ライフサイエンスコーパス: phospholipase C

1 was readily reversible by pretreatment with phospholipase C.

2 eptor complexes to activate Galphaq and thus phospholipase C.

3 nositol 1,4,5-trisphosphate receptors and/or phospholipase C.

4 of G protein-coupled receptors that activate phospholipase C.

5 s treated with phosphatidylinositol-specific phospholipase C.

6 in turn generated by a G protein-stimulated phospholipase C.

7 mechanism that involves phosphatidylcholine-phospholipase C.

8 Such inhibition is predominantly mediated by phospholipase C.

9 obe specific to phosphatidylcholine-specific phospholipase C.

10 distinct G proteins to redundantly activate phospholipase C.

11 ctivation of G protein, protein kinase C and phospholipase C.

12 ons to cause uncoupling of H1 receptors from phospholipase C.

13 bition of Na(+)/H(+) exchange or blockade of phospholipase C.

14 Assessments of Erk, Akt, phospholipase C 1gamma, and FAK pathways reveal no appar

15 by treatment of the crude lipid extract with phospholipase C, (3) subsequent multiple thin-layer chro

16 treatment with phosphatidylinositol-specific phospholipase C, a phospholipase C specific for the clea

17 ed that this effect of CGRP was dependent on phospholipase C activation and was prevented by the inhi

18 cAMP production in adipocytes but inhibited phospholipase C activation by the alpha-adrenergic recep

19 karyotes, and their production downstream of phospholipase C activation is controlled through a netwo

20 tly enhanced bone formation, indicating that phospholipase C activation is not required for increased

21 Restoration of PI(4,5)P2 levels after phospholipase C activation is therefore essential for a

22 erstand dynamic effects of receptor-mediated phospholipase C activation on excitability and other PI(

23 al step in satiety, is prevented by blocking phospholipase C activation or Ca(2+) entry.

24 aining these mutations, weaker inhibition by phospholipase C activation, and reduced expression of ch

25 g of the I-II linker could be reversed after phospholipase C activation, causing polyphosphoinositide

26 g strong stimulation of receptors coupled to phospholipase C activation.

27 and sustained Ca(2+) signal, which requires phospholipase C activity and plasma membrane Ca(2+) entr

28 Phospholipase C activity is critically involved in media

29 suggest a model where NRT1.1/AtNPF6.3 and a phospholipase C activity mediate the increase of Ca(2+)

30 ssed ETA-WT signaling but failed to decrease phospholipase C activity mediated by the phosphorylation

31 The phospholipase C activity of mutant receptors in HEK-293

32 -O-Me-cAMP-AM, that gliclazide can stimulate phospholipase C activity via a partially pertussis toxin

33 evidence showing that active ARF6 increases phospholipase C activity, causing phosphatidylinositol 4

34 Both tolbutamide and gliclazide stimulated phospholipase C activity; however, only gliclazide did s

35 ated, resisted phosphatidylinositol-specific phospholipase C, aligned with raft markers, fluoresced w

36 of intracellular calcium, and inhibition of phospholipase C all result in suppression of chemokine-i

37 using phospholipase A1, phospholipase A2, or phospholipase C, allowing for a reliable determination o

38 ted pathogen in nature, produces a prototype phospholipase C, also called alpha-toxin, which plays a

39 ophagy and is sensitive to inhibitors of the phospholipase C and inositol 1,4,5-trisphosphate recepto

40 uch ROS generation was inhibited by blocking phospholipase C and inositol 1,4,5-trisphosphate-induced

41 from intracellular stores via activation of phospholipase C and opening of inositol trisphosphate (I

42 mation, has been attributed to hydrolysis by phospholipase C and phosphorylation by phosphatidylinosi

43 Phospholipase C and PI3 kinases 1 and 2, which are neces

44 se embryo at the 8-cell stage is directed by Phospholipase C and Protein kinase C and occurs in two p

45 the pharmacologic antagonists of Syk kinase, phospholipase C and protein kinase C, all downstream med

46 h P2Y(1) purinergic receptors, activation of phospholipase C and release of calcium from the intracel

47 to Galpha(q/11) leading to the activation of phospholipase C and the formation of diacylglycerol and

48 and activates the CamKKbeta-AMPK pathway via phospholipase C and the ryanodine receptor Ca(2+)-releas

49 ily to Galphaq, leading to the activation of phospholipase C and to the formation of diacylglycerol a

50 release that also depended on activation of phospholipase C and, for TLR 2/1, PI3-kinase.

51 egative of TRPC3 construct, or inhibition of phospholipase Cs and PKCs strongly inhibited the A(1)AR-

52 ssociated signaling pathway (G(q/11)-coupled phospholipase C) and the transactivated EGFR downstream

53 nd demonstrated that the export of protease, phospholipase C, and chitinase activities is T2SS depend

54 A2 (cPLA2), Src tyrosine kinases, p38 MAPK, phospholipase C, and intracellular calcium.

55 crease in glutamate release was dependent on phospholipase C, and it increased the hydrolysis of phos

56 Galphaq, on the other hand, signals through phospholipase C, and it remains unclear whether Galphaq-

57 ayers such as PAR1, Rho-associated kinase 2, phospholipase C, and proteins related to actin cytoskele

58 monary vasoconstriction that involved TRPC6, phospholipase C, and rho kinase.

59 identify toxins (ETX, Clostridium perfringes phospholipase C, and SEB) from blind spiked samples.

60 1 metabotropic glutamate receptors, Homer2, phospholipase C, and/or phosphotidylinositide-3 kinase f

61 epeated addition of agonist and blocked by a phospholipase C antagonist.

62 o express melanopsin and transduce light via phospholipase-C, apparently not acting through diacylgly

63 dated the prediction of the gamma isoform of phospholipase C as a component in the Galphaq pathway.

64 y due to the hydrolytic activity of Sac2 and phospholipase C, becoming undetectable for approximately

65 ported the coupling of dopamine signaling to phospholipase C beta (PLCbeta) both in vitro and in vivo

66 eved either by agonist-induced activation of phospholipase C beta or with a rapamycin-inducible syste

67 lated HUVEC migration and proliferation in a phospholipase C beta-dependent fashion and decreased Gal

68 effect of NAC on Galphaq palmitoylation and phospholipase C beta-mediated signaling in endothelial c

69 Phospholipase C-beta (PLC-beta) has been implicated to c

70 Mammalian phospholipase C-beta (PLC-beta) isoforms are stimulated

71 gamma subunits, and some Rho family GTPases, phospholipase C-beta (PLC-beta) isoforms hydrolyze phosp

72 Phospholipase C-beta (PLC-beta) isozymes hydrolyze the m

73 with the specific inhibitors of Gbetagamma, phospholipase C-beta (PLCbeta), or PKC, but not of prote

74 hototransduction pathway, which requires the phospholipase C-beta encoded by norpA (no receptor poten

75 MCMV is an activator of CREB, NF-kappaB, and phospholipase C-beta signaling pathways and has been imp

76 om Galpha(q) to the nucleus independently of phospholipase C-beta.

77 by which WDR26 enhances Gbetagamma-mediated phospholipase C beta2 (PLCbeta2) activation in leukocyte

78 strate 1 (Rac1)-dependent activation of both phospholipase C beta2 (Plcbeta2) and Plcbeta3.

79 ronchial aSMCs, through its association with phospholipase C beta2 and the stimulation of inositol 1,

80 ng components (i.e., G-protein gustducin and phospholipase C beta2).

81 correlated with an association of PP1c with phospholipase C beta3 (PLCbeta3), along with a concomita

82 /11 heterotrimeric G proteins, and in PLCB4 (phospholipase C beta4), the downstream effector of Galph

83 SHP-2 was identified to act upstream of phospholipase C beta4, linking it to the generation of n

84 Inhibitors of protein kinase C or phospholipase C blocked the development of DIR.

85 thuringiensis phosphatidylinositol-specific phospholipase C (BtPI-PLC) is a secreted virulence facto

86 rulence factor phosphatidylinositol-specific phospholipase C (BtPI-PLC), which specifically binds to

87 his signaling cascade requires activation of phospholipase C but is largely uncoupled from the inosit

88 Essentially only diacylglycerol released by phospholipase C but not by phospholipase D was implicate

89 ed by U73122, a pharmacological inhibitor of phospholipase C, but not by the nonfunctional phospholip

90 of the nerves requires the beta3 isoform of phospholipase C, but TRPA1 or other TRP channel are not

91 sphate counteracted the direct activation of phospholipase C by 2,4,6-trimethyl-N-[3-(trifluoromethyl

92 ed by cAMP (Epac) provokes inhibition of the phospholipase C by an as yet unknown mechanism.

93 ents of the platelet signaling cascades (ie, phospholipase C, [Ca(2+)]i, protein kinase C) and requir

94 lecular mechanism underlying this process: a phospholipase C/Ca(2+)/proline-rich tyrosine kinase 2/cJ

95 s involving a G-protein q, the activation of phospholipase C, calcium mobilization, and the release o

96 memory; conversely, a general and a specific phospholipase C-coupled D1R agonist (but not a D2R or ad

97 iquitous activation of Ca(2+) signaling upon phospholipase C-coupled receptor ligation leads quite na

98 ,5-trisphosphate (IP(3)) upon stimulation of phospholipase C-coupled receptors and the subsequent emp

99 In many cells, the activation of phospholipase C-coupled receptors hydrolyzes membrane ph

100 sis and ultimately to loss of signaling from phospholipase C-coupled receptors.

101 muscarinic receptor activation stimulates a phospholipase C-coupled signalling cascade involving the

102 2X1 receptors activated by ATP release via a phospholipase-C-coupled secretory pathway requiring both

103 rexpression of caveolin-1 increased receptor-phospholipase C coupling, resulting in initially larger

104 through TRPC3-encoded ROC by stimulating the phospholipase C/DAG/PKC cascade provide evidence for a n

105 urons and generate 2-AG through a Gq-protein-phospholipase C-DAGL cascade.

106 ition by the default PI(4,5)P2 lipid sensor, phospholipase C delta 1 pleckstrin homology domain (PLC

107 rance of the PI(4,5)P2-specific PH domain PH-phospholipase C delta-EGFP at the PM after Ca(2+) ionoph

108 Recombinant EF-hand domain of phospholipase C delta1 has a moderate affinity for anion

109 embrane binding domains from lactadherin and phospholipase C-delta1 to evaluate the feasibility of us

110 CD40 ligation in Muller cells triggered phospholipase C-dependent ATP release that caused P2X7-d

111 insulin secretion in a GPR43-, Galphaq-, and phospholipase C-dependent manner.

112 lipoproteins and subsequent signaling via a Phospholipase C-dependent mechanism to increase CD11c ex

113 roduced through the sequential activities of phospholipase C, diacylglycerol lipase, 5-lipo-oxygeneas

114 ein-coupled receptors (GPCRs), activated via phospholipase C-diacylglycerol signaling.

115 entiation (PTP) or through activation of the phospholipase-C-diacylglycerol pathway share characteris

116 -forming toxin listeriolysin O (LLO) and two phospholipase C enzymes.

117 Phospholipase C-epsilon (PLC) plays a critical role in G

118 te and diacylglycerol, PLC, unlike the other phospholipase C family members, is activated in a sustai

119 into secreted phosphatidylinositol-specific phospholipase C from Staphylococcus aureus, which lacks

120 Moreover, Tregs with defective phospholipase C gamma (PLCgamma) activation due to a Y14

121 a-estradiol (E2) activates the UPR through a phospholipase C gamma (PLCgamma)-mediated opening of EnR

122 s and lacks the final exon that includes the phospholipase C gamma 1 (PLCgamma1) binding site.

123 (MAPK), phosphoinositol-3 kinase (PI3K) and phospholipase C gamma 1 (PLCgamma1) pathways.

124 r activation of T cells (LAT), and activated phospholipase C gamma 1 (PLCgamma1), which all localize

125 f Syk, linker for activation of T cells, and phospholipase C gamma(1), critical signals for calcium r

126 Phospholipase C gamma-2 (PLCgamma2)-dependent calcium (C

127 docking site of the Gab adaptor proteins and phospholipase C gamma.

128 MC signaling mediators such as Lyn, Syk, and phospholipase C gamma; thus, a role for this adaptor in

129 gers different signaling pathways, including phospholipase C-gamma (PLC-gamma) and Akt cascades, cruc

130 tivation of Src tyrosine kinase to stimulate phospholipase C-gamma (PLC-gamma) which increases inosit

131 to the membrane by diacylglycerol (DAG) in a phospholipase C-gamma (PLCgamma)-dependent manner.

132 c-FOS, and the phosphorylation of ZAP70 and phospholipase C-gamma 1.

133 dendritic growth, whereas the activation of phospholipase C-gamma was found to be responsible for sp

134 naling pathways, including the activation of phospholipase C-gamma, which promotes the release of dia

135 Among the small Golgi hits, we focused on phospholipase C gamma1 (PLCgamma1).

136 In turn, H2O2 activates a Src kinase/phospholipase C-gamma1 (PLC-gamma1) signaling pathway an

137 ion of SFKs and proximal TCR signaling up to phospholipase C-gamma1 (PLC-gamma1).

138 c, phosphatidylinositol 3-kinase (PI3K), and phospholipase C-gamma1 (PLCgamma1) have all been implica

139 Despite the loss of LAT-dependent phospholipase C-gamma1 binding and activation, genetic a

140 ain-associated protein kinase 70 (ZAP70) and phospholipase C-gamma1 phosphorylation, were not impaire

141 f protein tyrosine phosphorylation of ZAP70, phospholipase C-gamma1, and protein kinase C-theta, and

142 ne 136 on LAT abrogates its interaction with phospholipase C-gamma1, causing severe ramifications on

143 Mice expressing a germline mutation in the phospholipase C-gamma1-binding site of linker for activa

144 s Vav-1, phosphatidylinositol 3' kinase, and phospholipase C-gamma1.

145 We find that phospholipase C gamma2 (PLCgamma2) accounts for LPS-indu

146 Phospholipase C gamma2 (PLCgamma2) is a critical regulat

147 on of a number of proteins including Syk and phospholipase C gamma2.

148 as well as the immediate downstream effector phospholipase C, gamma2 (PLCG2).

149 Mutations in the gene encoding phospholipase C-gamma2 (PLCgamma2) have been shown to be

150 PP2 abolished phosphorylations of Syk and Phospholipase C-gamma2.

151 tyrosines of Syk and the phosphorylation of phospholipase C-gamma2.

152 ase and indirectly its downstream substrate, phospholipase-C-gamma2, both important in B-cell signali

153 ogous expression systems or by activation of phospholipase C in native ciliated epithelial cells.

154 ngin D or 2-aminoethoxydiphenyl borate) or a phospholipase C inhibitor (U73122) attenuated Ca(2+) wav

155 hospholipase C, but not by the nonfunctional phospholipase C inhibitor analog U73343.

156 og GDP-beta-S (applied intracellularly), the phospholipase C inhibitor U-73122, and the diacylglycero

157 X) inhibitors, TRPC channel blockers and the phospholipase C inhibitor U-73122.

158 Treatment with phospholipase C inhibitor U73122 significantly reversed

159 B), or during block of IP3 production by the phospholipase C inhibitor U73122.

160 The selective M1 and M3 antagonists and the phospholipase C inhibitor, were able to prevent AEME-ind

161 s includes the calmodulin inhibitor W-7, the phospholipase-C inhibitor U73122, and anti-psychotic phe

162 retreatments with Ca(2+) channel blockers or phospholipase C inhibitors.

163 ucose, the alpha1-AR produced superoxide via phospholipase C, inositol triphosphate-induced Ca(2+) re

164 paired mitochondrial function and to involve phospholipase C/inositol 1,4,5-trisphosphate-mediated Ca

165 ion of B2 receptors, G protein activation of phospholipase C, InsP3 synthesis, and calmodulin activat

166 radicals, lipid peroxidation, activation of phospholipase C, IP3 receptors, and release of Ca(2+) fr

167 activity of the inositol phosphosphingolipid phospholipase C, Isc1, which is required for ceramide pr

168 ion in females through mGluR1 stimulation of phospholipase C, leading to inositol triphosphate (IP3)

169 This novel phospholipase C-like reaction is widespread.

170 Depletion of PI(4,5)P2 via phospholipase C-mediated hydrolysis leads to a decrease

171 in turn results in a complex that couples to phospholipase C-mediated intracellular calcium release.

172 ity to overcome M channel inhibition via two phospholipase C-mediated mechanisms, namely depletion of

173 g a variety of approaches, we also show that phospholipase C-mediated PIP2 hydrolysis is necessary an

174 ell death/senescence through repression of a phospholipase C-mediated signaling pathway, and arrest o

175 on of S1P and activation of S1P2/4 result in phospholipase C-mediated TRPC6 and rho kinase activation

176 Phospholipase C mediates TRP/TRPL opening, but the gatin

177 ernal GDP-beta-S or inhibiting OX1Rs, CB1Rs, phospholipase C or DAGL, and potentiated by inhibiting 2

178 Gallein had no effect on Gbetagamma-mediated phospholipase C or phosphoinositide 3-kinase (PI3K) gamm

179 ated by GDPbetaS, blocked by an inhibitor of phospholipase C or the calcium chelator 1,2-bis(o-aminop

180 ns by inhibiting PKC, its upstream activator phospholipase C, or the gamma-Pcdh binding partner focal

181 d by the miRNAs identified regulation of the phospholipase C pathway (miR200c, miR20b, and miR31throu

182 calcium permeable and activated through the phospholipase C pathway and by diacylglycerol.

183 Endothelin-1 activates the phospholipase C pathway, leading to activation of protei

184 tion of activated Galphaq independent of the phospholipase C pathway.

185 protein expression of MMPs and RANKL via the phospholipase C pathway.

186 of stimulation with agonists that engage the phospholipase C pathway.

187 homology to the phosphatidylcholine-specific phospholipase C (PC-PLC) of Pseudomonas fluorescens.

188 encodes a phosphatidylinositol (PI)-specific phospholipase C (PI-PLC) capable of hydrolyzing PI and c

189 ty of secreted phosphatidylinositol-specific phospholipase C (PI-PLC) enzymes is associated with bact

190 rulence factor phosphatidylinositol-specific phospholipase C (PI-PLC) from Bacillus thuringiensis , o

191 ococcus aureus phosphatidylinositol-specific phospholipase C (PI-PLC) is a secreted virulence factor

192 The activation of phosphoinositide-specific phospholipase C (PI-PLC) is one of the earliest response

193 )-induced activation of phosphatidylinositol-phospholipase C (PI-PLC) was studied with vesicles conta

194 are incubated with phosphoinositide-specific phospholipase C (PI-PLC).

195 from cells by phosphatidylinositol-specific phospholipase C (PIPLC) treatment is TFPIalpha, implying

196 TRPV1 is caused mainly by activation of the phospholipase C-PKC pathway following activation of the

197 framework for a mechanistic understanding of phospholipase C/PKC signaling in chemotactic gradient se

198 Outgrowth depends on phospholipase C (PLC) --> inositol trisphosphate --> Ca(

199 endogenous PIP2 either by serotonin-induced phospholipase C (PLC) activation or by a rapamycin-induc

200 ling cascade culminating in phosphoinositide-phospholipase C (PLC) activation, which generates the se

201 el inhibition by depletion of PI(4,5)P2 upon phospholipase C (PLC) activation.

202 1,4,5 trisphosphate (IP3 ) accumulation and phospholipase C (PLC) activity were significantly potent

203 icient CTLs due to residual calcium flux and phospholipase C (PLC) activity.

204 P2Y6-activated responses were abolished by phospholipase C (PLC) and inositol trisphosphate (IP3) r

205 eptors, and modulates Duox1 activity through phospholipase C (PLC) and intracellular calcium signalin

206 of key phototransduction proteins including phospholipase C (PLC) and the Ca(2+)-permeable transient

207 through a pathway that couples rhodopsin to phospholipase C (PLC) and the opening of transient recep

208 cium that are dependent on the activation of phospholipase C (PLC) and transient receptor potential c

209 signaling pathway mediated by G proteins and phospholipase C (PLC) beta1.

210 We observed a strong down-regulation of phospholipase C (PLC) beta3 in the DRGs of diabetic mice

211 CeA levels of mGluR1, GluN2B, Homer2a/b and phospholipase C (PLC) beta3, without significantly alter

212 Phospholipase C (PLC) converts phosphatidylinositol 4,5-

213 Phospholipase C (PLC) enzymes convert phosphatidylinosit

214 ically, both conditions entail activation of phospholipase C (PLC) enzymes, which hydrolyze phosphoin

215 Ca(2+) -induced activation of phospholipase C (PLC) has been implied in the regulation

216 the activation of phosphoinositide-specific phospholipase C (Plc) in nuclei of mammalian cells durin

217 f cued fear memory by redundantly activating phospholipase C (PLC) in the basolateral amygdala (BLA).

218 ) depletion and P2 purinergic receptor (P2R)/phospholipase C (PLC) inhibition.

219 dependent on [IP3] and were not perturbed by phospholipase C (PLC) inhibition.

220 Intra-shell administration of a phospholipase C (PLC) inhibitor (40.0 mum U73122) or a p

221 he tyrosine kinase Syk inhibitor OXSI-2, the phospholipase C (PLC) inhibitor neomycin, and either the

222 IP(3), but inhibited by either applying the phospholipase C (PLC) inhibitor U73112 or depleting ER C

223 by astrocytes is prevented by BAPTA-AM or a phospholipase C (PLC) inhibitor.

224 l inflammation was also inhibited by using a phospholipase C (PLC) inhibitor.

225 [a nonselective COX inhibitor], neomycine [a phospholipase C (PLC) inhibitor] or furegrelate [a throm

226 Phosphoinositide-specific phospholipase C (PLC) is an important family of enzymes

227 Phosphoinositide-specific phospholipase C (PLC) is involved in Ca(2)(+) mediated s

228 Phospholipase C (PLC) isozymes are important signaling m

229 tors and receptor tyrosine kinases, activate phospholipase C (PLC) isozymes to hydrolyze phosphatidyl

230 pacity to monitor spatiotemporal activity of phospholipase C (PLC) isozymes with a PLC-selective sens

231 the G-protein-coupled receptor (GPCR)-Gq/11-phospholipase C (PLC) pathway.

232 channels TRPC4 and -5 via the Gq/11 protein-phospholipase C (PLC) signaling pathway has remained elu

233 we used on-tissue treatment with buffer-free phospholipase C (PLC) to near-quantitatively degrade PCs

234 imple and homogeneous fluorescence assay for phospholipase C (PLC) was developed on the basis of the

235 Inhibition of phospholipase C (PLC) with U73122 did not inhibit either

236 boundary as merely a substrate for PI3K and phospholipase C (PLC), and is now an established lipid m

237 (NAPE-PLD), diacylglycerol lipase (DAGL), or phospholipase C (PLC), and their metabolism is mediated

238 PM8) channels are thought to be regulated by phospholipase C (PLC), but neither the specific PLC isof

239 f cation channels regulated by activation of phospholipase C (PLC), has been implicated in this respo

240 catalyze activation of G proteins coupled to phospholipase C (PLC), or activation of G(i/o) proteins

241 nd is not blunted by inhibitors of Src, PKC, phospholipase C (PLC), PI3K, or soluble MMPs.

242 e (PI4P) hydrolysis by a specific isoform of phospholipase C (PLC), PLCepsilon, at the nuclear envelo

243 the fibroblast growth factor (FGF) receptor, phospholipase C (PLC), protein kinase C (PKC) and phosph

244 inds its two major classes of effectors, the phospholipase C (PLC)-beta isozymes and Rho guanine nucl

245 RF1 couples CXCR2 to its downstream effector phospholipase C (PLC)-beta2, forming a macromolecular co

246 inositol-1,4,5-trisphosphate generation from phospholipase C (PLC)-dependent hydrolysis of PI(4,5)P(2

247 In Drosophila, a phospholipase C (PLC)-mediated signaling cascade, couple

248 r cells is mediated by a G protein-activated phospholipase C (PLC).

249 ownstream from receptors that signal through phospholipase C (PLC).

250 th-blocking peptides (GBP), acts through the phospholipase C (PLC)/Ca(2+) signalling cascade to media

251 requires G protein alpha q subunit (Galphaq)/phospholipase C (PLC)beta1 activities and protein kinase

252 requires G protein alpha q subunit (Galphaq)/phospholipase C (PLC)beta1/protein kinase C (PKC) activi

253 resulting in the inhibition of canonical Lck-phospholipase C (PLC)gamma-dependent TCR signaling.

254 ET-1 also stimulated p-phospholipase C (PLC)gamma1 levels.

255 Phosphorylated LAT binds Grb2, Gads, and phospholipase C (PLC)gamma1 to mediate T cell activation

256 d adhesion induced the activation of Src and phospholipase C (PLC)gamma2, which mediated Ca(2+) relea

257 altered the abundance of PIP2 by activating phospholipase-C (PLC), using a scavenging peptide, and i

258 Phospholipase C (Plc1p) is required for the initial step

259 forming cytolysin listeriolysin O (LLO), two phospholipases C (PlcA and PlcB), and ActA.

260 itment of TRPC3 or phosphoinositide-specific phospholipase C (PLCgamma) to the AT1R-beta-arrestin-1 s

261 Pseudomonas aeruginosa hemolytic phospholipase C (PlcH) degrades phosphatidylcholine (PC)

262 rient source and an inducer of the hemolytic phospholipase C, PlcH.

263 e determinants of pathogenesis: two secreted phospholipases C (PLCs; PlcA and PlcB) and a surface pro

264 A sperm-specific phospholipase C (PLCZ1) has emerged as the likely candid

265 ceptor subunits, spleen tyrosine kinase, and phospholipase C), production of several cytokines and ch

266 e receptors (A1ARs) triggers a Gi-Gbetagamma-phospholipase C-protein kinase C (PKC) cascade that prom

267 op and analyze a reaction-diffusion model of phospholipase C/protein kinase C (PKC) signaling, which

268 2C heteromers amplified the 5-HT-mediated Gq/phospholipase C response and triggered melatonin-induced

269 ated crude lipid extracts, pretreatment with phospholipase C resulted in clear-cut mass spectra.

270 ere could be used to annotate plant-specific phospholipase C sequences.

271 d define a negative feedback mechanism in Gq/Phospholipase C signaling through RGS2 protein upregulat

272 ignaling, cardiac beta-adrenergic signaling, phospholipase C signaling, glutamate receptor signaling,

273 t is UVA-specific and requires G protein and phospholipase C signaling, thus contributing to UVA-indu

274 n channels that are activated in response to phospholipase C signaling.

275 phatidylinositol-specific phospholipase C, a phospholipase C specific for the cleavage of glycosylpho

276 in Na/K-ATPase signaling, such as caveolin, phospholipase C, Src, and the IP3 receptor.

277 ate were synthesized and potently stimulated phospholipase C stimulation in astrocytoma cells express

278 Bacterial phosphatidylinositol-specific phospholipase C targets PI and glycosylphosphatidylinosi

279 hosphatase (TbPIP5Pase) or overexpression of phospholipase C (TbPLC) derepresses numerous silent ESs

280 cerophosphodiesterase GDE3 as a GPI-specific phospholipase C that cleaves and releases uPAR with cons

281 In particular, Ca(2+)-dependent phospholipase C, the intercellular diffusion of inositol

282 ion of cell-surface receptors that couple to phospholipase C to generate the second messenger inosito

283 We conclude that histamine activates phospholipase C to release intracellular Ca(2+) that ind

284 itol (PI) by targeting bacterial PI-specific phospholipase C to the PIS domain impairs recruitment of

285 monstrate that phosphatidylinositol-specific phospholipase C-treated EA.hy926 cells and PIGA-mutant T

286 aracterization in crude lipid extracts after phospholipase C treatment, thereby avoiding laborious an

287 is sensitive to deglycosidases, trypsin, and phospholipase C treatment.

288 abundant phosphatidylcholine head groups via phospholipase C treatment.

289 More detailed studies revealed phospholipase C-triggered release of AtTLP3 from the PM,

290 Inhibitors of phospholipase C (U-73122), IP3 (2-APB), ryanodine recept

291 d protein kinase A (PKA) via Gsalpha but not phospholipase C via Gq/11 (D/D mice), PTH significantly

292 -2-decanoylamino-3-morpholino-1-propanol and phospholipase C), we demonstrated that PSV could recogni

293 eam G protein-coupled receptors can activate phospholipase C, we then tested the effects of antagonis

294 ASR activates the NLRP3 inflammasome through phospholipase C, which catalyses inositol-1,4,5-trisphos

295 resistant to pretreatment with extracellular phospholipase C, which cleaves lipid moieties like those

296 nistic studies indicate that EDNRA activates phospholipase C, which then 1) increases the MMP1 protei

297 Sperm-specific phospholipase C zeta (PLCzeta) activates embryo developm

298 yte at fertilisation, a process initiated by phospholipase C zeta (PLCzeta), a sperm-specific protein

299 cytoplasmic sperm injection or expression of phospholipase C zeta.

300 Sperm-specific phospholipase C-zeta (PLCzeta) is widely considered to b