ライフサイエンスコーパス: PLD

1 PLD activation and VWF secretion induced by Stx1B were a

2 PLD are characterized by the formation and progressive e

3 PLD catalyzes the hydrolysis of phosphatidylcholine into

4 PLD has an acceptable safety profile in patients with ad

5 PLD is a downstream target of the GTPase Rheb, which is

6 PLD patients scored higher on the PLD-Q total score than

7 PLD produces phosphatidic acid (PA), a bioactive lipid i

8 PLD represents a potential target for the rational devel

9 PLD should be considered as congenital diseases of chola

10 PLD, because of PC2 deficiency, represents the first exa

11 PLD-Q is a valid, reproducible, and sensitive disease-sp

12 PLDs are caused by mutations in genes involved in intrac

13 PLDs were found to be able to catalyze phospholipid head

14 We identified 16 PLD-related symptoms (total score 0-100 points) by liter

15 cells, these kinases greatly enhance (>200%) PLD activity following protein-protein interaction throu

16 ch (n = 200) and United States (US; n = 203) PLD patients.

17 were randomly assigned (patupilone, n = 412; PLD, n = 417).

18 t of rapamycin (mTOR)/S6 kinase pathway in a PLD- and endocytosis-dependent manner, with both pharmac

19 Catalytically active PLD enhanced expression of EGFR in human breast cancer c

20 by reconstitution with catalytically active PLD.

21 Although PLD has been widely implicated in the generation of PA n

22 PIP(2) and PLD may themselves promote autophagosome biogenesis by i

23 known about the connection between AMPK and PLD.

24 D severity stages (Gigot classification) and PLD-Q total scores of PLD patients with general controls

25 se Cbeta3 (PLCbeta3), PLCdelta1, DGKzeta and PLD are all downstream of receptor activation.

26 imal models of polycystic kidney disease and PLD, and might be developed as therapeutics for these di

27 or the olaparib 200 mg, olaparib 400 mg, and PLD groups, respectively.

28 8% for olaparib 200 mg, olaparib 400 mg, and PLD, respectively; differences were not statistically si

29 rimary end point, between the patupilone and PLD arms (P = .195; hazard ratio, 0.93; 95% CI, 0.79 to

30 endosomes defined by the presence of PKC and PLD (the pericentrion), which results in significant dif

31 more beneficial for the treatment of PKD and PLD.

32 2.7 months for the vintafolide plus PLD and PLD-alone arms, respectively (hazard ratio [HR], 0.63; 9

33 nsfer DNA knockout lines for all Arabidopsis PLD genes revealed that PLDdelta is involved in penetrat

34 fic questionnaire that can be used to assess PLD-related symptoms in clinical care and future researc

35 ) together with basic pK(a) values to assign PLD inducing potential to a compound.

36 Correlation between PLD-Q total score and EORTC symptom scale (The Netherlan

37 mportance of functional interactions between PLD and Rac in the biological response of cell migration

38 While inhibition of both PLD and DGK had no effect on the overall ERK activity, i

39 y, this condition was also dependent on both PLD and mTOR activity.

40 These biological effects also required both PLD activity and mTOR function, with both the PLD inhibi

41 cogenic signaling pathway that requires both PLD and mTOR, and suggest that inhibitors of PLD or mTOR

42 ts is the generation of phosphatidic acid by PLD.

43 ion of PLD by AMPK and regulation of AMPK by PLD and PA.

44 Substrate phosphorylation was blocked by PLD inhibitors and was not observed in response to activ

45 The second is evidenced by PLD association with the growth factor receptor-bound pr

46 stabilization also occurred, as indicated by PLD resistance to cycloheximide-induced EGFR protein deg

47 fatty acid chains, such as those produced by PLD, are capable of displacing DEPTOR and activating mTO

48 nhibition of phosphatidic acid production by PLD increased the penetration rate of Bgh spores on wild

49 found that PA was generated sequentially by PLD and DGK in epidermal growth factor (EGF)-stimulated

50 c questionnaires lack sensitivity to capture PLD-related symptoms, a prerequisite to determine effect

51 type BBSomes were introduced into bbs cells, PLD was rapidly removed from the mutant cilia, indicatin

52 me-dependent mechanism for exporting ciliary PLD.

53 To test discriminative validity, we compared PLD-Q total scores of patients with different PLD severi

54 opment of a direct, specific, and continuous PLD assay that is based on the chelation-enhanced fluore

55 ment in OS compared with the active control, PLD.

56 Conversely, PLD activation and VWF exocytosis induced by Stx2B were

57 phase of a process that continuously cycles PLD through cilia.

58 ssociated signaling protein phospholipase D (PLD) accumulates abnormally in cilia of Chlamydomonas re

59 influenza virus stimulates phospholipase D (PLD) activity and that PLD co-localizes with influenza d

60 FAM83B expression increases Phospholipase D (PLD) activity, and that suppression of PLD1 activity pre

61 te (PIP(2)) and in inducing phospholipase D (PLD) activity.

62 StxB transiently increased phospholipase D (PLD) activity.

63 s contain a light-dependent phospholipase D (PLD) activity.

64 idic acid (PA) generated by phospholipase D (PLD) and diacylglycerol kinase (DGK).

65 of the PA-producing enzyme phospholipase D (PLD) and increased localization of PLD1 to ATG16L1-posit

66 We show here that phospholipase D (PLD) and its enzymatic reaction product, phosphatidic ac

67 Phospholipase D (PLD) and its product, phosphatidic acid, have been estab

68 verexpression of the enzyme phospholipase D (PLD) and its reaction product, phosphatidic acid (PA).

69 as the ED peptide activates phospholipase D (PLD) and MMP2, but not MMP9.

70 Phospholipase D (PLD) and small GTPases are vital to cell signaling.

71 Phospholipase D (PLD) catalyzes the conversion of phosphatidylcholine to

72 The membrane-active enzyme phospholipase D (PLD) catalyzes the hydrolysis of the phosphodiester bond

73 disruption of A. baumannii phospholipase D (PLD) caused a reduction in the organism's ability to thr

74 ted as a helicase domain, a phospholipase D (PLD) domain, a DUF1998 domain and a gene of unknown func

75 of cellular PA synthesis by phospholipase D (PLD) enzymes is reported.

76 Phospholipase D (PLD) enzymes play a double vital role in cells: they mai

77 and Bce14579I belong to the phospholipase D (PLD) family of endonucleases that are widely distributed

78 Phospholipase D (PLD) generates a metabolite, phosphatidic acid, that fac

79 riments were performed with phospholipase D (PLD) in a Ca(2+) dependent fashion.

80 of phosphatidic acid (PA), phospholipase D (PLD) is strongly involved in vesicular trafficking and c

81 Phospholipase D (PLD) proteins are enzymes that catalyze the hydrolysis o

82 Phospholipase D (PLD) signaling plays a critical role in cell growth and

83 The Phospholipase D (PLD) superfamily is linked to neurological disease, canc

84 ggested that sperm activate phospholipase D (PLD) to elevate phosphatidic acid (PA).

85 (PA), which is generated by phospholipase D (PLD) via hydrolysis of phosphatidylcholine.

86 mall molecule inhibitors of phospholipase D (PLD), an enzyme that produces phosphatidic acid in cells

87 on of the mTORC1 regulator, phospholipase D (PLD), and recapitulated with the addition of the PLD pro

88 bolic pathways generate PA: phospholipase D (PLD), diacylglycerol kinase (DGK), and lysophosphatidic

89 he enzyme that produces it, phospholipase D (PLD), downregulate EGFR expression.

90 dic acid, as synthesized by phospholipase D (PLD), enhances cancer cell survival.

91 sphatidic acid, produced by phospholipase D (PLD), has been shown to take part in both abiotic and bi

92 tween the signaling protein phospholipase D (PLD), phosphatidic acid (PA), and a specific set of micr

93 s a similar overall fold as phospholipase D (PLD), phosphatidylserine synthase (PSS) and tyrosyl-DNA

94 breast cancers in vitro is phospholipase D (PLD), which is also involved in cell migration.

95 of an enzymatically active phospholipase D (PLD), with the PLD2 isoform being more relevant than PLD

96 esis and the product of the phospholipase D (PLD)-catalyzed hydrolysis of phosphatidylcholine.

97 amycin) signaling through a phospholipase D (PLD)-dependent increase in the concentration of phosphat

98 and PKCbetaII induces their phospholipase D (PLD)-dependent internalization and translocation to a su

99 11 clearly demonstrate that phospholipase D (PLD)-dependent production of membrane phosphatidic acid

100 d mediated through RhoA and phospholipase D (PLD).

101 ibuted to the activation of phospholipase D (PLD).

102 olinergic agonists activate phospholipase D (PLD).

103 ion is dependent on PKC and phospholipase D (PLD).

104 ted by the signaling enzyme phospholipase D (PLD).

105 -x thin films using pulsed laser deposition (PLD) enables improving their superconducting transition

106 lm was grown by the pulsed laser deposition (PLD) method and it exhibits a broad transparent window f

107 glass substrates by pulsed laser deposition (PLD) technique.

108 glass substrates by pulsed laser deposition (PLD) technique.

109 The developed PLD-Q was validated in Dutch (n = 200) and United States

110 it 1D channels with pore limiting diameters (PLDs) of 1.64, 2.90, 5.06, 5.28, 8.57, 8.83, 11.86, and

111 LD-Q total scores of patients with different PLD severity stages (Gigot classification) and PLD-Q tot

112 Treatment of polycystic liver disease (PLD) focuses on symptom improvement.

113 Polycystic liver disease (PLD) is a member of the cholangiopathies, a group of liv

114 t in patients with polycystic liver disease (PLD), short-term treatment with somatostatin analogues (

115 kidney disease and polycystic liver disease (PLD), the normally nonproliferative hepato-renal epithel

116 nial aneurysms and polycystic liver disease (PLD), which can be severe and associated with significan

117 cause progressive polycystic liver disease (PLD).

118 Polycystic liver diseases (PLD) are inherited disorders of the biliary epithelium,

119 or fearful whole-body point-light displays (PLDs) as adapters and were then asked to perform an expl

120 on within the pyrophosphorylase-like domain (PLD) of eIF2Bepsilon for nucleotide exchange.

121 ng through its N-terminal prion-like domain (PLD) to the C-terminal domain of RNA polymerase II.

122 requires low-complexity prion-like domains (PLDs) within paraspeckle proteins.

123 Autosomal-dominant PLD (ADPLD) with no or very few renal cysts is a separat

124 etics determined the delivery of DOX and DOX-PLD to the same tumor phenotype, collagen content determ

125 chemotherapy-loaded pegylated liposome (DOX-PLD) in tumor vasculature.

126 content determined the extravasation of DOX-PLD to different tumor phenotypes.

127 meability of that vessel permeability to DOX-PLD, indicating that collagen content may offer a biophy

128 mbined with pegylated liposomal doxorubicin (PLD) compared with PLD alone.

129 nvestigated pegylated liposomal doxorubicin (PLD) in a clearly defined patient population with advanc

130 th those of pegylated liposomal doxorubicin (PLD) in patients with platinum-refractory or -resistant

131 laparib and pegylated liposomal doxorubicin (PLD) in this patient population.

132 Since pegylated liposomal doxorubicin (PLD) was the most prevalent formulation in these clinica

133 al reductions in planktonic larval duration (PLD) associated with ocean warming, given current socioe

134 ect determination of choline released during PLD-catalyzed phosphatidylcholine hydrolysis, making its

135 We report here that elevated PLD activity in human cancer cells is dependent on both

136 und an adaptation after-effect for emotional PLDs, indicating the existence of a neural representatio

137 CF-7 breast cancer cells have low endogenous PLD enzymatic activity and cell invasion, concomitant wi

138 hotoreceptors, during illumination, enhanced PLD activity was sufficient to clear RLVs from the cell

139 ed by the key phospholipid metabolism enzyme PLD.

140 for DISARM-mediated defence, with the fifth (PLD) being redundant for defence against some of the pha

141 Therefore, the parallel in vitro assay for PLD was discontinued.

142 dian PFS of 5.5 compared with 1.5 months for PLD alone (HR, 0.38; 95% CI, 0.17 to 0.85; P = .013).

143 We calculate a latency time of <650 mus for PLD activation by mixing.

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 gy, we find that the eIF2Bepsilon and -gamma PLDs and a shared second domain predicted to form a left

147 This easy to handle PLD assay constitutes, to our knowledge, the first direc

148 Thus, during illumination, PLD activity couples endocytosis of RLVs with their recy

149 ssect PA-dependent signaling pathways, image PLD activity in disease, and remodel intracellular membr

150 ssion of AMPK activity led to an increase in PLD activity, and conversely, activation of AMPK suppres

151 s well as the starvation-induced increase in PLD activity, are altered by wortmannin, a phosphatidyli

152 ggesting that, given potential reductions in PLD due to ocean warming, future marine reserve networks

153 ific questionnaire that assesses symptoms in PLD (PLD-Q).

154 The increased PLD activity is engaged by hyperactivation of epidermal

155 determining a compound's potential to induce PLD than the combined use of basic pK(a) and ClogP value

156 Amino acid- and glucose-induced PLD and mTORC1 activity were also dependent on the GTPas

157 At the cellular level, PLD and its reaction product, phosphatidate, interact wi

158 with opposite effects on cellular PA levels, PLD inhibition had opposite effects on EGFR internalizat

159 unique, unanticipated phospholipase D-like (PLD) domain at the C terminus that binds membranes.

160 53) and members of the phospholipase D-like (PLD) family, are related to proteins that modify membran

161 cin (DOX), delivered by pegylated liposomes (PLD), to murine lung (3LL) and breast (4T1) tumors.

162 In polycystic liver (PLD) and kidney (PKD) diseases, increased cyclic adenosi

163 low from other compartments or by modulating PLD activity independently of the mammalian target of ra

164 tudies using a combination of small molecule PLD inhibitors and siRNA knockdowns establish phosphatid

165 t mice and the development of small molecule PLD-specific inhibitors, in vivo roles for PLD1 in cance

166 pore-forming peptide gramicidin A to monitor PLD activity, the work presented here reveals the kineti

167 However, most PLD assays developed so far are either discontinuous or

168 Sp1 is involved in regulating baseline NAPE-PLD expression but not in the transcriptional suppressio

169 hosphatidylethanolaminephospholipase D (NAPE-PLD), diacylglycerol lipase (DAGL), or phospholipase C (

170 osphatidylethanolamine-phospholipase D (NAPE-PLD), glycerophosphodiesterase (GDE1), and CB1R protein

171 lethanolamine-specific phospholipase D (NAPE-PLD), which catalyzes the production of PEA and other li

172 osphatidylethanolamine phospholipase D [NAPE-PLD] and diacylglycerol lipase alpha [DAGLalpha]) in the

173 tional activation of the genes encoding NAPE-PLD, GDE1, and CB1R proteins, respectively.

174 a compensatory mechanism distinct from NAPE-PLD.

175 Moreover, NAPE-PLD-deficient mice fail to mount a normal inflammatory r

176 d in peritoneal macrophages from mutant NAPE-PLD-deficient mice, in which PEA is produced through a c

177 t that proinflammatory stimuli suppress NAPE-PLD expression and PEA biosynthesis in macrophages and t

178 lation of histone proteins bound to the NAPE-PLD promoter, an effect that is blocked by the histone d

179 these results indicate that DGKzeta, but not PLD, plays an important role in mechanically induced inc

180 mbination miR-887+miR-3619 abolished >90% of PLD enzymatic activity.

181 ased ABA- and H(2)O(2)-induced activation of PLD and stomatal sensitivity to ABA.

182 edly though, we found that the activation of PLD is not necessary for the mechanically induced increa

183 ential novel therapeutic target for cases of PLD.

184 We assessed the correlation of PLD-Q total score with European Organization for Researc

185 There was no correlation of PLD-Q total score with liver volume (NL, r = 0.138; P =

186 stered to receive a maximum of six cycles of PLD 20 mg/m2 on days 1 and 15, every 28 days (one cycle)

187 C, allowing for a reliable determination of PLD activity in crude protein extract samples.

188 ions for on-going therapeutic development of PLD small molecule inhibitors.

189 d, indicating that the inhibitory effects of PLD and PA on AMPK activity are mediated by mTOR.

190 11 preclinical studies comparing efficacy of PLD and conventional doxorubicin in tumor-bearing mice.

191 The efficacy of PLD seems promising.

192 However, the efficacy of PLD was greater than expected.

193 Importantly, entry of PLD into cilia is BBSome and IFT independent.

194 This is the story of the evolution of PLD from being involved in a large number of seemingly u

195 on in later starvation induces expression of PLD-targeting microRNA 203 (miR-203), miR-887, miR-3619-

196 signed to receive an intravenous infusion of PLD 30 mg/m(2) followed by a 3-hour infusion of trabecte

197 Inhibition of PLD activity or shRNA-mediated PLD1 knockdown abolished

198 Pharmacological inhibition of PLD and genetic ablation of PLD1 in mouse cells decrease

199 Inhibition of PLD enzymatic activity and subsequent Akt activation dec

200 Furthermore, inhibition of PLD results in higher levels of Tau and p62 aggregates i

201 d two different small-molecule inhibitors of PLD activity (5-fluoro-2-indolyl des-chlorohalopemide an

202 PLD and mTOR, and suggest that inhibitors of PLD or mTOR would be beneficial in cancers where PKC ove

203 chemical inhibition and RNA interference of PLD delayed viral entry and reduced viral titers in vitr

204 The particular involvement of PLD in cell migration is accomplished: (a) through the a

205 In this study, the involvement of PLD in the interaction between Arabidopsis (Arabidopsis

206 ustained PKC activity and the involvement of PLD in this process.

207 her a protein-protein disruption nor lack of PLD activity completely negates cup formation or phagocy

208 During illumination, loss of PLD resulted in an enhanced reduction in rhabdomere size

209 chanism, we determined that the machinery of PLD-induced cell invasion is mediated by phosphatidic ac

210 lated from both PCK rats (an animal model of PLD) and humans with PLD.

211 udies using inhibitors and overexpression of PLD proteins indicate that PLD1 and PLD2 play positive r

212 ce for the emerging tumorigenic potential of PLD, the role of the microenvironment, and putative conn

213 levels of phosphatidic acid, the product of PLD activity and were rescued by reconstitution with cat

214 l starvation, an elevated PA (the product of PLD enzymatic activity) activates mTOR and S6K, known to

215 The product of PLD, phosphatidic acid, activates the enhancer in a rapa

216 rovide evidence for reciprocal regulation of PLD by AMPK and regulation of AMPK by PLD and PA.

217 hat DGKzeta is a novel negative regulator of PLD activity in this system that occurs through an inhib

218 Reproducibility of PLD-Q was excellent (NL, r = 0.94; US, 0.96).

219 ot classification) and PLD-Q total scores of PLD patients with general controls and polycystic kidney

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 Suppression of PLD activity resulted in elevated AMPK activity.

223 ct as adaptation to the emotional content of PLDs.

224 ance against Bgh, and chemical inhibition of PLDs in plants mutated in PLDdelta indicated that this i

225 ncreases in mTORC1 activity are dependent on PLD.

226 day or 400 mg twice per day continuously or PLD 50 mg/m(2) intravenously every 28 days.

227 GFR), and JAK3) that are activated by it, or PLD becomes the target substrate.

228 of trabectedin 1.1 mg/m(2) every 3 weeks or PLD 50 mg/m(2) every 4 weeks.

229 (10 mg/m(2) intravenously every 3 weeks) or PLD (50 mg/m(2) intravenously every 4 weeks).

230 the lipid-metabolizing enzyme phospholipaseD(PLD) is a novel regulator of Akt inGBM.Studies using a c

231 Phospholipidosis (PLD) is a lysosomal storage disorder induced by compound

232 questionnaire that assesses symptoms in PLD (PLD-Q).

233 5.0 and 2.7 months for the vintafolide plus PLD and PLD-alone arms, respectively (hazard ratio [HR],

234 Vintafolide plus PLD is the first combination to demonstrate an improveme

235 ellular motility, and as such, they have put PLD at center stage in cancer research.

236 ipids, but the functions of CT153 and the PZ PLDs (pzPLDs) are unknown.

237 -887, miR-3619-5p, and miR-182, which reduce PLD translation.

238 nced decreased connectivity but when reduced PLD was added as an effect, ~65% of connections were wea

239 nectin, which was blocked by down-regulating PLD or Rap1A or by treatment with a beta1 integrin neutr

240 was mild PKD and variable, including severe, PLD.

241 tly under ocean warming because of shortened PLDs.

242 iseases (ADPLD), which result in significant PLD with minimal PKD.

243 The porous MOM with the smallest PLD suitable for physisorption, dia-7i-1-Co, was thereby

244 However, after prolonged (>12-h) starvation, PLD levels return to basal or lower levels.

245 nd conversely, activation of AMPK suppressed PLD activity.

246 mutation of lysine 230 of FAM83B suppressed PLD activity and MAPK signaling.

247 egorization of the emotion expressed in test PLDs.

248 ates phospholipase D (PLD) activity and that PLD co-localizes with influenza during infection.

249 In conclusion, we propose that PLD is involved in defense signaling in nonhost resistan

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 Here we show that PLD, although highly active, is not responsible for the

255 Biochemical analysis showed that PLD deficiency affected activation of the PI3K pathway a

256 Together these data suggest that PLD facilitates the rapid endocytosis of influenza virus

257 an increase in cellular PA, suggesting that PLD activity negatively regulates PA synthesis by other

258 The PLD pathway is also responsive to nutrients.

259 al feedback mechanism involving AMPK and the PLD/mTOR signaling node in cancer cells with therapeutic

260 binant Vigna unguiculata PLD, as well as the PLD from Streptomyces chromofuscus, cabbage, or peanuts,

261 LD activity and mTOR function, with both the PLD inhibitor FIPI and rapamycin reducing cell growth by

262 was higher in the patupilone arm than in the PLD arm (15.5% v 7.9%; odds ratio, 2.11; 95% CI, 1.36 to

263 (43%) and hand-foot syndrome (41.8%) in the PLD arm.

264 nuclear localization sequence located in the PLD.

265 , and recapitulated with the addition of the PLD product phosphatidic acid (PA).

266 ablish phosphatidic acid, the product of the PLD reaction, as an essential component for the membrane

267 late scale, thus allowing measurement of the PLD-catalyzed reaction rate parameters.

268 PLD patients scored higher on the PLD-Q total score than general controls (NL, 42 vs. 17;

269 r with IPOD sites or with PB/SG requires the PLD, whose activity is differentially regulated by the N

270 genously added phosphatidic acid rescued the PLD-inhibition phenotype, but only when PTPD2 was presen

271 termine whether cholinergic agonists use the PLD pathway to alter protein secretion and to identify t

272 brane phospholipid biosynthesis, whereas the PLD and DGK pathways are activated in response to growth

273 autophagy was restored by treatment with the PLD product, phosphatidic acid (PA) or adenoviral PLD1 e

274 dentified extensive interactions between the PLDs and left-handed beta helix domains that form the eI

275 Thus, PLD and PA are intrinsic components of cell adhesion, wh

276 ptor stimulations have been shown to lead to PLD activation and PA generation.

277 ens were randomly assigned at a 2:1 ratio to PLD (50 mg/m(2) intravenously [IV] once every 28 days) w

278 Median PFS was 7.3 months with trabectedin/PLD v 5.8 months with PLD (hazard ratio, 0.79; 95% CI, 0

279 Inhibition of PLD2, one of the two PLD members, was sufficient to eliminate most of the PA

280 Unexpectedly, PLD inhibition caused an increase in cellular PA, sugges

281 g the purified recombinant Vigna unguiculata PLD, as well as the PLD from Streptomyces chromofuscus,

282 P = .66) for combined olaparib doses versus PLD.

283 ur FeSexTe1-x thin films were fabricated via PLD using a Fe0.94Se0.45Te0.55 target, the precisely mea

284 PA upon receptor stimulation; however, when PLD is blocked, the cell compensates by increasing PA pr

285 direct evidence for a feedback loop, whereby PLD induction upon starvation leads to PA, which induces

286 a spatio-temporal manner that coincides with PLD activity timing.

287 ed liposomal doxorubicin (PLD) compared with PLD alone.

288 ine (8HQ) following Ca(2+) complexation with PLD-generated PA.

289 ats (an animal model of PLD) and humans with PLD.

290 ot an F666D mutant that cannot interact with PLD, was sufficient to enhance cell growth and increase

291 F663D) that is defective in interaction with PLD and in internalization.

292 onths with trabectedin/PLD v 5.8 months with PLD (hazard ratio, 0.79; 95% CI, 0.65 to 0.96; P = .0190

293 We analyzed data from 107 patients with PLD from 3 randomized placebo-controlled trials (67 rece

294 collected data from individual patients with PLD to identify subgroups that benefit most from SA ther

295 proved health perception among patients with PLD, and had an acceptable side effect profile.

296 alysis of data from individual patients with PLD, treatment with somatostatin analogues is equally ef

297 mice, healthy individuals, and patients with PLD.

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.