ライフサイエンスコーパス: methyl-beta-cyclodextrin

1 terol repletion fully reversed the effect of methyl beta-cyclodextrin.

2 d when cholesterol stores were depleted with methyl-beta-cyclodextrin.

3 ynamin-2 mutant (K44A) or treated cells with methyl-beta-cyclodextrin.

4 ane order and by cholesterol depletion using methyl-beta-cyclodextrin.

5 ately 50% when cholesterol is extracted with methyl-beta-cyclodextrin.

6 xidase uptake after cholesterol depletion by methyl-beta-cyclodextrin.

7 ition of human red blood cell cholesterol to methyl-beta-cyclodextrin.

8 cells with the cholesterol-depleting agent, methyl-beta-cyclodextrin.

9 disrupted by cholesterol depletion utilizing methyl-beta-cyclodextrin.

10 holesterol-rich domains during extraction by methyl-beta-cyclodextrin.

11 was eliminated by cholesterol depletion with methyl-beta-cyclodextrin.

12 ed from this compartment upon treatment with methyl-beta-cyclodextrin.

13 by extraction of cholesterol with filipin or methyl-beta-cyclodextrin.

14 rs with the cholesterol-sequestering reagent methyl-beta-cyclodextrin.

15 d then treated with the cholesterol chelator methyl-beta-cyclodextrin.

16 issociated ciliary neurons by treatment with methyl-beta-cyclodextrin.

17 of cholesterol-rich membrane microdomains by methyl-beta-cyclodextrin.

18 lines, even after cholesterol depletion with methyl-beta-cyclodextrin.

19 es in response to external perturbation with methyl-beta-cyclodextrin.

20 ane lipid rafts, similar to positive control methyl-beta-cyclodextrin.

21 Hz) and after disruption of lipid rafts with methyl-beta-cyclodextrin.

22 do so following disruption of caveolae with methyl-beta-cyclodextrin.

23 rved after incubating dissociated cells with methyl-beta-cyclodextrin.

24 l by incubating neonatal cardiomyocytes with methyl-beta-cyclodextrin.

25 to nonraft domains, similar to the action of methyl-beta-cyclodextrin.

26 ere removed from erythrocyte membranes using methyl-beta-cyclodextrin.

27 ng three independent methods: 1) exposure to methyl-beta-cyclodextrin, 2) treatment with the HMG-CoA

28 mM sulfobutylether-beta-cyclodextrin, 40 mM methyl-beta-cyclodextrin, 5 mM carbonate buffer at pH 10

29 Treatment of cells with methyl-beta-cyclodextrin (a cholesterol-depleting agent)

30 Treatment of human T cells with methyl-beta-cyclodextrin, a cholesterol chelator, preven

31 tion of this Akt subspecies was ablated with methyl-beta-cyclodextrin, a cholesterol-binding compound

32 With the use of methyl-beta-cyclodextrin, a cholesterol-depleting agent

33 Indeed, methyl-beta-cyclodextrin, a cholesterol-sequestering age

34 Pretreating neutrophils with methyl-beta-cyclodextrin, a lipid raft-disrupting agent,

35 r cells were more sensitive to inhibition by methyl-beta-cyclodextrin, a sterol-chelating agent.

36 Disruption of caveolae by 2 mmol/L methyl-beta-cyclodextrin abolished ACh-induced NOi produ

37 Methyl-beta-cyclodextrin added apically to (MPK)CCD(14)

38 Treatment of human ARPE 19 cells with methyl beta-cyclodextrin after FasL induction of apoptos

39 Disrupting lipid raft by methyl-beta-cyclodextrin also blocked neurite outgrowth.

40 y, disruption of the clustered caveolae with methyl-beta-cyclodextrin also dispersed the Cav-actin st

41 Pharmacological raft disruption using methyl-beta-cyclodextrin also increased CD44-ezrin copre

42 Signaling prompted by cholesterol efflux to methyl-beta-cyclodextrin also was prevented, indicating

43 Methyl beta-cyclodextrin, an inhibitor of caveola format

44 olemmal sites and this was prevented by 2 mm methyl-beta-cyclodextrin, an agent that disrupts caveola

45 Using the lipid raft disruptors methyl-beta-cyclodextrin and filipin, we demonstrated th

46 he metalloprotease inhibitor batimastat, and methyl-beta-cyclodextrin and filipin, which block lipid

47 Membrane treatments with methyl-beta-cyclodextrin and glycosphingolipid synthesis

48 at the cholesterol-binding heptasaccharides, methyl-beta-cyclodextrin and OH-propyl-beta-cyclodextrin

49 rylation/activation was also decreased after methyl-beta-cyclodextrin and statin treatment but increa

50 urons, through cholesterol-scavenging drugs (methyl-beta-cyclodextrin) and the enzymatic breakdown of

51 Treatment with the inhibitors nystatin, methyl-beta-cyclodextrin, and genistein, as well as tran

52 Chitosan chloride and methyl-beta-cyclodextrins appear therefore suitable to f

53 We identified heptakis(2,6-di-O-methyl)-beta-cyclodextrin as a potent enhancer of choles

54 Using methyl-beta-cyclodextrin as a delivery vehicle, we show

55 res and their acute cholesterol depletion by methyl-beta-cyclodextrin as a tool to describe the physi

56 ed cell bilayer and exits the membrane using methyl-beta-cyclodextrin as an acceptor.

57 filling and occupancy of binding sites; (ii) methyl-beta-cyclodextrin, as a FA acceptor, to observe t

58 ith siRNA, or extraction of cholesterol with methyl beta-cyclodextrin, attenuated UMB18 antiviral act

59 s were found to be soluble when treated with methyl-beta-cyclodextrin before extraction with ice-cold

60 K562 cells treated with paraformaldehyde or methyl-beta-cyclodextrin before ligand coupling were les

61 Abolishing CEM formation (methyl-beta-cyclodextrin) blocked OxPAPC-mediated Rac1 a

62 nt of T-cells with the lipid raft inhibitor, methyl-beta-cyclodextrin, blocked the association betwee

63 ion of cholesterol from confluent cells with methyl-beta-cyclodextrin both induced tyrosine phosphory

64 nternalization was reduced by treatment with methyl-beta-cyclodextrin but not filipin.

65 Depletion of cholesterol from rafts with methyl-beta-cyclodextrin caused a redistribution of TNFR

66 In endothelial cells, HDL and methyl-beta-cyclodextrin caused comparable eNOS activati

67 bacteria with cholesterol extraction reagent methyl-beta-cyclodextrin caused their ultrastructural ch

68 on of membrane cholesterol by treatment with methyl-beta-cyclodextrin (CD) or by culturing cells in l

69 sses, endothelial cells were pretreated with methyl-beta-cyclodextrin (CD) or filipin to ablate raft

70 xin by phosphate-buffered saline (PBS), 0.1% methyl-beta-cyclodextrin (CD), or CD plus cholesterol (0

71 Dynamin inhibitors, chlorpromazine, methyl-beta-cyclodextrin, chloroquine, and concanamycin

72 Control cells were treated with methyl-beta-cyclodextrin-cholesterol at a molar ratio th

73 rosome but following cholesterol efflux with methyl-beta-cyclodextrin, clusters containing zona-bindi

74 BAPTA-AM or disruption of lipid rafts using methyl beta-cyclodextrin completely abrogated IFN-gamma-

75 tro with excess cholesterol by a cholesterol/methyl-beta-cyclodextrin complex, phenocopying SR-BI KO

76 r 72 h with cholesterol by using cholesterol:methyl-beta-cyclodextrin complexes, leading to approxima

77 lization of D3 that is blocked by sucrose or methyl-beta-cyclodextrin-containing medium.

78 and that disrupting lipid raft formation by methyl-beta-cyclodextrin decreased NO production and apo

79 ion of sgk1 with the apical surface, whereas methyl-beta-cyclodextrin decreased the association of sg

80 Here we measured the rate at which methyl-beta-cyclodextrin depletes cholesterol from a sup

81 ng, and internalization were not affected by methyl-beta-cyclodextrin depletion, whereas envelope cho

82 of cholesterol in the virus envelope, using methyl-beta-cyclodextrin depletion.

83 epletion of plasma membrane cholesterol with methyl-beta-cyclodextrin did not affect forskolin-stimul

84 Methyl-beta-cyclodextrin did not alter total cell surfac

85 disruption of lipid rafts by treatment with methyl-beta-cyclodextrin did not decrease the GTPase act

86 Cholesterol depletion with methyl-beta-cyclodextrin did not prevent the increase in

87 he cholesterol-depleting reagent saponin and methyl-beta-cyclodextrin differentially disrupted the fo

88 Using this method, we determined that methyl-beta-cyclodextrin differentially extracts cholest

89 lesterol depletion of alpha T3-1 cells using methyl-beta-cyclodextrin disrupted GnRHR but not c-raf k

90 odstream parasites with cholesterol-specific methyl-beta-cyclodextrin disrupts both membrane liquid o

91 Disruption of lipid rafts with methyl-beta-cyclodextrin disrupts the functional associa

92 id rafts with the cholesterol-depleting drug methyl-beta-cyclodextrin disrupts the raft localization

93 Disruption of the membrane with methyl-beta-cyclodextrin dissociates the EGFR/GM3/caveol

94 Pretreatment of virions with methyl-beta-cyclodextrin efficiently depleted envelope c

95 We previously reported that methyl-beta-cyclodextrin eliminates caveolae and blocks

96 aft disruption by cholesterol depletion with methyl-beta-cyclodextrin eliminates these light rafts.

97 ntroduced into these vesicles using a second methyl-beta-cyclodextrin exchange step.

98 Methyl-beta-cyclodextrin extracted OA from individual si

99 mbrane cholesterol by metabolic depletion or methyl-beta-cyclodextrin extraction was found to both in

100 thermore, knockdown of caveolae formation by methyl-beta-cyclodextrin failed to prevent wild-type cav

101 Cholesterol depletion with methyl-beta-cyclodextrin, filipin, or cholesterol oxidas

102 xposure of Hep3B cells to the raft disrupter methyl-beta-cyclodextrin for 1-10 min followed by IL-6 s

103 Treatment of HSV-1-infected Vero cells with methyl beta-cyclodextrin from 2 to 9 h postentry reduced

104 e data show that cholesterol, solubilized by methyl-beta-cyclodextrin, greatly reduced the levels of

105 Methyl beta-cyclodextrin had no effect on Ca(2+) store d

106 eNOS activation, whereas cholesterol-loaded methyl-beta-cyclodextrin had no effect.

107 thermore, the disruption of SM-rich rafts by methyl-beta-cyclodextrin impaired myosin activation and

108 king in response to postprandial micelles or methyl-beta-cyclodextrin in cultured enterocytes, and it

109 Treatment of cells with methyl-beta-cyclodextrin increased the hydrolysis rate a

110 ied that depleting cellular cholesterol with methyl-beta-cyclodextrin increased the resilience of str

111 port here that depletion of cholesterol with methyl-beta-cyclodextrin increases cell surface (125)I-E

112 endogenous cholesterol from oocytes using a methyl-beta-cyclodextrin incubation procedure without ca

113 ion of NF-kappaB and MAPKs was unaffected by methyl-beta-cyclodextrin indicating that, in airway smoo

114 ally extracted upon cholesterol depletion by methyl-beta-cyclodextrin, indicating that they were asso

115 In A431 cells, depletion of cholesterol with methyl-beta-cyclodextrin induced an increase in both bas

116 Cholesterol depletion by methyl-beta-cyclodextrin induced IL-8 synthesis in a dos

117 We previously described a technique in which methyl-beta-cyclodextrin-induced lipid exchange is used

118 A methyl-beta-cyclodextrin-induced lipid exchange techniqu

119 Methyl-beta-cyclodextrin induces activation of p38 and C

120 Depletion of membrane cholesterol by methyl-beta-cyclodextrin inhibited AEA binding, blocked

121 In 3T3L-1 adipocytes, apoAI, HDL, and methyl-beta-cyclodextrin inhibited chemotactic factor ex

122 Extraction of membrane cholesterol with methyl-beta-cyclodextrin inhibited infection by virions

123 dies showed that cholesterol depletion using methyl-beta-cyclodextrin inhibited preimplantation devel

124 We demonstrate that methyl-beta-cyclodextrin is more potent than hydroxyprop

125 annot occur, demonstrate that treatment with methyl-beta-cyclodextrin leads to an increase in intrins

126 Acute exposure of LLC-PK1 cells to methyl beta-cyclodextrin led to parallel decreases in ce

127 Similar to methyl-beta-cyclodextrin, leptin reduces beta-secretase

128 Infectivity was exquisitely sensitive to methyl-beta-cyclodextrin (M beta CD) and nystatin, which

129 his blue shift disappeared after exposure to methyl-beta-cyclodextrin (m beta CD), which disrupts lip

130 ith BKV and the cholesterol-depleting agents methyl beta cyclodextrin (MBCD) and nystatin (Nys), drug

131 We used a combination of methyl-beta cyclodextrin (MBCD), lovastatin, and cholest

132 Methyl-beta-cyclodextrin (MBCD) can efficiently capture

133 Among cyclodextrins (CDs), methyl beta cyclodextrin (MbetaCD) is the most efficient

134 tretch signaling, we disrupted caveolae with methyl beta-cyclodextrin (MbetaCD).

135 epletion of plasma membrane cholesterol with methyl-beta-cyclodextrin (MbetaCD) caused activation of

136 tment of cells with the raft disrupting drug methyl-beta-cyclodextrin (MbetaCD) caused activation of

137 Methyl-beta-cyclodextrin (MbetaCD) completely blunted th

138 Disruption of LR with methyl-beta-cyclodextrin (MbetaCD) decreased NHE3 activi

139 ling membrane-proteins in lipid rafts, while methyl-beta-cyclodextrin (MbetaCD) has been a major tool

140 atment with the cholesterol-extracting agent methyl-beta-cyclodextrin (MbetaCD) not only disrupted th

141 t of peripheral blood lymphocytes (PBL) with methyl-beta-cyclodextrin (MbetaCD) or cytochalasin reduc

142 rupting rafts by removal of cholesterol with methyl-beta-cyclodextrin (MbetaCD) or destabilizing the

143 epletion of plasma membrane cholesterol with methyl-beta-cyclodextrin (MbetaCD) relocalized raft-resi

144 Cholesterol depletion by methyl-beta-cyclodextrin (MbetaCD) remodels the plasma m

145 Extraction with methyl-beta-cyclodextrin (MbetaCD) removed pUL37x1/vMIA

146 Treatment of cells with methyl-beta-cyclodextrin (MbetaCD) significantly reduced

147 Using methyl-beta-cyclodextrin (MbetaCD) to deplete membrane c

148 To test this hypothesis, we used methyl-beta-cyclodextrin (MbetaCD) to load mouse periton

149 gated the effect of cholesterol depletion by methyl-beta-cyclodextrin (MbetaCD) treatment on influenz

150 eceptor mediates this signaling specificity, methyl-beta-cyclodextrin (MbetaCD) treatment was used to

151 was sensitive to cholesterol depletion with methyl-beta-cyclodextrin (MbetaCD) was detected.

152 The cholesterol depleting agent methyl-beta-cyclodextrin (mbetaCD) was used to disrupt l

153 ntum chagasi promastigotes were treated with methyl-beta-cyclodextrin (MbetaCD), a sterol-chelating r

154 mbrane cholesterol levels were reduced using methyl-beta-cyclodextrin (mbetaCD), as confirmed by Ampl

155 he cells with the caveolae-disrupting agent, methyl-beta-cyclodextrin (mbetaCD), selectively inhibite

156 Methyl-beta-cyclodextrin (MbetaCD), which disassembles c

157 We show here that methyl-beta-cyclodextrin (MbetaCD), which disrupts DIMs

158 g in lipid rafts, we pretreated animals with methyl-beta-cyclodextrin (MbetaCD), which disrupts lipid

159 fragments were depleted of cholesterol with methyl-beta-cyclodextrin (mbetaCD).

160 Pretreatment with lipid raft disruptor (Methyl-beta-cyclodextrin, MbetaCD) and oxidative stress

161 Lipid raft/caveolae disruptors (methyl-beta-cyclodextrin (MCD) and Nystatin) and Ang II

162 Acute depletion of cholesterol with 5 mm methyl-beta-cyclodextrin (MCD) caused a substantial incr

163 In addition, cholesterol reduction by methyl-beta-cyclodextrin (MCD) disrupted rafts and shift

164 sly shown that depletion of cholesterol with methyl-beta-cyclodextrin (MCD) disrupts caveolar microdo

165 atment with the cholesterol depleting agent, methyl-beta-cyclodextrin (MCD), significantly inhibited

166 STARD4 with that of a simple sterol carrier, methyl-beta-cyclodextrin (MCD), when STARD4 and MCD were

167 be disrupted by cholesterol depletion using methyl-beta-cyclodextrin (MCD).

168 us laevis oocytes with cholesterol-depleting methyl-beta-cyclodextrin (MebetaCD) stimulates phosphory

169 Spherical chitosan chloride and methyl-beta-cyclodextrin microparticles loaded with DFO

170 Membrane cholesterol depletion with methyl-beta-cyclodextrin mimicked the effects of AC6 sil

171 e, cholesterol depletion of macrophages with methyl-beta-cyclodextrin normalized FC content between t

172 The use of dynasore, PitStop2, methyl-beta-cyclodextrin, nystatin, and filipin (specifi

173 minated by disruption of caveolae with 10 mM methyl beta-cyclodextrin or by small interfering RNA dir

174 Finally, depletion of either cholesterol by methyl beta-cyclodextrin or caveolin-1 by siRNA signific

175 We showed that cholesterol depletion by methyl beta-cyclodextrin or filipin did not affect virus

176 e current study, cholesterol, solubilized by methyl- beta-cyclodextrin or ethanol, was added to the c

177 FP; however, this trafficking was blocked by methyl-beta-cyclodextrin or by caveolin knockdown.

178 ither short-term cholesterol chelation using methyl-beta-cyclodextrin or by stable knockdown of caveo

179 Methyl-beta-cyclodextrin or caveolin knockdown significa

180 Depletion of cholesterol through methyl-beta-cyclodextrin or cholesterol oxidase abolishe

181 s disrupted by lipid raft perturbation using methyl-beta-cyclodextrin or cholesterol oxidase.

182 henomena, we used growth media enriched with methyl-beta-cyclodextrin or cholesterol to reduce or ele

183 e microdomains by acute exposure of cells to methyl-beta-cyclodextrin or chronic exposure to differen

184 gonists, but the response was not reduced by methyl-beta-cyclodextrin or CPM antibody.

185 ontent was depleted by exposing the cells to methyl-beta-cyclodextrin or enriched by exposing the cel

186 Treatment with either methyl-beta-cyclodextrin or filipin III to disrupt chole

187 disrupted by pretreatment of the cells with methyl-beta-cyclodextrin or Filipin III, hence implicati

188 Conversely, cholesterol-depletion with methyl-beta-cyclodextrin or formaldehyde fixation had no

189 th agents that deplete membrane cholesterol (methyl-beta-cyclodextrin or lovastatin) disrupted caveol

190 tion was rescued by cholesterol depletion by methyl-beta-cyclodextrin or mevastatin.

191 rthermore, pretreatment of the bacteria with methyl-beta-cyclodextrin or NBD-cholesterol deprived the

192 with cholesterol-sequestering drugs such as methyl-beta-cyclodextrin or nystatin and then exposed to

193 Correspondingly, pharmacological (methyl-beta-cyclodextrin) or genetic disruption of caveo

194 icient toxoids or pretreatment of cells with methyl-beta-cyclodextrin) or osmotic protection of targe

195 urthermore, cholesterol lowering by statins, methyl-beta-cyclodextrin, or filipin also activates PKA

196 ced either in vitro, by treatment with 25 mM methyl-beta-cyclodextrin, or in vivo, by subjecting anim

197 ated by using Cab-O-sil, medium treated with methyl-beta-cyclodextrin, or serum-free medium.

198 Pretreatment of IECs with methyl-beta-cyclodextrin partially blocks OMV-induced ho

199 Tetradeca-2,6-O-methyl-beta-cyclodextrin, per-2,6-OMe-beta-CD, is an unu

200 pid ratio from intact cells does not reflect methyl-beta-cyclodextrin plasma membrane extraction prop

201 e dynamin (K44A) or cholesterol depletion by methyl-beta-cyclodextrin prevented EGFR internalization.

202 Cholesterol depletion by methyl-beta-cyclodextrin prevented Kit-mediated activati

203 In parallel, methyl-beta-cyclodextrin primes the human PMN for subseq

204 ecryption of tissue factor was achieved with methyl-beta-cyclodextrin prior to complete disruption of

205 ng either m1 or m3 muscarinic receptors with methyl-beta-cyclodextrin produced a loss of localization

206 ate to inhibit IP(3)Rs negated the effect of methyl-beta-cyclodextrin, providing further support that

207 Methyl beta-cyclodextrin quantitatively extracted both c

208 Extraction of cholesterol with methyl-beta-cyclodextrin reduced comets, establishing th

209 holesterol in human fibroblasts (WI-38) with methyl-beta-cyclodextrin-reduced TF activity at the cell

210 Methyl-beta-cyclodextrin removed cholesterol from both c

211 This contrasts with the inhibitory effect of methyl-beta-cyclodextrin reported for other P2X subtypes

212 r cholesterol levels by brief treatment with methyl-beta-cyclodextrin resulted in a 100-fold reductio

213 th lipid rafts, yet disruption of rafts with methyl-beta-cyclodextrin resulted in a 3-fold stimulatio

214 of mouse brain plasma membrane vesicles with methyl-beta-cyclodextrin resulted in a significant reduc

215 letion of cellular cholesterol with the drug methyl-beta-cyclodextrin resulted in inhibition of palmi

216 Depletion of membrane cholesterol by methyl-beta-cyclodextrin resulted in reduced Na(+)-depen

217 h the cholesterol-binding agents filipin and methyl-beta-cyclodextrin resulted in the inhibition of s

218 these domains by cholesterol extraction with methyl-beta-cyclodextrin resulted in the release of viri

219 Treatment of plasma membrane vesicles with methyl-beta-cyclodextrin resulting in 75% cholesterol de

220 ol with 2-hydroxypropyl beta-cyclodextrin or methyl beta-cyclodextrin reversibly inhibited CT-induced

221 Cholesterol depletion and repletion with methyl-beta-cyclodextrin reversibly altered PI4KIIalpha

222 dextrin or enriched by exposing the cells to methyl-beta-cyclodextrin saturated with cholesterol.

223 al region that is palmitoylated and mediates methyl-beta-cyclodextrin-sensitive self-association of p

224 ys (amiloride, cytochalasin D, nystatin, and methyl-beta-cyclodextrin) showed that hCTR1 degradation

225 Cholesterol depletion with methyl-beta-cyclodextrin slowed Ras diffusion by a visco

226 sterol-binding agents filipin, nystatin and methyl beta-cyclodextrin specifically block FimH-mediate

227 ly, acute cholesterol depletion induced with methyl-beta-cyclodextrin stimulated relocation of NPC1L1

228 We find that cholesterol depletion with methyl-beta-cyclodextrin substantially reduces stimulate

229 s by extraction of cellular cholesterol with methyl-beta-cyclodextrin suffers from various adverse ef

230 asma membrane cholesterol is extracted using methyl beta-cyclodextrin, suggesting that lipid raft mic

231 inhibited by the cholesterol-depleting drug, methyl beta-cyclodextrin, suggesting that the physiologi

232 rnalization as does disruption of rafts with methyl-beta-cyclodextrin, suggesting raft exit enables i

233 dispersed after cholesterol extraction with methyl-beta-cyclodextrin, suggesting that the majority o

234 ion of membrane cholesterol by treating with methyl-beta-cyclodextrin suppressed deoxycholic acid (DC

235 cells with the cholesterol chelating agent, methyl-beta-cyclodextrin, that is thought to disrupt lip

236 cholesterol-sequestering drugs nystatin and methyl-beta-cyclodextrin, the dynamin-specific inhibitor

237 We used methyl beta-cyclodextrin to deplete cholesterol from pol

238 NF signaling in ECs, cells were treated with methyl-beta-cyclodextrin to disrupt caveolae.

239 ment of cells co-expressing CPM and B1R with methyl-beta-cyclodextrin to disrupt lipid rafts reduced

240 We have overcome these limitations using methyl-beta-cyclodextrin to solubilize VLCFA for rapid d

241 Some cells were incubated with methyl-beta-cyclodextrin (to deplete cholesterol from me

242 ycin A1, hypertonic sucrose) or lipid rafts (methyl-beta-cyclodextrin) to treat restrictive cells and

243 ntinuous sucrose density gradients, and that methyl-beta-cyclodextrin treatment causes a redistributi

244 Biochemical membrane fractionation and methyl-beta-cyclodextrin treatment demonstrated that thi

245 e found that depleting endogenous 7-DHC with methyl-beta-cyclodextrin treatment enhances Hedgehog act

246 ing sucrose gradient ultracentrifugation and methyl-beta-cyclodextrin treatment that CLEC-2 transloca

247 and increased to approximately 79 pN/mum by methyl-beta-cyclodextrin treatment to sequester membrane

248 virus, simian virus 40, was not affected by methyl-beta-cyclodextrin treatment.

249 Methyl-beta-cyclodextrin was also used to examine the re

250 DHE delivered via methyl-beta-cyclodextrin was delivered to both the apica

251 Treatment with methyl-beta-cyclodextrin was not associated with cytotox

252 r VIIa/tissue factor activity decrypted with methyl-beta-cyclodextrin was quantitatively similar to t

253 In addition, eNOS activation by methyl-beta-cyclodextrin was SR-BI dependent.

254 -soluble cholesterol (cholesterol mixed with methyl-beta-cyclodextrin), we observed an increase in DA

255 By using DHE loaded on methyl-beta-cyclodextrin, we followed this cholesterol a

256 owing a hypo-osmotic shock or treatment with methyl-beta-cyclodextrin were found to increase clusteri

257 which sequesters cholesterol) had no effect, methyl-beta-cyclodextrin (which extracts cholesterol) re

258 Incubation with methyl-beta-cyclodextrin, which disrupts caveolae, or wi

259 VECs treated with hypertonic medium and with methyl-beta-cyclodextrin, which disrupts lipid rafts.

260 ission, we treated hippocampal cultures with methyl-beta-cyclodextrin, which reversibly binds cholest

261 Methyl-beta-cyclodextrin, which sequesters cholesterol a

262 dramatically reduced by prior complexing of methyl-beta-cyclodextrin with cholesterol.

263 LTCC antagonist or disrupting caveolae with methyl-beta-cyclodextrin, with an associated approximate