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1 sPLA2-IIA also bound to alpha4beta1.
4 f human group IIA secreted phospholipase A2 (sPLA2-IIA), a bactericidal enzyme induced during acute i
7 ment significantly attenuated PLA2 activity, sPLA2-IIA mRNA and protein levels, and PtdCho-PLC activi
8 s Ptd-Cho levels by differentially affecting sPLA2-IIA, PtdCho-PLC, and CCTalpha after transient foca
10 ) levels yet lower oxLDL/LDL (P = 0.006) and sPLA2-IIA mass (P = 0.04), probably reflecting LD with P
12 ggest that both secretory PLA2 (sPLA2)-V and sPLA2-IIA (encoded, respectively, by the neighbouring PL
16 hydrolysis of the mitochondrial membrane by sPLA2-IIA yields inflammatory mediators (ie, lysophospho
17 6 C allele associated with lower circulating sPLA2-IIA mass (38% to 44%) and sPLA2 enzyme activity (3
18 enzyme activity in inbred strains containing sPLA2-IIA mutations; these strains were also associated
19 ggest that, in the airway, S. aureus escapes sPLA2-IIA-mediated killing through adenosine-mediated in
20 3 and alpha4beta1 may serve as receptors for sPLA2-IIA and mediate pro-inflammatory action of sPLA2-I
22 Using transgenic mice that express human sPLA2-IIA, we demonstrate that this enzyme is crucial fo
23 egulation of secretory phospholipase A2 IIA (sPLA2 IIA) mRNA and protein expression, increased PLA2 a
25 substrate of secreted phospholipase A2 IIA (sPLA2-IIA), a phospholipase otherwise specific for bacte
26 d activity of secreted phospholipase A2 IIA (sPLA2-IIA), present in inflammatory fluids, and platelet
27 rkers, secretory phospholipase A2 group IIA (sPLA2-IIA) and compares with other biomarkers on their p
32 adenosine production (adsA strain) increased sPLA2-IIA expression in guinea pig airways and was clear
34 atory action of sPLA2-IIA, and that integrin-sPLA2-IIA interaction is a novel therapeutic target.
36 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
37 mice, we show that the coordinated action of sPLA2-IIA and 12-LO promotes inflammatory arthritis.
38 2-IIA and mediate pro-inflammatory action of sPLA2-IIA, and that integrin-sPLA2-IIA interaction is a
41 n a previous study, a selective inhibitor of sPLA2-IIA (LY315920NA/S-5920) was well tolerated and app
42 c peptide, and a small molecule inhibitor of sPLA2-IIA ameliorated drusen accumulation in AMD/MD iPSC
43 Continuous 7-day infusion of an inhibitor of sPLA2-IIA had no beneficial effect on 28-day all-cause m
44 sive GBS disease contain increased levels of sPLA2-IIA compared with normal sera from healthy individ
46 l in ED and was analysed for serum levels of sPLA2-IIA, high-sensitive C-reactive protein (CRP), proc
47 nd the catalytically inactive H47Q mutant of sPLA2-IIA induced cell proliferation and ERK1/2 activati
49 found in neutrophils only in the presence of sPLA2-IIA and 12-LO in an in vivo model of autoimmune in
53 uggests that cytokine induction up-regulates sPLA2 IIA protein expression, resulting in altered lipid
54 er, the M-type receptor is species-specific: sPLA2-IIA binds to the M-type receptor in rodents and ra
59 t is entirely due to sPLA2-IIA, showing that sPLA2-IIA might represent an important component of humo
64 t the bactericidal effect is entirely due to sPLA2-IIA, showing that sPLA2-IIA might represent an imp
66 significantly attenuated infarction volume, sPLA2 IIA protein expression, PLA2 activity and signific