ライフサイエンスコーパス: cholesterol depletion

1 s reduced (-24.5%) following statin-mediated cholesterol depletion.

2 f inhibition by AME is distinct from that by cholesterol depletion.

3 y disrupting the integrity of lipid rafts by cholesterol depletion.

4 secretion, with normal secretion restored by cholesterol depletion.

5 l orientation in response to statin-mediated cholesterol depletion.

6 ngly dependent on temperature conditions and cholesterol depletion.

7 inding, but binding is sensitive to membrane cholesterol depletion.

8 The suppression was fully reversible by cholesterol depletion.

9 viral gp41 fusion protein that counteracted cholesterol depletion.

10 when fully solubilized and were resistant to cholesterol depletion.

11 )P2] to the plasma membrane is reduced after cholesterol depletion.

12 nger facilitative effect on the current than cholesterol depletion.

13 t/PKB in response to EGF are not affected by cholesterol depletion.

14 by cholesterol feeding but was increased by cholesterol depletion.

15 ased by dietary cholesterol and decreased by cholesterol depletion.

16 M cholesterol and show endoplasmic reticulum cholesterol depletion.

17 tion but did not affect virus sensitivity to cholesterol depletion.

18 general, activation of SREBPs occurs during cholesterol depletion.

19 tegrin alpha2 expression were unchanged upon cholesterol depletion.

20 ut was unaffected by caveolin-1 knockdown or cholesterol depletion.

21 -beta in the absence of Dab2 is disrupted by cholesterol depletion.

22 SREBP-2 LDLR promoter binding in response to cholesterol depletion.

23 ctivation and current facilitation following cholesterol depletion.

24 (2) human prostate cells exposed acutely to cholesterol depletion.

25 -cholesterol diet, and facilitated following cholesterol depletion.

26 liminated by the Tyr(4)(5)(8) mutation or by cholesterol depletion.

27 ects that are difficult to ascribe solely to cholesterol depletion.

28 ndent endocytosis, which is not sensitive to cholesterol depletion.

29 dense regions of the sucrose gradient after cholesterol depletion.

30 cell biomechanics following statin-mediated cholesterol depletion.

31 Fluvastatin-mediated cholesterol depletion (-27.8%) lowered VSMC migration di

32 Concomitantly, cholesterol depletion abolished ouabain-induced recruitm

33 Cholesterol depletion abolished prostaglandin E1-stimula

34 on demonstrated that inhibition of Cav-1 and cholesterol depletion abrogated C5b-9 exo-vesiculation,

35 Immunofluorescence reveals that cholesterol depletion abrogates sarcomeric organization,

36 for SREBP/Sp1 regulation whereby lipoprotein cholesterol depletion activates caveolin-1 transcription

37 Transient anchorage was abolished by cholesterol depletion, addition of the Src family kinase

38 Finally, we show that cholesterol depletion affects a raft subpool and blocks

39 Cholesterol depletion, after Fas ligand activation of ap

40 with anti-transferrin receptor antibody and cholesterol depletion agents completely abolished endoge

41 In contrast, cholesterol depletion allowed random transport of the 2A

42 MBCD, this effect could not be explained by cholesterol depletion alone, as cholesterol repletion di

43 Cholesterol depletion also blocked insulin-dependent pho

44 Cholesterol depletion also changed the density and speci

45 Cholesterol depletion also enhances in vivo EGF receptor

46 Cholesterol depletion also increases membrane tension, C

47 Mild membrane cholesterol depletion also inhibited constitutive endocy

48 Cholesterol depletion also inhibited S100B-induced effec

49 Cholesterol depletion also inhibits EGF internalization

50 Statin-induced cholesterol depletion also modestly activated the epider

51 Cholesterol depletion also resulted in the collapse of t

52 Cholesterol depletion also significantly attenuated GnRH

53 testine and liver largely reflect a state of cholesterol depletion and a decrease in intestinal sensi

54 ively monitor the change in lipid phase upon cholesterol depletion and apoptosis.

55 y we examined the effects of target membrane cholesterol depletion and cytoskeletal changes on human

56 r rendered cells resistant to the effects of cholesterol depletion and decreased the basal level of p

57 lustering of MHC I molecules by two methods, cholesterol depletion and direct cross-linking of a dime

58 olipids in caveolae/lipid rafts, followed by cholesterol depletion and displacement of important sign

59 between DiO-C16 and DiI-C16 is sensitive to cholesterol depletion and disruption of liquid order (Lo

60 detergent resistant, but are insensitive to cholesterol depletion and do not require the transmembra

61 ll isolation, but isolation was inhibited by cholesterol depletion and enhanced by cholesterol loadin

62 ignaling pathways as a direct consequence of cholesterol depletion and identify the EGFR-PLD2-Ras-MAP

63 Cholesterol depletion and magnetic immunoisolation studi

64 induction of apoptosis resulted in cellular cholesterol depletion and markedly reduced the incidence

65 residues (i.e., BiP) are essential for both cholesterol depletion and potent cancer cell inhibition.

66 In contrast, we confirmed that cholesterol depletion and raft disruption strongly inhib

67 Cholesterol depletion and repletion with methyl-beta-cyc

68 We also provide evidence that cholesterol depletion and SREBP activation are signals f

69 ed pO(2) led to alteration of lipid rafts by cholesterol depletion and structural changes and was ass

70 studies suggest a novel role for endothelial cholesterol depletion and subsequent SREBP activation in

71 f Vav1 phosphorylation that was sensitive to cholesterol depletion and to inhibition of actin polymer

72 horylation of Vav1 that was not sensitive to cholesterol depletion and to inhibition of actin polymer

73 of the trimer) increased virus resistance to cholesterol depletion and to the surface-acting agents.

74 sis of affected skin showed evidence of both cholesterol depletion and toxic metabolic accumulation.

75 To test this hypothesis, we performed cholesterol-depletion and repletion assays and used chol

76 rbations, including transmembrane potential, cholesterol depletion, and PM curvature.

77 Responses to cholesterol depletion are often taken as evidence of a r

78 lso protected the red cells against lysis by cholesterol depletion as if substituting for the extract

79 esterol, and that cancer-cell stiffening via cholesterol depletion augments T-cell cytotoxicity and e

80 specialized membrane microdomains that upon cholesterol depletion become disrupted and release the c

81 tion of dendriplexes was strongly reduced by cholesterol depletion before transfection.

82 Correspondingly, cholesterol depletion blocked effector translocation int

83 ularly important because their disruption by cholesterol depletion blocks the ability of BDNF to rend

84 With cholesterol depletion, both ligand binding and signaling

85 own InsP3R2 or inducing its dysfunction with cholesterol depletion, Bsep redistributed intracellularl

86 nted by Clostridium difficile toxin B and by cholesterol depletion, but was unaffected by inhibition

87 Therefore, cholesterol depletion by beta-cyclodextrin abrogates bot

88 Here we show that cholesterol depletion by beta-cyclodextrin disrupts cave

89 Cholesterol depletion by beta-cyclodextrin results in th

90 o lysosomal degradation of neogenin and that cholesterol depletion by filipin blocks both HJV endocyt

91 Even cholesterol depletion by itself stimulated Erk activatio

92 We showed that cholesterol depletion by methyl beta-cyclodextrin or fil

93 is study, we have investigated the effect of cholesterol depletion by methyl-beta-cyclodextrin (Mbeta

94 Cholesterol depletion by methyl-beta-cyclodextrin (Mbeta

95 sed rat hippocampal cultures and their acute cholesterol depletion by methyl-beta-cyclodextrin as a t

96 Cholesterol depletion by methyl-beta-cyclodextrin induce

97 eduction in insulin secretion was rescued by cholesterol depletion by methyl-beta-cyclodextrin or mev

98 Cholesterol depletion by methyl-beta-cyclodextrin preven

99 ol since dominant-negative dynamin (K44A) or cholesterol depletion by methyl-beta-cyclodextrin preven

100 gradients, and were partially extracted upon cholesterol depletion by methyl-beta-cyclodextrin, indic

101 udged by horseradish peroxidase uptake after cholesterol depletion by methyl-beta-cyclodextrin.

102 Cholesterol depletion caused a decrease in the diffusion

103 , whereas in the alpha C418W mutant the same cholesterol depletion caused a dramatic gain-in-function

104 data show that disruption of lipid rafts by cholesterol depletion caused an enhancement of virus par

105 Ultrastructural studies indicate that acute cholesterol depletion causes accumulation of flat-coated

106 Cholesterol depletion causes dispersion of syntaxin 3 bu

107 Cholesterol depletion causes morphology changes of domai

108 due to multiple effects of MbetaCD-mediated cholesterol depletion causing disruption of lipid rafts,

109 Additionally, on cholesterol depletion, cell membranes display higher int

110 However, cholesterol depletion completely ablated the regulation

111 Cholesterol depletion completely prevented FXI binding t

112 l-cell fusion induced by MHV was retarded by cholesterol depletion, consistent with the association o

113 Differences in sensitivity to cholesterol depletion could not be explained by variatio

114 Cholesterol depletion, decreased caveolin, and increased

115 ane systems or by biochemical fractionation (cholesterol depletion, decreased temperature, and choles

116 sterol-enriched membrane rafts, and cellular cholesterol depletion decreases Abeta formation.

117 ins and functional experiments revealed that cholesterol depletion decreases channel sensitivity to c

118 However, cholesterol depletion did not affect the observed rate c

119 Interestingly, cholesterol depletion did not prevent initial activation

120 re increased in intestines of animals on the cholesterol depletion diet but minimally suppressed if a

121 nd increased in intestines of animals on the cholesterol-depletion diet.

122 Cholesterol depletion diminished the cell membrane mean

123 As a result, cholesterol depletion diminishes Akt activity in both re

124 its inhibition of tyrosine phosphorylation, cholesterol depletion disrupts the interactions of aggre

125 However, cholesterol depletion does not alter the magnitude of ch

126 Unexpectedly, cholesterol depletion does not visibly alter the distrib

127 CNGA2-expressing HEK 293 cells revealed that cholesterol depletion dramatically reduced the apparent

128 ulated by cellular cholesterol levels; acute cholesterol depletion elicited a rapid induction of VLC-

129 In contrast, cholesterol depletion exacerbated apoptotic death in a K

130 ellular cholesterol during endosomal escape; cholesterol depletion from host cells impairs K(+) accum

131 he apoA-I binding protein (AIBP) facilitated cholesterol depletion from inflammarafts and reversed ne

132 plexes were shifted to a higher density upon cholesterol depletion from intact cells or cell lysate.

133 Cholesterol depletion from the apical membrane leads to

134 s in virus particle density, suggesting that cholesterol depletion from the HIV-1 envelope membrane r

135 We conclude that cholesterol depletion from the plasma membrane by MbetaC

136 We conclude that cholesterol depletion from the plasma membrane by MbetaC

137 Moderate cholesterol depletion from the viral membrane sped fusio

138 Abeta production depending on the extent of cholesterol depletion, generating controversy.

139 We also show that although cholesterol depletion had no apparent effect on the inte

140 lipid rafts exclusion at the iNKIS, whereas cholesterol depletion had no effect on actin disruption

141 Cholesterol depletion had no effect on the induction of

142 duction in glutamate uptake, suggesting that cholesterol depletion has a direct effect on the functio

143 In contrast, cholesterol depletion has no effect on E-selectin-depend

144 processing is not clearly understood because cholesterol depletion has pleiotropic effects on Golgi m

145 2+) signals in SkHep1 cells, suggesting that cholesterol depletion has similar effects among polarize

146 No effect of cholesterol depletion, however, was seen on viral bindin

147 ion in response to 25-hydroxycholesterol and cholesterol depletion, impairs CERT Golgi localization,

148 roclustering was measured after 27% membrane cholesterol depletion in a cell line expressing WT integ

149 Moreover, cholesterol depletion in adipocytes by treating the cell

150 We show that cholesterol depletion in cells does not inhibit the form

151 Cholesterol depletion in MDCK cells greatly restricted A

152 itself through SR-B1-mediated intracellular cholesterol depletion in SHH MB cells.

153 s as well as cellular proliferation, whereas cholesterol depletion in the cell membrane abrogated Akt

154 GAb uptake was attenuated following membrane cholesterol depletion in vitro and ex vivo, indicating t

155 using GT1-7 hypothalamic cells subjected to cholesterol depletion in vitro using three independent m

156 anced proliferation of prostate cells, while cholesterol depletion increased ATF3 levels and inhibite

157 Our study thus demonstrates that cholesterol depletion increases membrane tension and its

158 We suggest that cholesterol depletion increases the stiffness of the mem

159 m mobilization was only partially reduced by cholesterol depletion, indicating that this treatment di

160 equent virus internalization is sensitive to cholesterol depletion, indicating the involvement of a c

161 reduction in the outward current was due to cholesterol depletion induced by MCD rather than a direc

162 Interestingly, acute cholesterol depletion induced with methyl-beta-cyclodext

163 sphorylated E2 state relative to E1, and the cholesterol depletion-induced slowing of ATP phosphoryla

164 Disruption of lipid rafts through cholesterol depletion inhibited PI3K localization to mem

165 in cholesterol-containing microdomains, and cholesterol depletion inhibits the stability of these cl

166 d diffusion coefficients were measured after cholesterol depletion, irrespective of the integrins bei

167 ndependent of protein expression levels, and cholesterol depletion is commonly used to test the raft-

168 These results support a model in which cholesterol depletion is coupled through PIP(2) to enhan

169 r control conditions but can be activated by cholesterol depletion, knockdown of caveolin-1 expressio

170 Cholesterol depletion, known to decrease lipid bilayer s

171 Similar findings were obtained upon chemical cholesterol depletion, leading directly to syntaxin-1 cl

172 th methyl-beta-cyclodextrin resulting in 75% cholesterol depletion leads to commensurate decreases in

173 Cholesterol depletion led to almost complete confinement

174 tural integrity and function of LR caused by cholesterol depletion likely inhibited the initial stage

175 Similarly, cholesterol depletion lowered thermodynamic but enhanced

176 eta-cyclodextrin depletion, whereas envelope cholesterol depletion markedly affected influenza virus

177 It is concluded that statin-mediated cholesterol depletion may coordinate vascular smooth mus

178 gether, it is concluded that statin-mediated cholesterol depletion may coordinate VSMC migration and

179 This result indicates that after cholesterol depletion molecules in the more ordered doma

180 integrin association was not disrupted upon cholesterol depletion, occurred in high density sucrose

181 Cholesterol depletion of alpha T3-1 cells using methyl-b

182 rol on membrane stiffness of lipid bilayers, cholesterol depletion of bovine aortic endothelial cells

183 Cholesterol depletion of infected cells drastically alte

184 This impairment was reversed with cholesterol depletion of isolated endosomes or with high

185 ages and endothelial cells seem to occur via cholesterol depletion of LRs.

186 Furthermore, cholesterol depletion of macrophages with methyl-beta-cy

187 This localization was supported by cholesterol depletion of membranes, which ablated STAT5

188 Cholesterol depletion of native intestinal plasma membra

189 cholesterol for H-Ras activation was probed; cholesterol depletion of rafts using methyl-betacyclodex

190 Here we report that cholesterol depletion of serum-starved COS-1 cells with

191 pression of CD44 on monocytes and subsequent cholesterol depletion of TAMs.

192 ma ligands, but was decreased in response to cholesterol depletion of the membrane.

193 the Reelin signaling cascade is impaired by cholesterol depletion of the plasma membrane.

194 Cholesterol depletion of virus did not affect the abilit

195 ent of all lipoproteins was attenuated, with cholesterol depletion of VLDL and enrichment of HDL.

196 asma membrane PI(4,5)P2 mimic the effects of cholesterol depletion on actin organization and on later

197 igating functional and structural effects of cholesterol depletion on Lyn/FcepsilonRI interactions.

198 However, the effects of cholesterol depletion on protein and lipid diffusion in

199 There was a marked effect of cholesterol depletion on the cell-surface distribution a

200 Upon cholesterol depletion, only 12% of the AChR-containing v

201 Most importantly, cholesterol depletion or blocking cholesterol synthesis

202 phorylation are inhibited by either membrane cholesterol depletion or overexpression of RGS1 in proge

203 moreover, it was only slightly inhibited by cholesterol depletion or SFK inhibition and depended com

204 atin myotoxicity may be due to intracellular cholesterol depletion, or interference with oxidative ph

205 lpain 2 is recruited to lipid rafts and that cholesterol depletion perturbs calpain 2 localization, s

206 Using cholesterol depletion, pharmacological inhibitors, RNA i

207 Cholesterol depletion postinfection did not affect WNV g

208 In response to cholesterol depletion, PP2A directly interacted with SRE

209 red cells against the hemolysis elicited by cholesterol depletion, presumably by substituting for th

210 Disruption of lipid rafts by cholesterol depletion prevented the TNF-alpha-dependent

211 For cholesterol depletion, rat salivary epithelial A5 cells

212 monstrated that disruption of lipid rafts by cholesterol-depletion reagent blocked the agonist-induce

213 Cholesterol depletion redistributed the BK channels to n

214 Although acute cholesterol depletion reduced sphingolipid domain abunda

215 Cholesterol depletions reduced plaque development 2- to

216 AIBP- and HDL-mediated cholesterol depletion reduces lipid rafts, interferes wi

217 tion of squared displacements confirmed that cholesterol depletion reduces prestin confinement.

218 ational order is also seen to be affected by cholesterol depletion, reflecting the strong interplay b

219 Proof is provided that statin-mediated cholesterol depletion remodels total vascular smooth mus

220 Cholesterol depletion resulted in dissociation of CPE fr

221 ilar to disruptions of actin polymerization, cholesterol depletion results in an increase in the fiss

222 Mechanistically, cholesterol depletion results in displacement of KLF11 f

223 cholesterol-rich membranes, and we find that cholesterol depletion significantly reduces viral infect

224 ity-independent mechanism, whereas overnight cholesterol depletion slightly increased both protein an

225 urements with the probe eosin indicated that cholesterol depletion stabilizes the unphosphorylated E2

226 Cholesterol depletion studies indicate a role for choles

227 Cholesterol depletion studies showed that the TF associa

228 utilization of rafts in Th1 and Th2 cells by cholesterol depletion studies, which alters calcium sign

229 esponses of mu- and delta-opioid agonists to cholesterol depletion suggest that mu-opioid receptors a

230 In addition, its relative insensitivity to cholesterol depletion suggests that the interactions of

231 cytes led to enhanced channel activity while cholesterol depletion suppressed I(K,ACh).

232 showed an increased kinetic sensitivity in a cholesterol depletion test, demonstrating that palmitoyl

233 EV11-207R is significantly less sensitive to cholesterol depletion than infection by EV11-207, confir

234 Desialylated PrP(C) was less sensitive to cholesterol depletion than PrP(C) and was not released f

235 ond, after treatment with SHH, but not after cholesterol depletion, the molecules that remain in the

236 ipoprotein A-I binding protein, non-specific cholesterol depletion, TLR4 mis-sense rats and a TLR4 in

237 Cholesterol depletion to disrupt LRs abolished LTB(4)-in

238 ated macrophages (TAM) through CD44-mediated cholesterol depletion to generate an immunosuppressive t

239 We propose a mechanism in which cholesterol depletion triggers a signaling cascade, culm

240 independent of cholesterol concentration as cholesterol depletion using cyclodextrins did not alter

241 After cholesterol depletion using cyclodextrins, Golgi and api

242 In vivo cholesterol depletion using lovastatin resulted in the l

243 resistant membranes that can be disrupted by cholesterol depletion using methyl-beta-cyclodextrin (MC

244 Complementary functional studies showed that cholesterol depletion using methyl-beta-cyclodextrin inh

245 perature dependence of membrane order and by cholesterol depletion using methyl-beta-cyclodextrin.

246 chain after disruption of the lipid rafts by cholesterol depletion using methyl-betacyclodextrin.

247 We show that acute cholesterol depletion, using beta-methyl-cyclodextrin, s

248 al integrity of lipid rafts was disrupted by cholesterol depletion utilizing methyl-beta-cyclodextrin

249 Cholesterol depletion was also observed to extract a poo

250 ABCA1 overexpression or cholesterol depletion was sufficient to reduce albuminur

251 -CoA synthase mRNAs, in response to cellular cholesterol depletion, was prevented when cells expresse

252 Using controlled cholesterol depletion, we found that a cholesterol-depen

253 ) or 4% cholestyramine and 0.15% lovastatin (cholesterol-depletion) were fed to hamsters for 2 weeks.

254 By contrast, cholesterol depletion, which impairs lipid raft formatio

255 he divergence was even more pronounced after cholesterol depletion, which reduced thermodynamic stabi

256 Cholesterol depletion with beta-cyclodextrin causes a si

257 Dispersion of lipid rafts on the cells by cholesterol depletion with beta-cyclodextrin resulted in

258 uch as digitonin and acetone/methanol, while cholesterol depletion with beta-methyl-cyclodextrin and

259 fect was significantly decreased by membrane cholesterol depletion with beta-methyl-cyclodextrin, the

260 A minimal cholesterol depletion with beta-methylcyclodextrin atten

261 Nevertheless, cholesterol depletion with cyclodextrin augments agonist

262 A1 deficiency and was partially prevented by cholesterol depletion with cyclodextrin.

263 ost important finding of this study was that cholesterol depletion with dextrin induced eNOS phosphor

264 ssociated CH-2 complex that was sensitive to cholesterol depletion with methyl-beta-cyclodextrin (Mbe

265 Cholesterol depletion with methyl-beta-cyclodextrin did

266 Raft disruption by cholesterol depletion with methyl-beta-cyclodextrin elim

267 Membrane cholesterol depletion with methyl-beta-cyclodextrin mimi

268 Cholesterol depletion with methyl-beta-cyclodextrin slow

269 We find that cholesterol depletion with methyl-beta-cyclodextrin subs

270 Cholesterol depletion with methyl-beta-cyclodextrin, fil

271 g pattern, but the pattern was eliminated by cholesterol depletion with methyl-beta-cyclodextrin.

272 t similar rates in the two lines, even after cholesterol depletion with methyl-beta-cyclodextrin.

273 Conversely, cholesterol-depletion with methyl-beta-cyclodextrin or f