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 the enzymatic action of dPLCXD, an atypical phospholipase C.

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

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

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

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

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

13 Phospholipase C, a key enzyme playing critical roles in

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

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

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

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

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

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

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

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

22 Vibration caused phospholipase C activation, transient increases in cytos

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

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

25 Phospholipase C activity is critically involved in media

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

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

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

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

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

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

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

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

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

35 pathway involving phosphoinositide-specific phospholipase C and diacylglycerol lipase alpha is known

36 A agonist A61603-stimulated phosphoinositide-phospholipase C and myocyte contraction.

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

38 naling pathways activated by CD44, including phospholipase C and phosphoinositide 3-kinase (PI3K), al

39 In contrast, inhibition of phospholipase C and phosphoinositide 3-kinase did not pr

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

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

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

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

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

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

46 ion of IP3 (inositol-1,4,5-trisphosphate) by phospholipase-C and accordingly were not stimulated by p

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

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

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

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

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

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

53 1 metabotropic glutamate receptors, Homer2, phospholipase C, and/or phosphotidylinositide-3 kinase f

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

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

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

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

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

59 ipase C gamma and G protein-coupled receptor/phospholipase C beta activities.

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

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

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

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

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

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

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

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

68 This function depends on an alternative phospholipase C-beta enzyme, encoded by PLC21C, presumab

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

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

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

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

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

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

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

76 /11 heterotrimeric G proteins, and in PLCB4 (phospholipase C beta4), the downstream effector of Galph

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

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

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

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

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

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

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

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

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

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

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

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

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

90 rt because of its potentiation downstream of phospholipase C-coupled receptors that regulate phosphoi

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

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

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

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

95 a somatic p.S745L (c.2234 G > A) mutation in phospholipase C delta 1 (PLCD1), a proposed tumor suppre

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

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

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

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

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

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

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

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

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

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

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

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

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

109 m channel currents (G(i)), and activation of phospholipase C (G(q)).

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

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

112 Phospholipase C Gamma 1 (PLCG1) is frequently mutated in

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

114 Phospholipase C gamma 1 (Plcgamma1) has been implicated

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

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

117 eam of the gene encoding the B cell-specific phospholipase C gamma 2 (PLCG2), a B cell-specific enzym

118 Inhibition of the phospholipase C gamma 2 (PLCG2)/inositol 1,4,5-trisphosp

119 mics depend on both receptor tyrosine kinase/phospholipase C gamma and G protein-coupled receptor/pho

120 GE(2) interfered with the phosphorylation of phospholipase C gamma-1 and extracellular signal-regulat

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

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

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

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

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

126 Direct activation of the human phospholipase C-gamma isozymes (PLC-gamma1, -gamma2) by

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

128 disclosed many mutations in PLCG2, encoding phospholipase C-gamma(2) (PLCgamma(2)).

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

130 at activation of tropomyosin kinase B (TrkB)-phospholipase-C-gamma-1 (PLCgamma1) signaling induced by

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

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

133 , leads to the recruitment and activation of phospholipase C-gamma1 (PLC-gamma1), an important effect

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

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

136 of linker of activation of T cells (LAT) and phospholipase C-gamma1 (PLCgamma1), signaling proteins t

137 osensor based on the tandem SH2 domains from phospholipase C-gamma1 (PLCgamma1), tSH2-WT, has been us

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

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

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

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

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

143 Phospholipase C gamma2 (PLCgamma2) is a critical regulat

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

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

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

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

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

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

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

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

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

153 Treatment with phospholipase C inhibitor U73122 significantly reversed

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

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

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

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

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

159 bnormalities in the PLC/IP3/PKC/ERK pathway (phospholipase C/inositol 1,4,5-triphosphate/protein kina

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

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

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

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

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

165 This novel phospholipase C-like reaction is widespread.

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

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

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

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

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

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

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

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

174 (1) receptors for ATP; and (4) inhibitors of phospholipase C or IP3 receptors.

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

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

177 Inhibition of G (betagamma,) phospholipase C, or protein kinase C mimicked agonist re

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

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

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

181 -protein-coupled receptors that activate the phospholipase C pathway, leading to the hydrolysis of ph

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

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

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

185 lation induced by vibration was dependent on phospholipase C pathways, including calcium, protein kin

186 product of the phosphatidylcholine-specific phospholipase C (PC-PLC) of L. monocytogenes, is a poten

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

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

193 in O (LLO) and phosphatidylinositol-specific phospholipase C (PI-PLC).

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

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

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

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

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

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

200 1,4,5 trisphosphate (IP3 ) accumulation and phospholipase C (PLC) activity were significantly potent

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

202 ototransduction in Drosophila is mediated by phospholipase C (PLC) and Ca(2+)-permeable TRP channels,

203 Stimulating the same receptors activated phospholipase C (PLC) and decreased plasma membrane PI(4

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

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

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

210 te coupling of the receptor to activation of phospholipase C (PLC) but not phospholipase D (PLD).

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

212 s been shown to activate a calcium-sensitive phospholipase C (PLC) enzyme and to lead to a robust dec

213 Phospholipase C (PLC) enzymes are key virulence factors

214 Phospholipase C (PLC) enzymes convert phosphatidylinosit

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

216 tein (GP) VI, or the GPVI signaling effector phospholipase C (PLC) gamma2.

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

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

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

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

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

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

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 Phospholipase C (PLC) isozymes are important signaling m

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

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

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

231 receptors, in which melatonin transactivates phospholipase C (PLC) through 5-HT(2C) .

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

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

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

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

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

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

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

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

240 For ED, phospholipase C (PLC), phospholipase A2 (PLA2) and a mix

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 istically, intra-sciatic MBP(84-104) induced phospholipase C (PLC)-driven (females) and phosphoinosit

246 elta) was phosphorylated at threonine 505 by phospholipase C (PLC)-mediated signaling at the early st

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

248 ily by virtue of its role as a substrate for phospholipase C (PLC).

249 riginate with IP(3) generated from PIP(2) by phospholipase C (PLC).

250 PI(4,5)P(2) hydrolysis is mediated by phospholipase C (PLC).

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

252 factor (PDGF) requires signaling through the phospholipase C (PLC)/protein kinase C (PKC) pathway.

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

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

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

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

257 Phospholipase C (PLC)s degrade phosphatidylinositol-4, 5

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

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

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

261 predicted virulence factors, the presence of phospholipase C (plcC), which is a major virulence facto

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

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

264 xperiments revealed that AGB1 interacts with phospholipase Cs (PLCs), and Ca(o) induced InsP3 product

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

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

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

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

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

270 etabotropic P2Y(1) receptors, recruitment of phospholipase C, release of Ca(2+) from the internal sto

271 2C heteromers amplified the 5-HT-mediated Gq/phospholipase C response and triggered melatonin-induced

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

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

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

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

276 adaptive immune response, integrin, PTEN and phospholipase C signaling, serotonin and tryptophan meta

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

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

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

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

281 Bacterial phosphatidylinositol-specific phospholipase C targets PI and glycosylphosphatidylinosi

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

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

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

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

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

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

288 ation of phosphatidylcholine biosynthesis by phospholipase C treatment induces the partial nuclear-to

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

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

291 abundant phosphatidylcholine head groups via phospholipase C treatment.

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

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

294 -2-decanoylamino-3-morpholino-1-propanol and phospholipase C), we demonstrated that PSV could recogni

295 ototransduction in Drosophila is mediated by phospholipase C, which activates TRP cation channels by

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

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

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