コーパス検索結果 (left1)
通し番号をクリックするとPubMedの該当ページを表示します
1 PLC activity was found to depend upon the electrostatic
2 PLC localization is largely intracellular and its compar
3 PLC-beta isoforms also function as GTPase-activating pro
4 PLC-derived organoid cultures preserve the histological
5 PLC-derived organoids are amenable for biomarker identif
6 PLC/inositol trisphosphate receptor (IP3R) and estrogen
12 Moreover, we determined that GLP-1 activates PLC, which increases submembrane diacylglycerol and ther
13 w that Ca(2+) influx through TRPV1 activates PLC and DAGK enzymes and that the latter limits formatio
16 on detection of coincident Gi/o, Ca(2+), and PLC signaling, which is further modulated by the small G
17 activated TrkB and downstream AKT, ERK, and PLC-gamma signaling in TNBC cells, increasing their inva
18 show that WNT signaling through Galphao and PLC-beta results in sustained Ca(2+) release via IP(3) a
19 cate that the mechanism by which Galphaq and PLC-beta3 mutually regulate each other is far more compl
20 turn, aberrant activation of PLC-gamma1 and PLC-gamma2 is implicated in inflammation, autoimmunity,
21 on followed by G(q) immunoprecipitation, and PLC activation by determining the inositol phosphate lev
25 ve, whereas those of coinhibiting mGluR5 and PLC were not, indicating that the efficacy of mGluR1 blo
26 beta(2) integrin activation (PKC, PI3K, and PLC) were similarly activated in both T cell subsets.
27 tion-dependently activated G(q) proteins and PLC in the hypothalamus and cerebellum but not in cortex
31 me Rho family GTPases, phospholipase C-beta (PLC-beta) isoforms hydrolyze phosphatidylinositol 4,5-bi
33 e was found for a direct interaction between PLC and the GTPases that mediate phospholipase activatio
34 block a highly specific interaction between PLC delta1-PH and PI(4,5)P2, encoded within the conforma
35 or the first time, the relationships between PLC activity and substrate presentation in lipid vesicle
36 ral studies showed how Galphaq and Rac1 bind PLC-beta, there is a lack of consensus regarding the Gbe
40 ific electrostatic interactions between BtPI-PLC and membranes vary as a function of the fraction of
41 tidylinositol-specific phospholipase C (BtPI-PLC) is a secreted virulence factor that binds specifica
42 tidylinositol-specific phospholipase C (BtPI-PLC), which specifically binds to phosphatidylcholine (P
43 esults lead to a quantitative model for BtPI-PLC interactions with cell membranes where protein bindi
44 at weak electrostatics, as observed for BtPI-PLC, might be a less unusual mechanism for peripheral me
46 -atom molecular dynamics simulations of BtPI-PLC interacting with PC-rich bilayers show that the prot
49 tly activated by diacylglycerols produced by PLC breakdown of phosphatidylinositol 4,5-bisphosphate (
50 either by serotonin-induced phospholipase C (PLC) activation or by a rapamycin-induced translocation
51 inating in phosphoinositide-phospholipase C (PLC) activation, which generates the second messengers d
53 ate (IP3 ) accumulation and phospholipase C (PLC) activity were significantly potentiated in hepatocy
54 n Drosophila is mediated by phospholipase C (PLC) and Ca(2+)-permeable TRP channels, but the function
55 he same receptors activated phospholipase C (PLC) and decreased plasma membrane PI(4,5)P(2) levels in
59 ctivate a calcium-sensitive phospholipase C (PLC) enzyme and to lead to a robust decrease in phosphat
62 (2+) -induced activation of phospholipase C (PLC) has been implied in the regulation of TRPM8 channel
66 Phosphoinositide-specific phospholipase C (PLC) is an important family of enzymes constituting a ju
67 tyrosine kinases, activate phospholipase C (PLC) isozymes to hydrolyze phosphatidylinositol 4,5-bisp
71 treatment with buffer-free phospholipase C (PLC) to near-quantitatively degrade PCs in fresh-frozen
73 ly a substrate for PI3K and phospholipase C (PLC), and is now an established lipid messenger pivotal
74 lglycerol lipase (DAGL), or phospholipase C (PLC), and their metabolism is mediated by several metabo
75 thought to be regulated by phospholipase C (PLC), but neither the specific PLC isoform nor the in vi
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 sciatic MBP(84-104) induced phospholipase C (PLC)-driven (females) and phosphoinositide 3-kinase-driv
82 rylated at threonine 505 by phospholipase C (PLC)-mediated signaling at the early stage of infection,
88 n alpha q subunit (Galphaq)/phospholipase C (PLC)beta1 activities and protein kinase C (PKC) phosphor
90 d LAT binds Grb2, Gads, and phospholipase C (PLC)gamma1 to mediate T cell activation, proliferation,
93 everal signaling pathways, including calcium-PLC-PKC-PKD1 pathway, NF-kappaB pathway, and MAP kinase
96 to the propagation of primary liver cancer (PLC) organoids from three of the most common PLC subtype
97 dy are major traits of primary liver cancer (PLC), which represent the second most common cause of ca
100 fic subpopulation of proximal luminal cells (PLCs), enriched in the periurethral region of the develo
101 After activation of phospholipase Cgamma (PLC-gamma), TRPC1 mediated Ca(2+) entry and triggered pr
104 PLC) organoids from three of the most common PLC subtypes: hepatocellular carcinoma (HCC), cholangioc
107 The MHC class I peptide loading complex (PLC) facilitates the assembly of MHC class I molecules w
108 lex class-I (MHC-I) peptide-loading complex (PLC) is a cornerstone of the human adaptive immune syste
109 al component of the peptide-loading complex (PLC), to which tapasin (TPN) recruits MHC class I (MHC I
112 the percent loss of hydraulic conductivity (PLC) and the content of nonstructural carbohydrates (NSC
113 t percentage loss of hydraulic conductivity (PLC) of about 40%-60%, were broadly consistent with sate
116 ositol 4,5-bisphosphate used in conventional PLC assays and will enable high-throughput screens to id
117 of the parental tumors and the corresponding PLC-PDXs show high conservation of the molecular feature
118 Although the stroke perilesional cortex (PLC) has been hypothesized as a potential site for a BMI
119 neuronal ensembles in rat prelimbic cortex (PLC) and assess altered intrinsic excitability after 10
120 yer V pyramidal neurons in prelimbic cortex (PLC) of FosGFP-transgenic rats, we found that operant fo
121 edict that trees would have reached critical PLC in widespread areas (i.e. it projected a low mortali
122 d that AGB1 interacts with phospholipase Cs (PLCs), and Ca(o) induced InsP3 production in Col but not
126 itol 1,4,5-trisphosphate and diacylglycerol, PLC, unlike the other phospholipase C family members, is
127 activation of common (AC/PKA) and distinct (PLC/PKC, intra-/extra-cellular calcium, PI3K/MAPK/mTOR)
128 lipase C delta 1 pleckstrin homology domain (PLC delta1-PH), is completely inhibited in the presence
130 Starch was converted to soluble sugar during PLC progression under drought, and the hydraulic conduct
132 cell-surface D1-mGlu5 heteromers exacerbated PLC signaling and intracellular calcium release in respo
133 ic rats to ablate selectively Fos-expressing PLC neurons that were active during operant food self-ad
134 , we assessed the presence of signs favoring PLC on HRCT (smooth or nodular septal lines, subpleural
137 ive value, and negative predictive value for PLC injuries were 55% (11 of 20), 97% (38 of 39), 92% (1
138 Although structures of isolated domains from PLC-gamma isozymes are available, these structures are i
139 etest-posttest study, patients with AMS from PLCs at 2 academic medical centers were recruited from J
140 ctive for some time following either Galphaq-PLC-beta3 dissociation or PLC-beta3-potentiated Galphaq
141 on-canonical signal transduction via Galphaq-PLC-IP3-Ca(2+) at the expense of canonical DRD1 Galphas
142 tivates a Src kinase/phospholipase C-gamma1 (PLC-gamma1) signaling pathway and Ca(2+) mobilization.
143 nt and activation of phospholipase C-gamma1 (PLC-gamma1), an important effector molecule for T cell a
144 and signal transducer phospholipase gamma2 (PLC-gamma2), and increased activation of PLC-gamma2 and
149 aling response as evidenced by a decrease in PLC-beta activation and IP3R-mediated calcium store rele
150 fore, intrinsic movement of the PH domain in PLC-beta modulates Gbetagamma access to its binding site
151 Our reporting of a projected increase in PLC incidence to 2030 in 30 countries serves as a baseli
155 a clinically useful tool that can be used in PLCs to help decrease worry about developing melanoma in
158 ysically interacts with the TCR intermediate PLC-gamma1, targeting it for proteasomal degradation aft
159 e specific SK channel antagonist apamin into PLC increased Fos expression but had no effect on food s
160 of the human phospholipase C-gamma isozymes (PLC-gamma1, -gamma2) by tyrosine phosphorylation is fund
163 ibition or genetic disruption of Lck kinase, PLC-gamma1 or the T cell receptor complex inhibits light
164 d Gbetagamma and the Alexa Fluor 594-labeled PLC-beta pleckstrin homology (PH) domain, we demonstrate
166 lated PH domain can compete with full-length PLC-beta3 for binding Gbetagamma but not Galphaq, Using
168 t high-resolution structure of a full-length PLC-gamma isozyme and use it to underpin a detailed mode
169 cs, including particle number (PNC), length (PLC), and surface area (PSC) concentrations, and myocard
173 signaling pathway involving Galphaq-mediated PLC activity is responsible for driving PKC-dependent ch
174 s greater than the EC50 for Galphaq-mediated PLC-beta3 activation and for the Galphaq GTPase-activati
176 in PNC within the size range of 10 - 100 nm, PLC, and PSC were associated with an increase of MI 6 h
180 to assess Ca(2+) responses in the absence of PLC activity indicates that IP3 receptor modulation by P
182 ns inhibited Galphaq-dependent activation of PLC-beta3 at least as effectively as a dominant-negative
183 eported the membrane-dependent activation of PLC-beta3 by Galphaq Therefore, XY-69 can replace radioa
184 bunits and did not inhibit the activation of PLC-beta3 by Gbeta1gamma2 In contrast, the peptide robus
185 the peptide robustly prevented activation of PLC-beta3 or p63RhoGEF by Galphaq; it also prevented G p
187 a2 (PLC-gamma2), and increased activation of PLC-gamma2 and its downstream pathways following B cell
189 creased cancer fitness and aggressiveness of PLC may be achieved by enhancing tumoral genomic complex
194 HRCT perform similarly for the diagnosis of PLC, with both being outperformed by (18)F-FDG PET/CT qu
195 F (CDC25 homology domain) and RA2 domains of PLC are required for long term protein kinase D (PKD) ac
196 learning increased intrinsic excitability of PLC Fos-expressing neuronal ensembles that play a role i
199 surrogate to define genomic heterogeneity of PLC linked to chromosomal instability and evasion of imm
204 measured the thermodynamics and kinetics of PLC-beta3 binding to Galphaq FRET and fluorescence corre
206 ylation increases the speed and magnitude of PLC-gamma1 activation and enhances T cell sensitivity to
208 R signaling, resulting in phosphorylation of PLC-g1, calcium influx, ROS generation, upregulation of
209 2, infection leads to the phosphorylation of PLC-gamma1 at Ser 1248 immediately after infection and i
210 Diacylglycerol (DAG), the lipid product of PLC that activates conventional PKCs, is focally enriche
212 nalysis, we found that the incidence rate of PLC and the mortality rates of severe end-stage liver di
214 mplications may lead to an increased risk of PLC that potentially offsets these gains is a concern.
215 not solvent-exposed in crystal structures of PLC-beta, necessitating conformational rearrangement to
218 ompleteness and assess the underreporting of PLC to the CR and to produce a more accurate estimate ba
219 ate the wide-ranging biomedical utilities of PLC-derived organoid models in furthering the understand
220 g candidates for reporting the activation of PLCs in live cells with high spatiotemporal resolution.
221 tool for measuring the real-time activity of PLCs as either purified enzymes or in cellular lysates.
224 ing either Galphaq-PLC-beta3 dissociation or PLC-beta3-potentiated Galphaq deactivation, is not suffi
226 phatidylcholine-specific phospholipase C (PC-PLC) of L. monocytogenes, is a potent inhibitor of intra
229 ous domains, indicated that DAG activates PI-PLC whenever it can generate fluid domains to which the
231 hosphoinositide-specific phospholipase C (PI-PLC) is one of the earliest responses triggered by the r
232 of phosphatidylinositol-phospholipase C (PI-PLC) was studied with vesicles containing PI, either pur
235 t 22 degrees C, DAG at 33 mol % increased PI-PLC activity in all of the mixtures, but not in pure PI
240 ostsynaptic TRPC channel opening by the PI3K-PLC signalling pathway in POMC neurons enhances spontane
241 ilizing a randomized, double-blind, placebo (PLC)-controlled, within-subject functional MRI study des
242 utaneous injection of EX (5 mug) or placebo (PLC) 30 minutes before a 75-g oral glucose tolerance tes
244 C4 and TRPC5 channel function, the Galpha(q)-PLC pathway inhibits channel activity by depleting PI(4,
246 ted Fos-expressing neuronal ensembles in rat PLC play an important role in learned operant food seeki
247 s at the level of G protein-coupled receptor PLC activity and/or IP3 metabolism to attenuate IP3 leve
250 netic lineage tracing, we show that RUNX1(+) PLCs are unaffected by androgen deprivation, and do not
251 llectively, our results reveal that RUNX1(+) PLCs is an intrinsic castration-resistant and self-susta
252 citation light induced a rapid (tau ~0.8 s), PLC-dependent decrease in fluorescence, representing dep
253 e evidence for the involvement of a specific PLC isoform in the regulation of cold sensitivity in mic
255 spholipase C (PLC), but neither the specific PLC isoform nor the in vivo relevance of this regulation
256 s of G(q)alpha and G11alpha, which stimulate PLC, leads to severe hyperphagic obesity, increased line
257 malize the differences in hormone-stimulated PLC activity, indicating calcium-dependent PLCs are not
258 stent with a Kd of 200 nm We determined that PLC-beta3 hysteresis, whereby PLC-beta3 remains active f
263 tor GDP-beta-S, anti-Galphaq antibodies, the PLC inhibitor U73122, and the PKC inhibitor GF109203X al
264 In contrast to all other TRPC channels, the PLC product diacylglycerol (DAG) is not sufficient for c
266 , delaying MHC class I dissociation from the PLC and their transit through the secretory pathway.
267 to induce MHC class I dissociation from the PLC, we investigated the interaction of ATP with the cha
268 a rat stroke model, we demonstrate here the PLC's capacity for neuroprosthetic control and physiolog
271 t, despite the disrupted connectivity in the PLC, it may serve as an effective target for neuroprosth
273 e showed that signaling abnormalities in the PLC/IP3/PKC/ERK pathway (phospholipase C/inositol 1,4,5-
274 complex, we report an atomistic model of the PLC and study its conformational dynamics on the multimi
276 nesis, we identify a hydrophobic face of the PLC-beta PH domain as the Gbetagamma binding interface.
277 Diacylglycerol (DAG), the product of the PLC-catalyzed PI(4,5)P(2) hydrolysis, activates protein
278 model also explains why mutant forms of the PLC-gamma isozymes found in several cancers have a wide
280 eic acids or GPCR antagonists stabilized the PLC components, Rb and p53, and sensitized mammary gland
281 esence of extracellular Ca(2+), and that the PLC-inositol 1,4,5-trisphosphate pathway, which controls
283 es suggest a functional asymmetry within the PLC resulting in greater significance of the TAP2/TPN in
285 e G (alphaq) protein that does not couple to PLC inhibited TRPM8 activity, and in cells expressing th
286 g by G(q)-protein-coupled receptors triggers PLC-mediated hydrolysis of PIP(2) into inositol 1,4,5-tr
290 e to Coronin-1-dependent calcium release via PLC-gamma1 signaling, which releases PI3K-dependent supp
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
297 nversion of NSCs is strongly associated with PLC variations during dehydration and rehydration proces
300 ric liver cancer patient-derived xenografts (PLC-PDXs) from 20 hepatoblastomas (HBs), 1 transitional