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1 ting imbalanced Lands' cycle by knockdown of phospholipase 2 (cPLA2) or overexpression of lysophospha
2 TT>deltaG, rs12979860 C>T, and patatin-like phospholipase-3 rs738409 C>G polymorphisms were genotype
3 In Gram-negative bacteria, outer membrane phospholipase A (OmpLA) is involved in outer-membrane li
4 tinized the unfolded state of outer-membrane phospholipase A (OmpLA) to provide a detailed view of it
5 chniques, we discover that ACT has intrinsic phospholipase A (PLA) activity, and that such activity d
8 d that the dominant mlaA* mutation activates phospholipase A, resulting in increased levels of lipopo
9 f genes encoding 13-lipoxygenases (LOXs) and phospholipase A-Igamma3 (At1g51440), a plastid lipase wi
11 proteins, which belong to the intracellular phospholipase A1 (iPLA1) family, have been predicted to
14 and no PA production could be detected using phospholipase A1, phospholipase A2, or phospholipase C,
15 doxin 6 (Prdx6), a bifunctional protein with phospholipase A2 (aiPLA2) and GSH peroxidase activities,
16 DX6 or inhibition of its calcium-independent phospholipase A2 (Ca(2+)-iPLA2) activity by MJ33 on fert
17 ls of MYC, we found an increase in cytosolic phospholipase A2 (cPLA2) activity with a preferential re
19 tease-activated receptors 1 and 4, cytosolic phospholipase A2 (cPLA2), Src tyrosine kinases, p38 MAPK
20 acid by phospholipase A2, and the cytosolic phospholipase A2 (cPLA2)alpha isoform has been specifica
24 vated levels of human lipoprotein-associated phospholipase A2 (Lp-PLA2) are associated with cardiovas
29 ybean seeds and positively characterised for phospholipase A2 (PLA2) activity, suggesting their plaus
32 the demonstration that lipid enzymes such as phospholipase A2 (PLA2) contain allosteric activator sit
35 n after lung challenge with S. pneumoniae As phospholipase A2 (PLA2) promotes the release of AA, we i
36 of cancer cells was critically dependent on phospholipase A2 (PLA2) to mobilize lysophospholipids an
37 le of sequestering and neutralizing venomous phospholipase A2 (PLA2), we demonstrate that broad-spect
38 hate (cAMP) and a subsequent inactivation of phospholipase A2 (PLA2), whose metabolites are known to
41 ), two in apolipoprotein B (APOB) and one in phospholipase A2 (PLA2G4A) that significantly associated
42 l. (2017) provide intriguing evidence that a phospholipase A2 (Pla2gb1) produced by epithelial cells
43 ays, we found expression levels of secretory phospholipase A2 (sPLA2), lysophospholipid acyltransfera
44 tional screen, we have identified a secreted phospholipase A2 (sPLA2)-like protein, BomoTx, from the
45 strong upregulation of the secreted group V phospholipase A2 (sPLA2-V), both at the mRNA and protein
49 l or Prdx6-D140A-knock-in mice that lack the phospholipase A2 activity (PLA2) of Prdx6; addition of e
50 easurement of prostaglandin E2 and cytosolic phospholipase A2 activity in membrane fractions of fibro
53 onses are elicited through lipid products of phospholipase A2 activity that acts on the membrane phos
55 r levels of hsCRP and lipoprotein-associated phospholipase A2 after AMI compared with men, and this r
56 2+) release from internal stores, activating phospholipase A2 and generating vasodilatory arachidonic
57 hetic enzymes includes (1) the activation of phospholipase A2 at the plasma membrane, resulting in a
58 urons caused the dissociation of cytoplasmic phospholipase A2 from PrP-containing membrane rafts and
59 Here we identify epithelial-cell-derived phospholipase A2 group 1B (PLA2g1B) as a host-derived en
60 04, n >/=5/group) for five other NBIA genes, phospholipase A2 group VI, fatty acid 2-hydroxylase, cer
61 esterol, adiponectin, lipoprotein-associated phospholipase A2 mass and activity, monocyte chemoattrac
67 le is known about the biological role of the phospholipase A2 receptor (PLA2R1) transmembrane protein
68 tly discovered podocyte antigens: the M-type phospholipase A2 receptor 1 (PLA2R) and thrombospondin t
69 bodies against the podocyte surface antigens phospholipase A2 receptor 1 (PLA2R1) and the recently id
71 e ExoU type III secretion enzyme is a potent phospholipase A2 secreted by the Gram-negative opportuni
72 ity to induce prostaglandin E2 and cytosolic phospholipase A2 synthesis in patients' fibroblasts.
73 d a novel cardiolipin hydrolysis reaction by phospholipase A2 to form diacylated cardiolipin progress
75 crophages, activation of group IVA cytosolic phospholipase A2(cPLA2alpha) by calcium- and mitogen-act
79 ion is the liberation of arachidonic acid by phospholipase A2, and the cytosolic phospholipase A2 (cP
80 d on a denatured form of the major allergen, phospholipase A2, associated with microbubbles (PLA2dena
81 (COX-2)/prostaglandin E2 signaling cascade (phospholipase A2, COX-2, multidrug resistance protein 4,
82 on could be detected using phospholipase A1, phospholipase A2, or phospholipase C, allowing for a rel
83 yclooxygenase-2 and phosphorylated cytosolic phospholipase A2, which was reflected in prostaglandin E
84 adult mice expressed more group 10 secretory phospholipase A2, Wnt5a, and transglutaminase 2 (Tgm2).
85 evels of prostaglandin E2 The non-functional phospholipase A2-activating protein and the associated n
86 a loss of function sequence variation in the phospholipase A2-activating protein encoding gene (PLAA)
94 c activity of soluble lipoprotein-associated phospholipase A2; at CYP2F1, with higher plasma interleu
99 dependent upon calcium-independent group VIA phospholipase A2beta (iPLA2beta) following infection of
100 ding to the activation of Ca(2+)-independent phospholipase A2gamma (iPLA2gamma) and the production of
102 reported previously that calcium-independent phospholipase A2gamma (iPLA2gamma) is cytoprotective aga
103 yl chains from CL by the calcium-independent phospholipase A2gamma (iPLA2gamma)-selective inhibitor (
105 rom non-failing hearts was calcium-dependent phospholipase A2zeta (cPLA2zeta) identified by sequentia
107 e truncated ExoU proteins partially restored phospholipase activity and cytotoxicity, indicating that
108 thogen, Pseudomonas aeruginosa Activation of phospholipase activity is induced by protein-protein int
110 e data indicate that cPLA2alpha, through its phospholipase activity, is a critical effector of G1 pha
117 ccelerated DHA catabolism (eg, activation of phospholipases and oxidation pathways) could explain the
118 tion in MATRILINEAL (MTL), a pollen-specific phospholipase, and that novel edits in MTL lead to a 6.7
122 thuringiensis phosphatidylinositol-specific phospholipase C (BtPI-PLC) is a secreted virulence facto
123 The activation of phosphoinositide-specific phospholipase C (PI-PLC) is one of the earliest response
125 endogenous PIP2 either by serotonin-induced phospholipase C (PLC) activation or by a rapamycin-induc
126 ling cascade culminating in phosphoinositide-phospholipase C (PLC) activation, which generates the se
128 1,4,5 trisphosphate (IP3 ) accumulation and phospholipase C (PLC) activity were significantly potent
132 tors and receptor tyrosine kinases, activate phospholipase C (PLC) isozymes to hydrolyze phosphatidyl
134 channels TRPC4 and -5 via the Gq/11 protein-phospholipase C (PLC) signaling pathway has remained elu
135 we used on-tissue treatment with buffer-free phospholipase C (PLC) to near-quantitatively degrade PCs
137 boundary as merely a substrate for PI3K and phospholipase C (PLC), and is now an established lipid m
138 (NAPE-PLD), diacylglycerol lipase (DAGL), or phospholipase C (PLC), and their metabolism is mediated
139 PM8) channels are thought to be regulated by phospholipase C (PLC), but neither the specific PLC isof
140 the fibroblast growth factor (FGF) receptor, phospholipase C (PLC), protein kinase C (PKC) and phosph
141 inds its two major classes of effectors, the phospholipase C (PLC)-beta isozymes and Rho guanine nucl
143 requires G protein alpha q subunit (Galphaq)/phospholipase C (PLC)beta1 activities and protein kinase
144 requires G protein alpha q subunit (Galphaq)/phospholipase C (PLC)beta1/protein kinase C (PKC) activi
145 itment of TRPC3 or phosphoinositide-specific phospholipase C (PLCgamma) to the AT1R-beta-arrestin-1 s
147 tly enhanced bone formation, indicating that phospholipase C activation is not required for increased
149 erstand dynamic effects of receptor-mediated phospholipase C activation on excitability and other PI(
150 from intracellular stores via activation of phospholipase C and opening of inositol trisphosphate (I
151 se embryo at the 8-cell stage is directed by Phospholipase C and Protein kinase C and occurs in two p
152 eved either by agonist-induced activation of phospholipase C beta or with a rapamycin-inducible syste
153 lated HUVEC migration and proliferation in a phospholipase C beta-dependent fashion and decreased Gal
154 effect of NAC on Galphaq palmitoylation and phospholipase C beta-mediated signaling in endothelial c
156 ronchial aSMCs, through its association with phospholipase C beta2 and the stimulation of inositol 1,
158 correlated with an association of PP1c with phospholipase C beta3 (PLCbeta3), along with a concomita
159 /11 heterotrimeric G proteins, and in PLCB4 (phospholipase C beta4), the downstream effector of Galph
160 sphate counteracted the direct activation of phospholipase C by 2,4,6-trimethyl-N-[3-(trifluoromethyl
162 ition by the default PI(4,5)P2 lipid sensor, phospholipase C delta 1 pleckstrin homology domain (PLC
163 r activation of T cells (LAT), and activated phospholipase C gamma 1 (PLCgamma1), which all localize
164 ernal GDP-beta-S or inhibiting OX1Rs, CB1Rs, phospholipase C or DAGL, and potentiated by inhibiting 2
167 phatidylinositol-specific phospholipase C, a phospholipase C specific for the cleavage of glycosylpho
168 cerophosphodiesterase GDE3 as a GPI-specific phospholipase C that cleaves and releases uPAR with cons
169 ion of cell-surface receptors that couple to phospholipase C to generate the second messenger inosito
170 itol (PI) by targeting bacterial PI-specific phospholipase C to the PIS domain impairs recruitment of
171 d protein kinase A (PKA) via Gsalpha but not phospholipase C via Gq/11 (D/D mice), PTH significantly
172 yte at fertilisation, a process initiated by phospholipase C zeta (PLCzeta), a sperm-specific protein
174 -2-decanoylamino-3-morpholino-1-propanol and phospholipase C), we demonstrated that PSV could recogni
175 treatment with phosphatidylinositol-specific phospholipase C, a phospholipase C specific for the clea
176 using phospholipase A1, phospholipase A2, or phospholipase C, allowing for a reliable determination o
178 Galphaq, on the other hand, signals through phospholipase C, and it remains unclear whether Galphaq-
179 1 metabotropic glutamate receptors, Homer2, phospholipase C, and/or phosphotidylinositide-3 kinase f
180 y due to the hydrolytic activity of Sac2 and phospholipase C, becoming undetectable for approximately
181 of the nerves requires the beta3 isoform of phospholipase C, but TRPA1 or other TRP channel are not
182 s involving a G-protein q, the activation of phospholipase C, calcium mobilization, and the release o
183 radicals, lipid peroxidation, activation of phospholipase C, IP3 receptors, and release of Ca(2+) fr
185 nistic studies indicate that EDNRA activates phospholipase C, which then 1) increases the MMP1 protei
187 gamma subunits, and some Rho family GTPases, phospholipase C-beta (PLC-beta) isoforms hydrolyze phosp
188 hototransduction pathway, which requires the phospholipase C-beta encoded by norpA (no receptor poten
189 iquitous activation of Ca(2+) signaling upon phospholipase C-coupled receptor ligation leads quite na
191 CD40 ligation in Muller cells triggered phospholipase C-dependent ATP release that caused P2X7-d
194 c, phosphatidylinositol 3-kinase (PI3K), and phospholipase C-gamma1 (PLCgamma1) have all been implica
197 g a variety of approaches, we also show that phospholipase C-mediated PIP2 hydrolysis is necessary an
201 lecular mechanism underlying this process: a phospholipase C/Ca(2+)/proline-rich tyrosine kinase 2/cJ
202 framework for a mechanistic understanding of phospholipase C/PKC signaling in chemotactic gradient se
203 op and analyze a reaction-diffusion model of phospholipase C/protein kinase C (PKC) signaling, which
204 e determinants of pathogenesis: two secreted phospholipases C (PLCs; PlcA and PlcB) and a surface pro
205 s includes the calmodulin inhibitor W-7, the phospholipase-C inhibitor U73122, and anti-psychotic phe
206 entiation (PTP) or through activation of the phospholipase-C-diacylglycerol pathway share characteris
207 e show that manipulation of the non-specific phospholipase C1, NPC1, alters silicon content in nodes
208 cellular levels of phosphoinositide-specific phospholipase Cbeta (PLCbeta) and its activator, Galphaq
211 alcium signals generated through the Galphaq/phospholipase Cbeta signaling pathway and that subjectin
212 f Gq signaling and its downstream components phospholipase Cbeta, protein kinase Cepsilon, calcineuri
214 -mediated interference screen, we identified phospholipase Cepsilon 1 (PLCepsilon1) as a crucial regu
215 rate that recruitment and phosphorylation of Phospholipase Cgamma (PLCgamma), a prototypical SH2 cont
216 deficiency did not affect phosphorylation of phospholipase Cgamma or Ca(2+) influx, it was associated
217 rosine kinase, spleen tyrosine kinase [SYK], phospholipase Cgamma), but had low alpha-BCR-induced sig
218 o interacts with the p85 subunit of PI3K and phospholipase Cgamma, enzymes that deplete plasma membra
221 association between BD and the gene encoding phospholipase Cgamma1 (PLCG1), its etiological basis rem
226 F) could directly activate EGCs via the TrkB-phospholipase Cgamma1 pathway, thereby inducing a signif
228 e Hck, Wiskott-Aldrich-syndrome protein, and phospholipase Cgamma2 were also involved in this pathway
232 characterization of an F. nucleatum Type Vd phospholipase class A1 autotransporter (strain ATCC 2558
234 ncreased activity of the PA-producing enzyme phospholipase D (PLD) and increased localization of PLD1
236 ther genes annotated as a helicase domain, a phospholipase D (PLD) domain, a DUF1998 domain and a gen
238 gh its production of phosphatidic acid (PA), phospholipase D (PLD) is strongly involved in vesicular
241 feedback loop between the signaling protein phospholipase D (PLD), phosphatidic acid (PA), and a spe
242 DNase II exhibits a similar overall fold as phospholipase D (PLD), phosphatidylserine synthase (PSS)
247 rpretations concerning the possible roles of phospholipase D and its biologically active product phos
249 s in chlamydial cytotoxins, guaBA-add, and a phospholipase D homolog developed normally in cell cultu
251 evidence that the plasma membrane localized phospholipase D, involved in the biosynthesis of PA, is
252 nd LEP localization in cells lacking Sma1, a phospholipase D-associated protein dispensable for initi
255 ally, elevated membrane tension acts through phospholipase D2 (PLD2) and the mammalian target of rapa
256 tments that inactivate the signalling enzyme phospholipase D2 (PLD2) by sequestering the enzyme from
258 d that Ca(2+) generates arachidonic acid via phospholipase D2 and diacylglycerol kinase rather than p
259 eveal that a signaling molecule generated by phospholipase D2 drives deposition of MT1-MMP at the sit
260 stream of ARF6 small GTPase and its effector phospholipase D2, directly phosphorylating the conserved
263 GS1) protein and a lipid-hydrolyzing enzyme, phospholipase Dalpha1 (PLDalpha1), both act as GTPase-ac
266 membrane-embedded protein or as a truncated phospholipase domain that remains associated with the ou
268 e genetic polymorphism I148M of patatin-like phospholipase domain-containing 3 (PNPLA3) is robustly a
269 isk variants of genes including patatin-like phospholipase domain-containing 3 and transmembrane 6 su
270 irectly activates expression of patatin-like phospholipase domain-containing enzyme 8 (PNPLA8) gene,
271 A sequence variation (I148M) in patatin-like phospholipase domain-containing protein 3 (PNPLA3) is st
273 rized serine hydrolase (PNPLA4, patatin-like phospholipase domain-containing protein 4) involved in a
276 tyrosine 783 (Y783) leading to activation of phospholipase function and subsequent production of the
277 n Grb2, src-kinase Lyn and signal transducer phospholipase gamma2 (PLC-gamma2), and increased activat
279 trated with the results against autotaxin, a phospholipase implicated in cardiovascular disease.
282 researchers to dissect the complex roles of phospholipases in lipid metabolism, cellular signaling a
283 These results point to RcsPLA2alpha as a phospholipase involved in acyl editing, adapted to speci
284 ng activity of H2O2; and was able to inhibit phospholipase, lipoxygenase and cyclooxygenase, three pr
286 ivated by SEB with or without inhibitors for phospholipases (PL) (-C or -D), or cycloheximide, or bre
287 ory lipid metabolism, free arachidonic acid, phospholipases (PLA2G10), and prostaglandin synthesis-re
288 n and wound closure by activating a Wnt-like phospholipase (PLC)/ protein kinase C (PKC) signaling ca
289 al virulence genes (Listeriolysin O, and two phospholipases plcA and plcB) in a concentration-depende
290 factor receptor-bound protein (Grb2) and the phospholipase Plcgamma1 compete for the same binding sit
296 activates specific myocardial mitochondrial phospholipases that increase Ca(2+)-dependent production
297 acids (HETEs) and attenuate the activity of phospholipases that promote the synthesis of protective
299 xplanation for the targeting of patatin-like phospholipases to the plasma membrane and define the MLD
300 y pathogens contain a family of patatin-like phospholipases, which have been shown to have phospholip
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