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1                                              PLD is a downstream target of the GTPase Rheb, which is
2                                              PLD patients scored higher on the PLD-Q total score than
3                                              PLD represents a potential target for the rational devel
4                                              PLD-MNA holds great promise as a novel, safe, effective,
5                                              PLD-MNA was packaged with a mixture of powdered peanut a
6                                              PLD-MNA was successfully laden with PNA/VD3/CpG powder a
7                                              PLD-MNA-mediated EPIT substantially reduced clinical all
8                                              PLD-Q is a valid, reproducible, and sensitive disease-sp
9                                              PLDs are also found in gut bacterial isolates that are u
10                                              PLDs are caused by mutations in genes involved in intrac
11                                              PLDs were found to be able to catalyze phospholipid head
12                             We identified 16 PLD-related symptoms (total score 0-100 points) by liter
13 ch (n = 200) and United States (US; n = 203) PLD patients.
14 ressed high interest in genetic testing as a PLD: age >=35 years (adjusted odds ratio [aOR], 1.75; 95
15 t of rapamycin (mTOR)/S6 kinase pathway in a PLD- and endocytosis-dependent manner, with both pharmac
16                         This gives rise to a PLD-dependent cutoff in TREK-1.
17                         Catalytically active PLD enhanced expression of EGFR in human breast cancer c
18  by reconstitution with catalytically active PLD.
19 ness of increased HCV screening to cover all PLD compared to the current approach, using a standard t
20 n center, rather than an offer to screen all PLD.
21                                     Although PLD has been widely implicated in the generation of PA n
22  and the need to examine such opinions among PLDs and transplant patients to enhance patient educatio
23 tion, we sought to determine whether ALN and PLD played a similar role in the ability of A. haemolyti
24  known about the connection between AMPK and PLD.
25 D severity stages (Gigot classification) and PLD-Q total scores of PLD patients with general controls
26 se Cbeta3 (PLCbeta3), PLCdelta1, DGKzeta and PLD are all downstream of receptor activation.
27                     Using PLD inhibitors and PLD knockout mice, we showed that PLD was necessary for
28    We validated the assay under knockout and PLD-overexpression conditions and then applied it to cha
29 endosomes defined by the presence of PKC and PLD (the pericentrion), which results in significant dif
30 rain of flies, anesthesia disrupts rafts and PLD(null) flies resist anesthesia.
31 powder-laden, dissolvable microneedle array (PLD-MNA) for epidermal delivery of powdered allergens an
32 fic questionnaire that can be used to assess PLD-related symptoms in clinical care and future researc
33                          Correlation between PLD-Q total score and EORTC symptom scale (The Netherlan
34                                         Both PLD isoforms were found to interact with Arf6 during Fcg
35                     While inhibition of both PLD and DGK had no effect on the overall ERK activity, i
36 y, this condition was also dependent on both PLD and mTOR activity.
37  These biological effects also required both PLD activity and mTOR function, with both the PLD inhibi
38 cogenic signaling pathway that requires both PLD and mTOR, and suggest that inhibitors of PLD or mTOR
39 ion of PLD by AMPK and regulation of AMPK by PLD and PA.
40 stabilization also occurred, as indicated by PLD resistance to cycloheximide-induced EGFR protein deg
41 fatty acid chains, such as those produced by PLD, are capable of displacing DEPTOR and activating mTO
42  found that PA was generated sequentially by PLD and DGK in epidermal growth factor (EGF)-stimulated
43 c questionnaires lack sensitivity to capture PLD-related symptoms, a prerequisite to determine effect
44 type BBSomes were introduced into bbs cells, PLD was rapidly removed from the mutant cilia, indicatin
45 emoenzymatic method for visualizing cellular PLD activity, yielded a panel of optoPLDs whose range of
46 D is only distantly related to characterized PLDs from pathogenic bacteria, suggesting a distinct evo
47 activities such as Streptomyces chromofuscus PLD or serum lipase.
48 me-dependent mechanism for exporting ciliary PLD.
49 d dynamics in human primary DCs by combining PLD pharmacological inhibition with a fluorescent PA sen
50 To test discriminative validity, we compared PLD-Q total scores of patients with different PLD severi
51 , but no phenotype has been shown connecting PLD to an anesthetic effect.
52 opment of a direct, specific, and continuous PLD assay that is based on the chelation-enhanced fluore
53  influenza virus stimulates phospholipase D (PLD) activity and that PLD co-localizes with influenza d
54  by the FcgammaR stimulates phospholipase D (PLD) activity and triggers the production of phosphatidi
55 FAM83B expression increases Phospholipase D (PLD) activity, and that suppression of PLD1 activity pre
56 s contain a light-dependent phospholipase D (PLD) activity.
57 idic acid (PA) generated by phospholipase D (PLD) and diacylglycerol kinase (DGK).
58  of the PA-producing enzyme phospholipase D (PLD) and increased localization of PLD1 to ATG16L1-posit
59           We show here that phospholipase D (PLD) and its enzymatic reaction product, phosphatidic ac
60 uggested the involvement of phospholipase D (PLD) and its product phosphatidic acid (PA) in podosome
61 verexpression of the enzyme phospholipase D (PLD) and its reaction product, phosphatidic acid (PA).
62 as the ED peptide activates phospholipase D (PLD) and MMP2, but not MMP9.
63 ted as a helicase domain, a phospholipase D (PLD) domain, a DUF1998 domain and a gene of unknown func
64 ms can hydrolyse PC using a phospholipase D (PLD) enzyme and further convert the released choline to
65 of cellular PA synthesis by phospholipase D (PLD) enzymes is reported.
66                             Phospholipase D (PLD) enzymes play a double vital role in cells: they mai
67 siological PA production by phospholipase D (PLD) enzymes.
68      In animals, the enzyme phospholipase D (PLD) has been shown to generate alcohol metabolites (e.g
69                             Phospholipase D (PLD) hydrolyzes membrane phospholipids to produce phosph
70 riments were performed with phospholipase D (PLD) in a Ca(2+) dependent fashion.
71  of phosphatidic acid (PA), phospholipase D (PLD) is strongly involved in vesicular trafficking and c
72                             Phospholipase D (PLD) proteins are enzymes that catalyze the hydrolysis o
73                             Phospholipase D (PLD) signaling plays a critical role in cell growth and
74                         The Phospholipase D (PLD) superfamily is linked to neurological disease, canc
75 (PA), which is generated by phospholipase D (PLD) via hydrolysis of phosphatidylcholine.
76 lvins (RvD1- RvD5) activate phospholipase D (PLD), a ubiquitously expressed membrane lipase enzyme ac
77 tors, arcanolysin (ALN) and phospholipase D (PLD), affect the ability of the bacteria to adhere to an
78 mall molecule inhibitors of phospholipase D (PLD), an enzyme that produces phosphatidic acid in cells
79 on of the mTORC1 regulator, phospholipase D (PLD), and recapitulated with the addition of the PLD pro
80 bolic pathways generate PA: phospholipase D (PLD), diacylglycerol kinase (DGK), and lysophosphatidic
81 he enzyme that produces it, phospholipase D (PLD), downregulate EGFR expression.
82 dic acid, as synthesized by phospholipase D (PLD), enhances cancer cell survival.
83 tween the signaling protein phospholipase D (PLD), phosphatidic acid (PA), and a specific set of micr
84 s a similar overall fold as phospholipase D (PLD), phosphatidylserine synthase (PSS) and tyrosyl-DNA
85    We exploited a microbial phospholipase D (PLD), which produces PA by phosphatidylcholine hydrolysi
86 e newly identified mediator phospholipase D (PLD), which promotes both mTORC1-dependent cell prolifer
87 esis and the product of the phospholipase D (PLD)-catalyzed hydrolysis of phosphatidylcholine.
88 amycin) signaling through a phospholipase D (PLD)-dependent increase in the concentration of phosphat
89 and PKCbetaII induces their phospholipase D (PLD)-dependent internalization and translocation to a su
90 wth factors also induce the phospholipase D (PLD)-phosphatidic acid (PA) pathway, required for mTORC1
91 ted by the signaling enzyme phospholipase D (PLD).
92 d mediated through RhoA and phospholipase D (PLD).
93 ibuted to the activation of phospholipase D (PLD).
94 ospholipase C (PLC) but not phospholipase D (PLD).
95 armacological inhibition of phospholipase D (PLD)2, which generates the signaling lipid phosphatidic
96       Arf6 silencing concomitantly decreased PLD activity as well as the levels of PA found on phagos
97 -x thin films using pulsed laser deposition (PLD) enables improving their superconducting transition
98 lm was grown by the pulsed laser deposition (PLD) method and it exhibits a broad transparent window f
99 glass substrates by pulsed laser deposition (PLD) technique.
100 strate by optimized pulsed laser deposition (PLD) technique.
101 irus (HCV) among people living in detention (PLD) is typically high in many countries including Switz
102                                The developed PLD-Q was validated in Dutch (n = 200) and United States
103 lished online, the Paravalvular Leak Device (PLD; Occlutech) was incorrectly described as having a "p
104 it 1D channels with pore limiting diameters (PLDs) of 1.64, 2.90, 5.06, 5.28, 8.57, 8.83, 11.86, and
105 LD-Q total scores of patients with different PLD severity stages (Gigot classification) and PLD-Q tot
106       Treatment of polycystic liver disease (PLD) focuses on symptom improvement.
107                    Polycystic liver disease (PLD) is a member of the cholangiopathies, a group of liv
108 lantation (LT) for polycystic liver disease (PLD) is rare, extremely challenging and hemorrhagic, wit
109 nial aneurysms and polycystic liver disease (PLD), which can be severe and associated with significan
110                   Polycystic liver diseases (PLDs) are genetic disorders characterized by progressive
111  or fearful whole-body point-light displays (PLDs) as adapters and were then asked to perform an expl
112 ation and dynamics of the prion-like domain (PLD) of Orb2A using a nonconventional liquid-state NMR s
113 ng through its N-terminal prion-like domain (PLD) to the C-terminal domain of RNA polymerase II.
114                          Prion-like domains (PLDs) can drive liquid-liquid phase separation (LLPS) in
115  requires low-complexity prion-like domains (PLDs) within paraspeckle proteins.
116                           Autosomal-dominant PLD (ADPLD) with no or very few renal cysts is a separat
117 er 2 scenarios: as a potential living donor (PLD), and as a patient awaiting transplantation.
118 etics determined the delivery of DOX and DOX-PLD to the same tumor phenotype, collagen content determ
119  chemotherapy-loaded pegylated liposome (DOX-PLD) in tumor vasculature.
120  content determined the extravasation of DOX-PLD to different tumor phenotypes.
121 meability of that vessel permeability to DOX-PLD, indicating that collagen content may offer a biophy
122 poside, and pegylated liposomal doxorubicin (PLD) in vivo, utilizing ovarian cancer xenografts.
123       Since pegylated liposomal doxorubicin (PLD) was the most prevalent formulation in these clinica
124 al reductions in planktonic larval duration (PLD) associated with ocean warming, given current socioe
125 grees C) as well as pelagic larval duration (PLD) for juveniles from the beginning of the season and
126 ect determination of choline released during PLD-catalyzed phosphatidylcholine hydrolysis, making its
127 und an adaptation after-effect for emotional PLDs, indicating the existence of a neural representatio
128 orescence, confocal microscopy, endocytosis, PLD activity, and cell viability assays, we show that ex
129 CF-7 breast cancer cells have low endogenous PLD enzymatic activity and cell invasion, concomitant wi
130 nted the subcellular locations of endogenous PLD activity as elicited by physiological agonists of G
131 ological or genetic inhibition of endogenous PLD prevented mTORC1 lysosomal translocation.
132 ethanol directly competes for the endogenous PLD product phosphatidic acid at lipid-binding sites wit
133 hotoreceptors, during illumination, enhanced PLD activity was sufficient to clear RLVs from the cell
134 ed by the key phospholipid metabolism enzyme PLD.
135 for DISARM-mediated defence, with the fifth (PLD) being redundant for defence against some of the pha
136                           ELLS during LT for PLD facilitates total hepatectomy with vena cava and cav
137                             Moreover, LT for PLD presents the highest mortality rate (12% to 18%) amo
138 11 to 2018, ELLS was performed during LT for PLD.
139                            The mechanism for PLD-mediated actions of Resolvin-D5 (RvD5) in polarizing
140  We calculate a latency time of <650 mus for PLD activation by mixing.
141 C6i conjugates open a therapeutic avenue for PLDs.
142 sing femtosecond pulsed laser deposition (fs-PLD).
143 l properties can be controlled by varying fs-PLD process parameters to prepare TiO(2) thin films, whi
144           Out of these myriads of functions, PLD is becoming recognized as a major player in cell mig
145                                     Further, PLD interacts with a variety of kinases (PKC, FES, EGF r
146                          This easy to handle PLD assay constitutes, to our knowledge, the first direc
147                   Thus, during illumination, PLD activity couples endocytosis of RLVs with their recy
148 ssect PA-dependent signaling pathways, image PLD activity in disease, and remodel intracellular membr
149 ssion of AMPK activity led to an increase in PLD activity, and conversely, activation of AMPK suppres
150 ggesting that, given potential reductions in PLD due to ocean warming, future marine reserve networks
151 ific questionnaire that assesses symptoms in PLD (PLD-Q).
152 he numbers (valence) of aromatic residues in PLDs determine the extent of temperature-dependent compa
153                                The increased PLD activity is engaged by hyperactivation of epidermal
154                            PNA/VD3/CpG-laden PLD-MNA was safe and required only 6 treatments and one
155                       At the cellular level, PLD and its reaction product, phosphatidate, interact wi
156 cin (DOX), delivered by pegylated liposomes (PLD), to murine lung (3LL) and breast (4T1) tumors.
157                         In polycystic liver (PLD) and kidney (PKD) diseases, increased cyclic adenosi
158 ogical and pathological effects of localized PLD signaling.
159 at the beginning of the season with a longer PLD, or at the end of the reproductive season.
160 tudies using a combination of small molecule PLD inhibitors and siRNA knockdowns establish phosphatid
161 t mice and the development of small molecule PLD-specific inhibitors, in vivo roles for PLD1 in cance
162                                However, most PLD assays developed so far are either discontinuous or
163 osphatidylethanolamine phospholipase D (NAPE-PLD) (EC 3.1.4.4) catalyzes the final step in the biosyn
164 osphatidylethanolamine phospholipase D (NAPE-PLD) catalyzes the cleavage of membrane NAPEs into bioac
165 osphatidylethanolamine phospholipase D (NAPE-PLD) is regarded as the main enzyme responsible for the
166 hosphatidylethanolaminephospholipase D (NAPE-PLD), diacylglycerol lipase (DAGL), or phospholipase C (
167 d inflammation, but a lack of effective NAPE-PLD inhibitors has been a major obstacle to elucidating
168 t to a previously unrecognized role for NAPE-PLD in the regulation of dopamine neuron function, which
169 ls and have significant selectivity for NAPE-PLD versus other tissue-associated lipases.
170                            Furthermore, NAPE-PLD silencing protects cathecolamine-producing SH-SY5Y c
171 tituted dichlorophenes potently inhibit NAPE-PLD in cultured cells and have significant selectivity f
172         Both also effectively inhibited NAPE-PLD activity in cultured HEK293 cells.
173 le acid lithocholic acid (LCA) inhibits NAPE-PLD activity (with an IC(50) of 68 mum), but LCA is also
174 acological tool compound to investigate NAPE-PLD function in vitro and in vivo.
175 ccumulation is enhanced in mice lacking NAPE-PLD, which display a substantial reduction in 6-OHDA-ind
176 jor obstacle to elucidating the role of NAPE-PLD and N-acyl-ethanolamide biosynthesis in these proces
177 utors to the neuroprotective effects of NAPE-PLD deletion, including suppression of Rac1 activity and
178 imidine-4-carboxamides as inhibitors of NAPE-PLD that led to the identification of LEI-401.
179 t selective small-molecule inhibitor of NAPE-PLD, ARN19874, has been reported (having an IC(50) of 34
180   To identify more potent inhibitors of NAPE-PLD, here we used a quenched fluorescent NAPE analog, PE
181                                 Reduced NAPE-PLD expression and activity may contribute to obesity an
182 -401) as the first potent and selective NAPE-PLD inhibitor that decreased NAEs in the brains of freel
183 these results indicate that DGKzeta, but not PLD, plays an important role in mechanically induced inc
184 mbination miR-887+miR-3619 abolished >90% of PLD enzymatic activity.
185 edly though, we found that the activation of PLD is not necessary for the mechanically induced increa
186 ential novel therapeutic target for cases of PLD.
187               We assessed the correlation of PLD-Q total score with European Organization for Researc
188                  There was no correlation of PLD-Q total score with liver volume (NL, r = 0.138; P =
189  C, allowing for a reliable determination of PLD activity in crude protein extract samples.
190 ions for on-going therapeutic development of PLD small molecule inhibitors.
191 d, indicating that the inhibitory effects of PLD and PA on AMPK activity are mediated by mTOR.
192 11 preclinical studies comparing efficacy of PLD and conventional doxorubicin in tumor-bearing mice.
193        This is the story of the evolution of PLD from being involved in a large number of seemingly u
194                        Directed evolution of PLD using yeast membrane display and IMPACT, a chemoenzy
195 on in later starvation induces expression of PLD-targeting microRNA 203 (miR-203), miR-887, miR-3619-
196                                Inhibition of PLD enzymatic activity and subsequent Akt activation dec
197 PLD and mTOR, and suggest that inhibitors of PLD or mTOR would be beneficial in cancers where PKC ove
198  chemical inhibition and RNA interference of PLD delayed viral entry and reduced viral titers in vitr
199                The particular involvement of PLD in cell migration is accomplished: (a) through the a
200 ustained PKC activity and the involvement of PLD in this process.
201                         Here we show loss of PLD blocks ethanol-mediated hyperactivity in Drosophila
202                 During illumination, loss of PLD resulted in an enhanced reduction in rhabdomere size
203 ly, powdered allergens delivered by means of PLD-MNA preferentially attracted immunoregulatory macrop
204 lated from both PCK rats (an animal model of PLD) and humans with PLD.
205 udies using inhibitors and overexpression of PLD proteins indicate that PLD1 and PLD2 play positive r
206 ce for the emerging tumorigenic potential of PLD, the role of the microenvironment, and putative conn
207  levels of phosphatidic acid, the product of PLD activity and were rescued by reconstitution with cat
208 l starvation, an elevated PA (the product of PLD enzymatic activity) activates mTOR and S6K, known to
209                               The product of PLD, phosphatidic acid, activates the enhancer in a rapa
210                            The proportion of PLD tested was predicted to increase from 13.6% to 67.0%
211 site in a transphosphatidylation reaction of PLD's lipid substrate, phosphatidylcholine.
212 soform-specific spatiotemporal regulation of PLD activity and further our understanding of the role o
213 e that Arf6 is involved in the regulation of PLD activity and PA synthesis required for efficient pha
214 rovide evidence for reciprocal regulation of PLD by AMPK and regulation of AMPK by PLD and PA.
215 hat DGKzeta is a novel negative regulator of PLD activity in this system that occurs through an inhib
216                           Reproducibility of PLD-Q was excellent (NL, r = 0.94; US, 0.96).
217   However, little is known about the role of PLD in M(1) receptor signaling in native systems, and it
218 ot classification) and PLD-Q total scores of PLD patients with general controls and polycystic kidney
219 ening strategy involves routine screening of PLD who indicate they are from HCV high-risk populations
220 dies revealed several intracellular sites of PLD-mediated PA synthesis.
221 ed for studying the substrate specificity of PLD, together with its kinetic parameters, using natural
222 (PM) induced by phorbol ester stimulation of PLD were rapidly internalized via apparent nonvesicular
223                               Suppression of PLD activity resulted in elevated AMPK activity.
224 that determine the overall phase behavior of PLDs.
225 that enables predictions of full binodals of PLDs from their sequences.
226 ull binodals that quantify concentrations of PLDs within coexisting dilute and dense phases as a func
227 ct as adaptation to the emotional content of PLDs.
228 dimerization system to create an optogenetic PLD (optoPLD).
229 GFR), and JAK3) that are activated by it, or PLD becomes the target substrate.
230 M3814 with PLD showed enhanced activity over PLD as a single agent.
231 the lipid-metabolizing enzyme phospholipaseD(PLD) is a novel regulator of Akt inGBM.Studies using a c
232 enables mimicry of endogenous, physiological PLD signaling.
233 questionnaire that assesses symptoms in PLD (PLD-Q).
234 ellular motility, and as such, they have put PLD at center stage in cancer research.
235 -887, miR-3619-5p, and miR-182, which reduce PLD translation.
236 nced decreased connectivity but when reduced PLD was added as an effect, ~65% of connections were wea
237 nectin, which was blocked by down-regulating PLD or Rap1A or by treatment with a beta1 integrin neutr
238 was mild PKD and variable, including severe, PLD.
239 tly under ocean warming because of shortened PLDs.
240 iseases (ADPLD), which result in significant PLD with minimal PKD.
241             The porous MOM with the smallest PLD suitable for physisorption, dia-7i-1-Co, was thereby
242 However, after prolonged (>12-h) starvation, PLD levels return to basal or lower levels.
243 nd conversely, activation of AMPK suppressed PLD activity.
244  mutation of lysine 230 of FAM83B suppressed PLD activity and MAPK signaling.
245 egorization of the emotion expressed in test PLDs.
246       The Arabidopsis (Arabidopsis thaliana) PLD family consists of 12 members, and for some of these
247 ates phospholipase D (PLD) activity and that PLD co-localizes with influenza during infection.
248              These findings demonstrate that PLD plays a critical role in the ability of M(1) PAMs to
249 melanogaster (fruit fly), demonstrating that PLD mediates behavioral responses to alcohol in vivo.
250 fore further validate the critical role that PLD plays in gas adsorption by porous MOMs.
251                                 We show that PLD expression is increased in four breast cancer cell l
252                            Here we show that PLD is a component of wild-type cilia but is enriched ap
253 y following PA flux in the cell we show that PLD is involved in an initial increase in PA upon recept
254             Biochemical analysis showed that PLD deficiency affected activation of the PI3K pathway a
255 bitors and PLD knockout mice, we showed that PLD was necessary for the induction of M(1)-dependent lo
256             Together these data suggest that PLD facilitates the rapid endocytosis of influenza virus
257                                          The PLD pathway is also responsive to nutrients.
258 al feedback mechanism involving AMPK and the PLD/mTOR signaling node in cancer cells with therapeutic
259 binant Vigna unguiculata PLD, as well as the PLD from Streptomyces chromofuscus, cabbage, or peanuts,
260 LD activity and mTOR function, with both the PLD inhibitor FIPI and rapamycin reducing cell growth by
261 lerosis complex subunit 2 (TSC2) exploit the PLD-PA pathway and thereby sustain mTORC1 activation at
262 can supplant water as the nucleophile in the PLD active site in a transphosphatidylation reaction of
263 nuclear localization sequence located in the PLD.
264 Genetic and in vitro characterization of the PLD from Escherichia coli MS 200-1 showed this enzyme is
265 e small GTPase Arf6 in the activation of the PLD isoforms during FcgammaR-mediated phagocytosis.
266 , and recapitulated with the addition of the PLD product phosphatidic acid (PA).
267 ablish phosphatidic acid, the product of the PLD reaction, as an essential component for the membrane
268 late scale, thus allowing measurement of the PLD-catalyzed reaction rate parameters.
269            PLD patients scored higher on the PLD-Q total score than general controls (NL, 42 vs. 17;
270 pH 4, where His residues are protonated, the PLD is disordered and flexible, except for a partially p
271 r with IPOD sites or with PB/SG requires the PLD, whose activity is differentially regulated by the N
272 genously added phosphatidic acid rescued the PLD-inhibition phenotype, but only when PTPD2 was presen
273 brane phospholipid biosynthesis, whereas the PLD and DGK pathways are activated in response to growth
274 autophagy was restored by treatment with the PLD product, phosphatidic acid (PA) or adenoviral PLD1 e
275 ent, a negative regulatory function for this PLD isoform is proposed.
276                           Unexpectedly, this PLD is only distantly related to characterized PLDs from
277                                        Thus, PLD and PA are intrinsic components of cell adhesion, wh
278 ore, biased M(1) PAMs that did not couple to PLD not only failed to potentiate orthosteric agonist-in
279 atients with massive hepatomegaly related to PLD: the exposure left lateral sectionectomy (ELLS).
280           Inhibition of PLD2, one of the two PLD members, was sufficient to eliminate most of the PA
281 g the purified recombinant Vigna unguiculata PLD, as well as the PLD from Streptomyces chromofuscus,
282                                        Using PLD inhibitors and PLD knockout mice, we showed that PLD
283 ur FeSexTe1-x thin films were fabricated via PLD using a Fe0.94Se0.45Te0.55 target, the precisely mea
284 ent electrophysiological responses that were PLD independent.
285  PA upon receptor stimulation; however, when PLD is blocked, the cell compensates by increasing PA pr
286          We propose an alcohol pathway where PLD produces lipid-alcohol metabolites that bind to and
287 direct evidence for a feedback loop, whereby PLD induction upon starvation leads to PA, which induces
288  net monetary benefit of screening the whole PLD population was CHF 23 298 046 and CHF 4298 per perso
289 a spatio-temporal manner that coincides with PLD activity timing.
290 ine (8HQ) following Ca(2+) complexation with PLD-generated PA.
291 re efficiently rescued upon cotreatment with PLD inhibitors and S1P.
292 ats (an animal model of PLD) and humans with PLD.
293 ot an F666D mutant that cannot interact with PLD, was sufficient to enhance cell growth and increase
294                The combination of M3814 with PLD showed enhanced activity over PLD as a single agent.
295      We analyzed data from 107 patients with PLD from 3 randomized placebo-controlled trials (67 rece
296 collected data from individual patients with PLD to identify subgroups that benefit most from SA ther
297 alysis of data from individual patients with PLD, treatment with somatostatin analogues is equally ef
298 ntly increased survival in mice treated with PLD compared to conventional doxorubicin (HR 0.39; 95% C
299 d polycystic kidney disease patients without PLD (22 points).
300 d polycystic kidney disease patients without PLD.

 
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