ライフサイエンスコーパス: cholesterol depletion

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

2 general, activation of SREBPs occurs during cholesterol depletion.

3 The suppression was fully reversible by cholesterol depletion.

4 when fully solubilized and were resistant to cholesterol depletion.

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

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

7 nger facilitative effect on the current than cholesterol depletion.

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

9 by cholesterol feeding but was increased by cholesterol depletion.

10 ased by dietary cholesterol and decreased by cholesterol depletion.

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

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

13 ctivation and current facilitation following cholesterol depletion.

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

15 -cholesterol diet, and facilitated following cholesterol depletion.

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

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

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

19 dense regions of the sucrose gradient after cholesterol depletion.

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

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

22 secretion, with normal secretion restored by cholesterol depletion.

23 Concomitantly, cholesterol depletion abolished ouabain-induced recruitm

24 Cholesterol depletion abolished prostaglandin E1-stimula

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

26 Immunofluorescence reveals that cholesterol depletion abrogates sarcomeric organization,

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

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

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

30 Cholesterol depletion, after Fas ligand activation of ap

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

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

33 Cholesterol depletion also blocked insulin-dependent pho

34 Cholesterol depletion also changed the density and speci

35 Cholesterol depletion also enhances in vivo EGF receptor

36 Cholesterol depletion also increases membrane tension, C

37 Mild membrane cholesterol depletion also inhibited constitutive endocy

38 Cholesterol depletion also inhibited S100B-induced effec

39 Cholesterol depletion also inhibits EGF internalization

40 Statin-induced cholesterol depletion also modestly activated the epider

41 Cholesterol depletion also resulted in the collapse of t

42 Cholesterol depletion also significantly attenuated GnRH

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

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

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

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

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

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

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

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

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

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

53 Cholesterol depletion and magnetic immunoisolation studi

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

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

56 Cholesterol depletion and repletion with methyl-beta-cyc

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

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

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

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

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

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

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

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

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

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

67 Correspondingly, cholesterol depletion blocked effector translocation int

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

69 With cholesterol depletion, both ligand binding and signaling

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

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

72 Therefore, cholesterol depletion by beta-cyclodextrin abrogates bot

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

74 Cholesterol depletion by beta-cyclodextrin results in th

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

76 Even cholesterol depletion by itself stimulated Erk activatio

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

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

79 Cholesterol depletion by methyl-beta-cyclodextrin induce

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

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

82 Cholesterol depletion by methyl-beta-cyclodextrin preven

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

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

85 Cholesterol depletion caused a decrease in the diffusion

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

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

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

89 Cholesterol depletion causes dispersion of syntaxin 3 bu

90 Cholesterol depletion causes morphology changes of domai

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

92 However, cholesterol depletion completely ablated the regulation

93 Cholesterol depletion completely prevented FXI binding t

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

95 Cholesterol depletion, decreased caveolin, and increased

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

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

98 Interestingly, cholesterol depletion did not prevent initial activation

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

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

101 Cholesterol depletion diminished the cell membrane mean

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

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

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

105 Unexpectedly, cholesterol depletion does not visibly alter the distrib

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

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

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

109 Cholesterol depletion from the apical membrane leads to

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

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

112 Moderate cholesterol depletion from the viral membrane sped fusio

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

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

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

116 Cholesterol depletion had no effect on the induction of

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

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

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

120 2+) signals in SkHep1 cells, suggesting that cholesterol depletion has similar effects among polarize

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

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

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

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

125 Cholesterol depletion in MDCK cells greatly restricted A

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 Cholesterol depletion, known to decrease lipid bilayer s

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

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

144 Cholesterol depletion led to almost complete confinement

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

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

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

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

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

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

151 Cholesterol depletion of infected cells drastically alte

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

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

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

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

156 Cholesterol depletion of native intestinal plasma membra

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

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

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

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

161 Cholesterol depletion of virus did not affect the abilit

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

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

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

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

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

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

168 Most importantly, cholesterol depletion or blocking cholesterol synthesis

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

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

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

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

173 Using cholesterol depletion, pharmacological inhibitors, RNA i

174 Cholesterol depletion postinfection did not affect WNV g

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

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

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

178 For cholesterol depletion, rat salivary epithelial A5 cells

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

180 Cholesterol depletion redistributed the BK channels to n

181 Although acute cholesterol depletion reduced sphingolipid domain abunda

182 Cholesterol depletions reduced plaque development 2- to

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

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

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

186 Cholesterol depletion resulted in dissociation of CPE fr

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

188 Mechanistically, cholesterol depletion results in displacement of KLF11 f

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

190 Cholesterol depletion studies showed that the TF associa

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

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

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

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

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

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

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

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

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

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

201 After cholesterol depletion using cyclodextrins, Golgi and api

202 In vivo cholesterol depletion using lovastatin resulted in the l

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

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

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

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

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

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

209 Cholesterol depletion was also observed to extract a poo

210 ABCA1 overexpression or cholesterol depletion was sufficient to reduce albuminur

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

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

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

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

215 Cholesterol depletion with beta-cyclodextrin causes a si

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

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

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

219 A minimal cholesterol depletion with beta-methylcyclodextrin atten

220 Nevertheless, cholesterol depletion with cyclodextrin augments agonist

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

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

223 Cholesterol depletion with methyl-beta-cyclodextrin did

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

225 Membrane cholesterol depletion with methyl-beta-cyclodextrin mimi

226 Cholesterol depletion with methyl-beta-cyclodextrin slow

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

228 Cholesterol depletion with methyl-beta-cyclodextrin, fil

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

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

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