ライフサイエンスコーパス: PLC

1 PLC activity was found to depend upon the electrostatic

2 PLC catalyzes the hydrolysis of phosphatidylcholine unit

3 PLC localization is largely intracellular and its compar

4 PLC-beta isoforms also function as GTPase-activating pro

5 PLC-beta isozymes are autoinhibited, and several protein

6 PLC-derived organoid cultures preserve the histological

7 PLC-derived organoids are amenable for biomarker identif

8 sms regulating the sensitivity to GPCR-Gq/11-PLC-dependent gating of a receptor-operated channel.

9 for conferring the sensitivity to GPCR-Gq/11-PLC-dependent gating on TRPC5.

10 scues the mutant's sensitivity to GPCR-Gq/11-PLC-dependent gating.

11 This inhibition is blocked by a PLC inhibitor (U73122, 1-(6-{[(17beta)-3-Methoxyestra-1,

12 ns despite their robust capacity to activate PLC-beta3 at membranes.

13 Moreover, we determined that GLP-1 activates PLC, which increases submembrane diacylglycerol and ther

14 A retrospective medical chart review of all PLC visits at an academic dermatology center from Octobe

15 to identify both orthosteric and allosteric PLC inhibitors.

16 on detection of coincident Gi/o, Ca(2+), and PLC signaling, which is further modulated by the small G

17 sphatidic acid (LPA) regulates PLC-beta1 and PLC-beta2 via two distinct pathways to enhance intestina

18 cate that the mechanism by which Galphaq and PLC-beta3 mutually regulate each other is far more compl

19 ular carcinoma-derived cell lines, Hep3B and PLC/PRF/5, that contain HBV integrants but do not produc

20 aused by manipulating beta2AR, D5R, M1R, and PLC.

21 The effects of co-infusing mGluR1 and PLC inhibitors were additive, whereas those of coinhibit

22 An intra-CeA infusion of mGluR1, mGluR5 and PLC inhibitors all dose-dependently reduced binge intake

23 The efficacy of mGluR1, mGluR5 and PLC inhibitors to reduce binge intake depended upon inta

24 ve, whereas those of coinhibiting mGluR5 and PLC were not, indicating that the efficacy of mGluR1 blo

25 ion is upstream of these neuromodulators and PLC, suggesting an important presynaptic role for cAMP/P

26 Rac1 and PLC are required for nutritional use of extracellular pr

27 stream signaling proteins, such as Zap70 and PLC-gamma1.

28 Phospholipase C-beta (PLC-beta) has been implicated to control myriad signalin

29 Mammalian phospholipase C-beta (PLC-beta) isoforms are stimulated by heterotrimeric G pr

30 me Rho family GTPases, phospholipase C-beta (PLC-beta) isoforms hydrolyze phosphatidylinositol 4,5-bi

31 Phospholipase C-beta (PLC-beta) isozymes hydrolyze the membrane lipid phosphat

32 e was found for a direct interaction between PLC and the GTPases that mediate phospholipase activatio

33 block a highly specific interaction between PLC delta1-PH and PI(4,5)P2, encoded within the conforma

34 or the first time, the relationships between PLC activity and substrate presentation in lipid vesicle

35 ral studies showed how Galphaq and Rac1 bind PLC-beta, there is a lack of consensus regarding the Gbe

36 Both PLC-gamma1-specific inhibitor and short hairpin RNA (shR

37 BtPI-PLC carries a negative net charge and its interfacial bi

38 BtPI-PLC interactions with the SUV surface are transient with

39 ific electrostatic interactions between BtPI-PLC and membranes vary as a function of the fraction of

40 tidylinositol-specific phospholipase C (BtPI-PLC) is a secreted virulence factor that binds specifica

41 tidylinositol-specific phospholipase C (BtPI-PLC), which specifically binds to phosphatidylcholine (P

42 esults lead to a quantitative model for BtPI-PLC interactions with cell membranes where protein bindi

43 at weak electrostatics, as observed for BtPI-PLC, might be a less unusual mechanism for peripheral me

44 To elucidate how BtPI-PLC searches for GPI-anchored proteins on the membrane s

45 -atom molecular dynamics simulations of BtPI-PLC interacting with PC-rich bilayers show that the prot

46 These data also suggest that BtPI-PLC does not directly sense curvature, but rather prefer

47 tly activated by diacylglycerols produced by PLC breakdown of phosphatidylinositol 4,5-bisphosphate (

48 either by serotonin-induced phospholipase C (PLC) activation or by a rapamycin-induced translocation

49 inating in phosphoinositide-phospholipase C (PLC) activation, which generates the second messengers d

50 depletion of PI(4,5)P2 upon phospholipase C (PLC) activation.

51 ate (IP3 ) accumulation and phospholipase C (PLC) activity were significantly potentiated in hepatocy

52 ates Duox1 activity through phospholipase C (PLC) and intracellular calcium signaling in vivo.

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

54 luR1, GluN2B, Homer2a/b and phospholipase C (PLC) beta3, without significantly altering protein expre

55 itions entail activation of phospholipase C (PLC) enzymes, which hydrolyze phosphoinositides.

56 (2+) -induced activation of phospholipase C (PLC) has been implied in the regulation of TRPM8 channel

57 y by redundantly activating phospholipase C (PLC) in the basolateral amygdala (BLA).

58 ] and were not perturbed by phospholipase C (PLC) inhibition.

59 2 purinergic receptor (P2R)/phospholipase C (PLC) inhibition.

60 a-shell administration of a phospholipase C (PLC) inhibitor (40.0 mum U73122) or a protein kinase C (

61 prevented by BAPTA-AM or a phospholipase C (PLC) inhibitor.

62 s also inhibited by using a phospholipase C (PLC) inhibitor.

63 OX inhibitor], neomycine [a phospholipase C (PLC) inhibitor] or furegrelate [a thromboxane A2 (TXA2)

64 Phosphoinositide-specific phospholipase C (PLC) is an important family of enzymes constituting a ju

65 Phospholipase C (PLC) isozymes are important signaling molecules, but few

66 tyrosine kinases, activate phospholipase C (PLC) isozymes to hydrolyze phosphatidylinositol 4,5-bisp

67 upled receptor (GPCR)-Gq/11-phospholipase C (PLC) pathway.

68 nd -5 via the Gq/11 protein-phospholipase C (PLC) signaling pathway has remained elusive so far.

69 treatment with buffer-free phospholipase C (PLC) to near-quantitatively degrade PCs in fresh-frozen

70 eous fluorescence assay for phospholipase C (PLC) was developed on the basis of the fluorescence quen

71 Inhibition of phospholipase C (PLC) with U73122 did not inhibit either ImAHP or IsAHP i

72 ly a substrate for PI3K and phospholipase C (PLC), and is now an established lipid messenger pivotal

73 lglycerol lipase (DAGL), or phospholipase C (PLC), and their metabolism is mediated by several metabo

74 thought to be regulated by phospholipase C (PLC), but neither the specific PLC isoform nor the in vi

75 regulated by activation of phospholipase C (PLC), has been implicated in this response.

76 on of G proteins coupled to phospholipase C (PLC), or activation of G(i/o) proteins coupled to the io

77 by inhibitors of Src, PKC, phospholipase C (PLC), PI3K, or soluble MMPs.

78 is by a specific isoform of phospholipase C (PLC), PLCepsilon, at the nuclear envelope.

79 owth factor (FGF) receptor, phospholipase C (PLC), protein kinase C (PKC) and phosphoinositide-3-kina

80 r classes of effectors, the phospholipase C (PLC)-beta isozymes and Rho guanine nucleotide exchange f

81 ceptors that signal through phospholipase C (PLC).

82 des (GBP), acts through the phospholipase C (PLC)/Ca(2+) signalling cascade to mediate the secretion

83 n alpha q subunit (Galphaq)/phospholipase C (PLC)beta1 activities and protein kinase C (PKC) phosphor

84 n alpha q subunit (Galphaq)/phospholipase C (PLC)beta1/protein kinase C (PKC) activity.

85 d LAT binds Grb2, Gads, and phospholipase C (PLC)gamma1 to mediate T cell activation, proliferation,

86 pathogenesis: two secreted phospholipases C (PLCs; PlcA and PlcB) and a surface protein (ActA).

87 everal signaling pathways, including calcium-PLC-PKC-PKD1 pathway, NF-kappaB pathway, and MAP kinase

88 protective efficacy on primary liver cancer (PLC) and other liver diseases has not been fully examine

89 that the incidence of primary liver cancer (PLC) has slowly declined over the last decades.

90 Primary liver cancer (PLC) is the sixth most common cancer worldwide and the s

91 to the propagation of primary liver cancer (PLC) organoids from three of the most common PLC subtype

92 After activation of phospholipase Cgamma (PLC-gamma), TRPC1 mediated Ca(2+) entry and triggered pr

93 a limited number of pigmented lesion clinic (PLC) visits at dermatology centers.

94 PLC) organoids from three of the most common PLC subtypes: hepatocellular carcinoma (HCC), cholangioc

95 ervical spine posterior ligamentous complex (PLC).

96 es a macromolecular peptide-loading complex (PLC) by recruiting tapasin.

97 The MHC class I peptide loading complex (PLC) facilitates the assembly of MHC class I molecules w

98 al component of the peptide-loading complex (PLC) important for efficient peptide loading onto MHC cl

99 al component of the peptide-loading complex (PLC), to which tapasin (TPN) recruits MHC class I (MHC I

100 ractions within the peptide-loading complex (PLC).

101 the classical MHC-I peptide-loading complex (PLC).

102 % percentage loss of hydraulic conductivity (PLC) and exposed to freeze-thaw cycles.

103 the percent loss of hydraulic conductivity (PLC) and the content of nonstructural carbohydrates (NSC

104 Consequently, PLCs control various cellular processes, and their aberr

105 ositol 4,5-bisphosphate used in conventional PLC assays and will enable high-throughput screens to id

106 of the parental tumors and the corresponding PLC-PDXs show high conservation of the molecular feature

107 Although the stroke perilesional cortex (PLC) has been hypothesized as a potential site for a BMI

108 neuronal ensembles in rat prelimbic cortex (PLC) and assess altered intrinsic excitability after 10

109 yer V pyramidal neurons in prelimbic cortex (PLC) of FosGFP-transgenic rats, we found that operant fo

110 y, we describe here a novel Zn(2+)-dependent PLC family present in Legionella, Pseudomonas, and fungi

111 d PLC activity, indicating calcium-dependent PLCs are not upregulated by alcohol.

112 ivated, whereas EDTA inhibited, PlcC-derived PLC activity.

113 itol 1,4,5-trisphosphate and diacylglycerol, PLC, unlike the other phospholipase C family members, is

114 und repair via spatial targeting of distinct PLC-betas within the cell.

115 activation of common (AC/PKA) and distinct (PLC/PKC, intra-/extra-cellular calcium, PI3K/MAPK/mTOR)

116 lipase C delta 1 pleckstrin homology domain (PLC delta1-PH), is completely inhibited in the presence

117 Starch was converted to soluble sugar during PLC progression under drought, and the hydraulic conduct

118 conclude that betaARs couple to a cAMP/Epac/PLC/Munc13/Rab3/RIM-dependent pathway to enhance glutama

119 Phospholipase C-epsilon (PLC) plays a critical role in G-protein-coupled receptor

120 ent needs while creating resources to expand PLC visits.

121 ic rats to ablate selectively Fos-expressing PLC neurons that were active during operant food self-ad

122 a signal-to-noise ratio of 3) of 0.21 nM for PLC, with high selectivity over other proteins, enzymes,

123 , both yielded Kd values of about 200 nm for PLC-beta3-Galphaq binding.

124 1 and TAP2 and the tapasin docking sites for PLC assembly are conserved in evolution, whereas element

125 ive value, and negative predictive value for PLC injuries were 55% (11 of 20), 97% (38 of 39), 92% (1

126 for infectivity is present on HBV RNAs from PLC/PRF/5 cells, while an L protein ORF that was truncat

127 etest-posttest study, patients with AMS from PLCs at 2 academic medical centers were recruited from J

128 ctive for some time following either Galphaq-PLC-beta3 dissociation or PLC-beta3-potentiated Galphaq

129 on-canonical signal transduction via Galphaq-PLC-IP3-Ca(2+) at the expense of canonical DRD1 Galphas

130 e kinase to stimulate phospholipase C-gamma (PLC-gamma) which increases inositol 1,4,5-trisphosphate

131 tivates a Src kinase/phospholipase C-gamma1 (PLC-gamma1) signaling pathway and Ca(2+) mobilization.

132 TCR signaling up to phospholipase C-gamma1 (PLC-gamma1).

133 sphoinositide-specific phospholipase gamma1 (PLC-gamma1) in mediating cell entry of influenza virus H

134 and signal transducer phospholipase gamma2 (PLC-gamma2), and increased activation of PLC-gamma2 and

135 t bind Gbetagamma in a FRET-based Gbetagamma-PLC-beta binding assay.

136 ordingly, the ability of a tumor to generate PLC-PDX is predictive of poor prognosis.

137 time the subtype-specific interplay of host PLC-gamma1 signaling and H1N1 virus that is critical for

138 es, suggesting a potential mechanism for how PLCs might interact with their target membranes.

139 P2E and P2M) and human HCC cell lines (Huh7, PLC/PRF/5, HLE, and HLF), that the TGFbeta signaling axi

140 cated Lsp-dependent export of PG-hydrolyzing PLC activity.

141 HDV virions assembled in PLC/PRF/5 cells were able to infect primary human hepato

142 aling response as evidenced by a decrease in PLC-beta activation and IP3R-mediated calcium store rele

143 fore, intrinsic movement of the PH domain in PLC-beta modulates Gbetagamma access to its binding site

144 Our reporting of a projected increase in PLC incidence to 2030 in 30 countries serves as a baseli

145 Blocking PH domain motion in PLC-beta by cross-linking it to the EF hand domain inhib

146 is the minimal Gbetagamma binding region in PLC-beta3.

147 sus regarding the Gbetagamma binding site in PLC-beta.

148 a clinically useful tool that can be used in PLCs to help decrease worry about developing melanoma in

149 ple downstream signaling pathways, including PLC/PKC, Rho/Rac, and YAP.

150 We have further shown that H1N1-induced PLC-gamma1 activation is downstream of epidermal growth

151 ion process and estimate freeze-thaw-induced PLC.

152 diameter) showed higher freeze-thaw-induced PLC.

153 ost cycle correlated positively with induced PLC, whereby species with wider conduits (hydraulic diam

154 ecan-9-yl potassium xanthate (D609) inhibits PLC (10 nM) with an IC50 value of 3.81 +/- 0.22 muM.

155 ysically interacts with the TCR intermediate PLC-gamma1, targeting it for proteasomal degradation aft

156 e specific SK channel antagonist apamin into PLC increased Fos expression but had no effect on food s

157 We further report that CB1-mediated intra-PLC opiate motivational signaling is mediated through a

158 Here we identify PLCdelta4 as the key PLC isoform involved in regulation of TRPM8 channels in

159 Here we identify PLCdelta4 as the key PLC isoform involved in regulation of TRPM8 in sensory d

160 ibition or genetic disruption of Lck kinase, PLC-gamma1 or the T cell receptor complex inhibits light

161 d Gbetagamma and the Alexa Fluor 594-labeled PLC-beta pleckstrin homology (PH) domain, we demonstrate

162 e that resulted in reduced formation of LAT, PLC-gamma, and AKT microclusters.

163 ic mutations of EF-1 residues in full-length PLC delta1 reduce enzyme activity but not because of dis

164 lated PH domain can compete with full-length PLC-beta3 for binding Gbetagamma but not Galphaq, Using

165 y as a dominant-negative form of full-length PLC-beta3.

166 Cross-linked PLC-beta does not bind Gbetagamma in a FRET-based Gbetag

167 Rapid activation of mbGR/PLC/PKC further leads to activation of known biomarkers

168 We found that mbGR/PLC/PKC signaling cascade exists in all cell types teste

169 signaling pathway involving Galphaq-mediated PLC activity is responsible for driving PKC-dependent ch

170 s greater than the EC50 for Galphaq-mediated PLC-beta3 activation and for the Galphaq GTPase-activati

171 luR5) or its downstream signaling molecules (PLC, PKC, IP3 receptors) markedly attenuated SKF38393-in

172 We projected new PLC cases to 2030 using age-period-cohort models (NORDPR

173 general approach for identification of novel PLC inhibitors, we developed a high-throughput assay bas

174 ary of 6280 compounds identified three novel PLC inhibitors that exhibited potent activities in two s

175 We hypothesized that the ability of PLC to function as a guanine nucleotide exchange factor

176 to assess Ca(2+) responses in the absence of PLC activity indicates that IP3 receptor modulation by P

177 aine seeking, in part, through activation of PLC and PKCgamma.

178 membranes are integral for the activation of PLC-beta isozymes by diverse modulators, and we propose

179 ns inhibited Galphaq-dependent activation of PLC-beta3 at least as effectively as a dominant-negative

180 eported the membrane-dependent activation of PLC-beta3 by Galphaq Therefore, XY-69 can replace radioa

181 bunits and did not inhibit the activation of PLC-beta3 by Gbeta1gamma2 In contrast, the peptide robus

182 the peptide robustly prevented activation of PLC-beta3 or p63RhoGEF by Galphaq; it also prevented G p

183 a2 (PLC-gamma2), and increased activation of PLC-gamma2 and its downstream pathways following B cell

184 alphaq GTPase-activating protein activity of PLC-beta.

185 We predicted the future burden of PLC in 30 countries around 2030.

186 Incident cases of PLC (International Classification of Diseases, Tenth Rev

187 rate interactions and as key determinants of PLC dynamics.

188 F (CDC25 homology domain) and RA2 domains of PLC are required for long term protein kinase D (PKD) ac

189 learning increased intrinsic excitability of PLC Fos-expressing neuronal ensembles that play a role i

190 Exposure of PLC-PDXs to standards of care or therapeutic options alr

191 The fraction of PLC-beta cross-linked is proportional to the fractional

192 The histology of PLC-PDXs is strikingly similar to that observed in prima

193 the G488R mutant, showing the importance of PLC-mediated PI(4,5)P2 depletion in this process.

194 nge intake involves a pathway independent of PLC activation.

195 tively decreasing PI(4,5)P2 independently of PLC potentiated the sensitizing effect of protein kinase

196 re significantly associated with injuries of PLC in patients with spine cervical trauma.

197 measured the thermodynamics and kinetics of PLC-beta3 binding to Galphaq FRET and fluorescence corre

198 Here we show that localization of PLC to the Golgi is required for activation of PKD in th

199 However, the regulatory mechanism of PLC is not yet understood in detail.

200 In addition, mutants of PLC-beta3 with crippled autoinhibition dramatically acce

201 R signaling, resulting in phosphorylation of PLC-g1, calcium influx, ROS generation, upregulation of

202 2, infection leads to the phosphorylation of PLC-gamma1 at Ser 1248 immediately after infection and i

203 ogical features and metastatic properties of PLC-derived organoids are preserved in vivo.

204 nalysis, we found that the incidence rate of PLC and the mortality rates of severe end-stage liver di

205 Increases in new cases and rates of PLC are projected in both sexes.

206 dulthood and subsequently reduce the risk of PLC and other liver diseases in young adults in rural Ch

207 mplications may lead to an increased risk of PLC that potentially offsets these gains is a concern.

208 not solvent-exposed in crystal structures of PLC-beta, necessitating conformational rearrangement to

209 There was an underreporting of PLC diagnosed by noninvasive methods; the incidence was

210 ompleteness and assess the underreporting of PLC to the CR and to produce a more accurate estimate ba

211 ate the wide-ranging biomedical utilities of PLC-derived organoid models in furthering the understand

212 g candidates for reporting the activation of PLCs in live cells with high spatiotemporal resolution.

213 tool for measuring the real-time activity of PLCs as either purified enzymes or in cellular lysates.

214 Mammals express six families of PLCs, each with both unique and overlapping controls ove

215 Despite the widespread importance of PLCs in human biology and disease, it has been impossibl

216 ylation at serine-16, which was dependent on PLC and PKCepsilon.

217 Information on PLC incidence and liver disease mortality were collected

218 mall hairpin RNA reduced both store-operated PLC activity and stimulation of TRPC1 SOCs.

219 Optos Panoramic 200MA imaging system (Optos PLC).

220 ing either Galphaq-PLC-beta3 dissociation or PLC-beta3-potentiated Galphaq deactivation, is not suffi

221 oscillations, which are dependent on the P2R/PLC/inositol trisphosphate/ER pathway.

222 sible for the activation of Duox1 via a P2YR/PLC/Ca(2+) signaling pathway and the production of H2O2,

223 sure by activating a Wnt-like phospholipase (PLC)/ protein kinase C (PKC) signaling cascade.

224 ous domains, indicated that DAG activates PI-PLC whenever it can generate fluid domains to which the

225 Real-time PCR and PI-PLC enzyme assays of the TCS mutants, coupled with SrrA

226 Shu1 cleavability by PI-PLC and its predicted hydropathy profile strongly sugges

227 emoving ephrinAs from axonal membranes by PI-PLC treatment abolishes this response.

228 ylinositol (PI)-specific phospholipase C (PI-PLC) capable of hydrolyzing PI and cleaving glycosyl-PI

229 hosphoinositide-specific phospholipase C (PI-PLC) is one of the earliest responses triggered by the r

230 of phosphatidylinositol-phospholipase C (PI-PLC) was studied with vesicles containing PI, either pur

231 hosphoinositide-specific phospholipase C (PI-PLC).

232 m and to oxidative stress and suggest how PI-PLC could contribute to the pathogenesis of S. aureus in

233 t 22 degrees C, DAG at 33 mol % increased PI-PLC activity in all of the mixtures, but not in pure PI

234 aureus (CA-MRSA) USA300 secreted the most PI-PLC.

235 ns long molecular dynamics simulation of PI-PLC at the surface of a lipid bilayer revealed a strikin

236 related motions between the two halves of PI-PLC may be more important for enzymatic activity than fo

237 rulent staphylococci, the contribution of PI-PLC to the capacity of S. aureus to cause disease remain

238 The Arabidopsis (Arabidopsis thaliana) PI-PLC gene family is composed of nine members.

239 Although the PI-PLC active site has no obvious lid, molecular-dynamics s

240 enesis of Pro(254) appears to stiffen the PI-PLC structure, but experimental mutations had minor effe

241 r goal in these studies was to understand PI-PLC in the context of S. aureus biology.

242 h the generation of small vesicles, which PI-PLC is known to degrade at higher rates.

243 both Pro residues is quite variable among PI-PLCs, it shows high conservation in virulence-associated

244 rvation in virulence-associated, secreted PI-PLCs that bind to the surface of cells.

245 ostsynaptic TRPC channel opening by the PI3K-PLC signalling pathway in POMC neurons enhances spontane

246 utaneous injection of EX (5 mug) or placebo (PLC) 30 minutes before a 75-g oral glucose tolerance tes

247 The present randomized placebo (PLC)-controlled within-subject pharmaco-functional magne

248 Plasma PLC levels were higher in patients with KD and CC+CG rs6

249 aq or Gbeta1gamma2 did not activate purified PLC-beta3 under these conditions despite their robust ca

250 in two separate assay formats with purified PLC isozymes in vitro.

251 ted Fos-expressing neuronal ensembles in rat PLC play an important role in learned operant food seeki

252 s at the level of G protein-coupled receptor PLC activity and/or IP3 metabolism to attenuate IP3 leve

253 s that lysophosphatidic acid (LPA) regulates PLC-beta1 and PLC-beta2 via two distinct pathways to enh

254 hormone-dependent responses, do not require PLC.

255 ce, while bubble expansion and the resulting PLC occur during thawing.

256 bstantial proportion of additional screening PLC visits exist and are desired by all patients with pi

257 e evidence for the involvement of a specific PLC isoform in the regulation of cold sensitivity in mic

258 ion, PlcC showed cell-associated PC-specific PLC activity after bacterial growth in broth.

259 spholipase C (PLC), but neither the specific PLC isoform nor the in vivo relevance of this regulation

260 s of G(q)alpha and G11alpha, which stimulate PLC, leads to severe hyperphagic obesity, increased line

261 malize the differences in hormone-stimulated PLC activity, indicating calcium-dependent PLCs are not

262 ibited G protein-coupled receptor-stimulated PLC activity in intact cell systems.

263 Further analyses demonstrate that PLC-gamma1 activation is required for viral postbinding

264 stent with a Kd of 200 nm We determined that PLC-beta3 hysteresis, whereby PLC-beta3 remains active f

265 These results provide evidence that PLC-PDX preclinical platform can strongly contribute to

266 3N2 viruses in cell culture, suggesting that PLC-gamma1 plays an important subtype-specific role in t

267 The PLC functions to facilitate and optimize MHC I-mediated

268 tor GDP-beta-S, anti-Galphaq antibodies, the PLC inhibitor U73122, and the PKC inhibitor GF109203X al

269 In contrast to all other TRPC channels, the PLC product diacylglycerol (DAG) is not sufficient for c

270 ic method, should be reported to the CR, the PLC incidence may not reflect the true rate.

271 , delaying MHC class I dissociation from the PLC and their transit through the secretory pathway.

272 to induce MHC class I dissociation from the PLC, we investigated the interaction of ATP with the cha

273 a rat stroke model, we demonstrate here the PLC's capacity for neuroprosthetic control and physiolog

274 Importantly, the PLC treatment did not decrease the high lateral resoluti

275 t, despite the disrupted connectivity in the PLC, it may serve as an effective target for neuroprosth

276 R) luminal, calcium-binding component of the PLC that is known to bind ATP.

277 nesis, we identify a hydrophobic face of the PLC-beta PH domain as the Gbetagamma binding interface.

278 ulin and is not an integral component of the PLC.

279 olongs the association of MHC class I on the PLC.

280 phosphate (PIP2), the mechanism by which the PLC pathway activates TRPC4/C5 remains unclear.

281 es suggest a functional asymmetry within the PLC resulting in greater significance of the TAP2/TPN in

282 ional valence switching mechanism within the PLC, controlling dissociable subcortical reward and aver

283 The results show that 98% of the PLCs reported to the CR were histologically verified; 80

284 unidentified tumor suppressor role for this PLC in animal models and, together with observations of

285 vealing a tumor suppressor function for this PLC.

286 ough Galpha(i/o), in addition to coupling to PLC through Galpha(q/11).

287 A reduction of substrate efflux due to PLC activation was also found with recombinant noradrena

288 ivate EGFR, but only H1N1 infection leads to PLC-gamma1 activation.

289 We propose that unliganded PLC-beta exists in equilibrium between a closed conforma

290 e host cytosol, WT L. monocytogenes utilized PLCs and ActA to avoid subsequent xenophagy.

291 e to Coronin-1-dependent calcium release via PLC-gamma1 signaling, which releases PI3K-dependent supp

292 was observed on ATGU (EX = 1.16 +/- 0.15 vs. PLC = 1.36 +/- 0.13 [mumol/min/L]/[mumol/min/kg]).

293 PK-dependent presynaptic inhibition, whereas PLC-mediated GABAergic feedback inhibition remains respo

294 etermined that PLC-beta3 hysteresis, whereby PLC-beta3 remains active for some time following either

295 data provide a molecular mechanism by which PLC mediates sustained signaling and by which astrocytes

296 An abnormal PFP was associated with PLC (P < .001) and arch (P = .006) injuries but not with

297 nversion of NSCs is strongly associated with PLC variations during dehydration and rehydration proces

298 include the small number of individuals with PLC, participants lost to follow-up, and the large propo

299 cribing membrane-mediated allosterism within PLC-beta isozymes.

300 ric liver cancer patient-derived xenografts (PLC-PDXs) from 20 hepatoblastomas (HBs), 1 transitional