beta cells with or without GX sPLA2 overexpression or exogenous addition.

212 he addition of IL-25 to PN increased luminal sPLA2 (P < 0.0001) and MUC2 (P < 0.02) compared with PN.

213 PN reduced luminal sPLA2 (P < 0.0001) and MUC2 (P <0.002) compared with cho

214 We conclude that GX sPLA2 plays a previously unrecognized role in negatively

215 Group X secretory phospholipase A2 (GX sPLA2) potently hydrolyzes membrane phospholipids to rel

216 are formed by internalization of the Group V sPLA2 previously associated with the outer cellular surf

217 cotropic hormone (ACTH) enhanced FLAG-pro-GX sPLA2 processing and phospholipase activity secreted by

218 ketone significantly suppressed FLAG-pro-GX sPLA2 processing and sPLA2 activity in Y1 cells, and it

219 PCs almost completely abolished FLAG-pro-GX sPLA2 processing in Y1 cells.

220 293 cells significantly enhanced FLAG-pro-GX sPLA2 processing, whereas siRNA-mediated knockdown of bo

221 Secretory phospholipase A2 (sPLA2) produces many inflammatory lipid mediators, and l

222 matory response, secretory phospholipase A2 (sPLA2) reaches its maximum levels in plasma, where it is

223 Different sPLA2's utilize different combinations of electrostatic

224 Secreted phospholipases A2 (sPLA2's) are enzymes that hydrolyze glycerophospholipids

225 ane association of two highly basic group II sPLA2's: Agkistrodon piscivorus piscivorus (AppD49) sPLA

226 cking group V secretory phospholipase A2 (gV-sPLA2) showed reduced eosinophilic pulmonary inflammatio

227 otein fold is similar to previously reported sPLA2 structures.

228 GX sPLA2 is produced as a pro-enzyme (pro-GX sPLA2) that contains an N-terminal 11-amino acid propept

229 for patient resuscitation was the source of sPLA2, the sPLA2 was measured in packed red blood cells,

230 oes not resemble that of the human group IIA sPLA2; the former is highly neutral, whereas the latter

231 n of the ability of the acidic human group X sPLA2 to kill Gram-positive bacteria.

232 er furin or PCSK6 enhanced the ability of GX sPLA2 to suppress liver X receptor reporter activity.

233 y was to characterize the plasma activity of sPLA2 type IIa in severely injured patients and to deter

234 a switch to a sequential induction of first sPLA2 (types IIa and V) that mediates the release of PAF

235 an studies suggest that both secretory PLA2 (sPLA2)-V and sPLA2-IIA (encoded, respectively, by the ne

236 causally related, because cells deficient in sPLA2-V exhibited decreased phagocytosis, and cells over

237 In parallel with increasing sPLA2-V expression levels, IL-4-treated macrophages exhi

238 Here, we use tSNPs of the sPLA2-V gene to investigate the association of PLA2G5 wi

239 evidence does not support a causal role for sPLA2-V in CHD.

240 investigate the hypothesized causal role of sPLA2-V in coronary heart disease (CHD) pathogenesis.

241 rt disease (CHD) risk, but no mass assay for sPLA2-V is available.

242 Collectively, our results show that sPLA2-V is required for efficient phagocytosis by IL-4-t

243 ls exists, and the only evidence linking the sPLA2-V isoform to atherosclerosis progression comes fro

244 sPLA2 activity and CHD, no assay to measure sPLA2-V levels exists, and the only evidence linking the

245 phism for PLA2G5 expression, a surrogate for sPLA2-V levels) and CHD events.

246 absence of an assay that directly quantifies sPLA2-V levels, we used PLA2G5 mRNA levels in a novel, m

247 PLA2G5 mRNA expression levels as a proxy for sPLA2-V levels.

248 on of the secreted group V phospholipase A2 (sPLA2-V), both at the mRNA and protein levels.

249 By supplementing sPLA2-V-deficient cells with LPE, phagocytosis of zymosa

250 human macrophages and provide evidence that sPLA2-V-derived LPE is involved in the process.

251 at ethanolamine lysophospholipid (LPE) is an sPLA2-V-derived product that may be involved in regulati

252 levels of LPE are selectively maintained by sPLA2-V.

253 ompasses several sPLA2 isoenzymes, including sPLA2-V.

254 t resuscitation was the source of sPLA2, the sPLA2 was measured in packed red blood cells, platelet c

255 The binding of sPLA2 was monitored using a fluorescein-sPLA2 conjugate.

256 The sPLA2 was observed to associate with the entire surface

257 The number of cells staining for sPLA2 was significantly less in benign epithelium (4%) a

258 o-GX sPLA2 expression construct (FLAG-pro-GX sPLA2), we determined that adrenocorticotropic hormone (

259 To further understand the role of group V sPLA2, we studied its localization in resting mouse peri

260 To elucidate the role of group V sPLA2, we used targeted gene disruption to generate mice

261 Tissue levels of sPLA2 were significantly decreased with PN compared with

262 e immunohistochemical staining for group IIA sPLA2, whereas 63 of 69 total cases (91%) of high-grade

263 cytes is group X secretory phospholipase A2 (sPLA2), which liberates large amounts of AA and the lyso

264 of Crotalus atrox-secreted phospholipase A2 (sPLA2) with giant unilamellar vesicles (GUVs) composed o

265 An inhibitor of sPLA2-X (ROC-0929) that does not inhibit other mammalian

266 ain lysophospholipid released in response to sPLA2-X activity, stimulates melanocyte dendricity.

267 al a relationship between epithelial-derived sPLA2-X and indirect AHR in asthma and that sPLA2-X serv

268 e treated human melanocytes with recombinant sPLA2-X and show that low levels of sPLA2-X stimulate bo

269 A rabbit polyclonal anti-sPLA2-X antibody identified sPLA2-X by Western blot.

270 We found that the effects of sPLA2-X are mediated predominantly by LPC, not AA, and w

271 polyclonal anti-sPLA2-X antibody identified sPLA2-X by Western blot.

272 The regulation of sPLA2-X gene (PLA2G10) expression was examined in primar

273 Eosinophils express the mammalian sPLA2-X gene (PLA2G10).

274 tion, our data suggest an important role for sPLA2-X in cutaneous pigmentation through the release of

275 The function of epithelial sPLA2-X in eicosanoid formation was examined using PLA2

276 We sought to examine sPLA2-X in the airway epithelium and airway wall of pati

277 The expression of sPLA2-X increases during in vitro epithelial differentia

278 Selective sPLA2-X inhibition attenuated the fMLP-mediated release

279 The sPLA2-X inhibitor reduced the phosphorylation of p38 and

280 We further demonstrate that sPLA2-X is activated before secretion from the cell duri

281 during cellular activation, indicating that sPLA2-X is involved in activating the MAPK cascade leadi

282 ents with asthma and that epithelial-derived sPLA2-X may be increased in association with indirect AH

283 Therapies targeting epithelial sPLA2-X may be useful in asthma.

284 Treatment of melanocytes with sPLA2-X or LPC induced phosphorylation of the zeta isofo

285 These results demonstrate that sPLA2-X plays a significant role in the formation of Cys

286 sPLA2-X potently reduced gene transfer of HIV-1 Env-pseu

287 We found that sPLA2-X protein is increased in the airways of patients

288 The sPLA2-X protein is located in the endoplasmic reticulum,

289 The sPLA2-X protein is regulated by proteolytic cleavage, su

290 sPLA2-X and indirect AHR in asthma and that sPLA2-X serves as an epithelial regulator of inflammator

291 ombinant sPLA2-X and show that low levels of sPLA2-X stimulate both tyrosinase activity and melanocyt

292 e used confocal microscopy to colocalize the sPLA2-X to intracellular structures.

293 sPLA2-X, to investigate the contribution of sPLA2-X to the measure of sPLA2 activity and coronary he

294 n humans, and the regulation and function of sPLA2-X within the epithelium.

295 Secretory phospholipase-A2 type X (sPLA2-X) is released by epidermal keratinocytes and we h

296 Secreted phospholipase A2 group X (sPLA2-X) plays a key role in regulating eicosanoid forma

297 A specific secretory PLA2, sPLA2-X, is shown here to neutralize human immunodeficie

298 dy and complement were sensitive to lysis by sPLA2-X, suggesting a novel mechanism of antiviral surve

299 to use genetic variants of PLA2G10, encoding sPLA2-X, to investigate the contribution of sPLA2-X to t

300 LA2-IVA, cPLA2-IVB, iPLA2-VI, sPLA2-IIE, and sPLA2-XIIA.