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1 terol repletion fully reversed the effect of methyl beta-cyclodextrin.
2 ynamin-2 mutant (K44A) or treated cells with methyl-beta-cyclodextrin.
3 ane order and by cholesterol depletion using methyl-beta-cyclodextrin.
4 ately 50% when cholesterol is extracted with methyl-beta-cyclodextrin.
5 xidase uptake after cholesterol depletion by methyl-beta-cyclodextrin.
6 ition of human red blood cell cholesterol to methyl-beta-cyclodextrin.
7 cells with the cholesterol-depleting agent, methyl-beta-cyclodextrin.
8 disrupted by cholesterol depletion utilizing methyl-beta-cyclodextrin.
9 holesterol-rich domains during extraction by methyl-beta-cyclodextrin.
10 ane lipid rafts, similar to positive control 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 l by incubating neonatal cardiomyocytes with methyl-beta-cyclodextrin.
20 Hz) and after disruption of lipid rafts with methyl-beta-cyclodextrin.
21 d when cholesterol stores were depleted 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 to nonraft domains, similar to the action of methyl-beta-cyclodextrin.
25 ere removed from erythrocyte membranes using methyl-beta-cyclodextrin.
26 ng three independent methods: 1) exposure to methyl-beta-cyclodextrin, 2) treatment with the HMG-CoA
27 mM sulfobutylether-beta-cyclodextrin, 40 mM methyl-beta-cyclodextrin, 5 mM carbonate buffer at pH 10
30 tion of this Akt subspecies was ablated with methyl-beta-cyclodextrin, a cholesterol-binding compound
39 y, disruption of the clustered caveolae with methyl-beta-cyclodextrin also dispersed the Cav-actin st
41 Signaling prompted by cholesterol efflux to methyl-beta-cyclodextrin also was prevented, indicating
43 olemmal sites and this was prevented by 2 mm methyl-beta-cyclodextrin, an agent that disrupts caveola
45 he metalloprotease inhibitor batimastat, and methyl-beta-cyclodextrin and filipin, which block lipid
47 at the cholesterol-binding heptasaccharides, methyl-beta-cyclodextrin and OH-propyl-beta-cyclodextrin
48 rylation/activation was also decreased after methyl-beta-cyclodextrin and statin treatment but increa
49 urons, through cholesterol-scavenging drugs (methyl-beta-cyclodextrin) and the enzymatic breakdown of
54 filling and occupancy of binding sites; (ii) methyl-beta-cyclodextrin, as a FA acceptor, to observe t
55 s were found to be soluble when treated with methyl-beta-cyclodextrin before extraction with ice-cold
56 K562 cells treated with paraformaldehyde or methyl-beta-cyclodextrin before ligand coupling were les
58 nt of T-cells with the lipid raft inhibitor, methyl-beta-cyclodextrin, blocked the association betwee
59 ion of cholesterol from confluent cells with methyl-beta-cyclodextrin both induced tyrosine phosphory
61 Depletion of cholesterol from rafts with methyl-beta-cyclodextrin caused a redistribution of TNFR
63 bacteria with cholesterol extraction reagent methyl-beta-cyclodextrin caused their ultrastructural ch
64 on of membrane cholesterol by treatment with methyl-beta-cyclodextrin (CD) or by culturing cells in l
65 sses, endothelial cells were pretreated with methyl-beta-cyclodextrin (CD) or filipin to ablate raft
66 xin by phosphate-buffered saline (PBS), 0.1% methyl-beta-cyclodextrin (CD), or CD plus cholesterol (0
69 rosome but following cholesterol efflux with methyl-beta-cyclodextrin, clusters containing zona-bindi
70 BAPTA-AM or disruption of lipid rafts using methyl beta-cyclodextrin completely abrogated IFN-gamma-
71 tro with excess cholesterol by a cholesterol/methyl-beta-cyclodextrin complex, phenocopying SR-BI KO
72 r 72 h with cholesterol by using cholesterol:methyl-beta-cyclodextrin complexes, leading to approxima
74 and that disrupting lipid raft formation by methyl-beta-cyclodextrin decreased NO production and apo
75 ion of sgk1 with the apical surface, whereas methyl-beta-cyclodextrin decreased the association of sg
77 ng, and internalization were not affected by methyl-beta-cyclodextrin depletion, whereas envelope cho
79 epletion of plasma membrane cholesterol with methyl-beta-cyclodextrin did not affect forskolin-stimul
81 disruption of lipid rafts by treatment with methyl-beta-cyclodextrin did not decrease the GTPase act
83 he cholesterol-depleting reagent saponin and methyl-beta-cyclodextrin differentially disrupted the fo
85 lesterol depletion of alpha T3-1 cells using methyl-beta-cyclodextrin disrupted GnRHR but not c-raf k
86 odstream parasites with cholesterol-specific methyl-beta-cyclodextrin disrupts both membrane liquid o
88 id rafts with the cholesterol-depleting drug methyl-beta-cyclodextrin disrupts the raft localization
92 aft disruption by cholesterol depletion with methyl-beta-cyclodextrin eliminates these light rafts.
95 mbrane cholesterol by metabolic depletion or methyl-beta-cyclodextrin extraction was found to both in
96 thermore, knockdown of caveolae formation by methyl-beta-cyclodextrin failed to prevent wild-type cav
98 xposure of Hep3B cells to the raft disrupter methyl-beta-cyclodextrin for 1-10 min followed by IL-6 s
99 Treatment of HSV-1-infected Vero cells with methyl beta-cyclodextrin from 2 to 9 h postentry reduced
100 e data show that cholesterol, solubilized by methyl-beta-cyclodextrin, greatly reduced the levels of
103 thermore, the disruption of SM-rich rafts by methyl-beta-cyclodextrin impaired myosin activation and
104 king in response to postprandial micelles or methyl-beta-cyclodextrin in cultured enterocytes, and it
106 ied that depleting cellular cholesterol with methyl-beta-cyclodextrin increased the resilience of str
107 port here that depletion of cholesterol with methyl-beta-cyclodextrin increases cell surface (125)I-E
108 endogenous cholesterol from oocytes using a methyl-beta-cyclodextrin incubation procedure without ca
109 ion of NF-kappaB and MAPKs was unaffected by methyl-beta-cyclodextrin indicating that, in airway smoo
110 ally extracted upon cholesterol depletion by methyl-beta-cyclodextrin, indicating that they were asso
111 In A431 cells, depletion of cholesterol with methyl-beta-cyclodextrin induced an increase in both bas
113 We previously described a technique in which methyl-beta-cyclodextrin-induced lipid exchange is used
119 dies showed that cholesterol depletion using methyl-beta-cyclodextrin inhibited preimplantation devel
121 annot occur, demonstrate that treatment with methyl-beta-cyclodextrin leads to an increase in intrins
124 Infectivity was exquisitely sensitive to methyl-beta-cyclodextrin (M beta CD) and nystatin, which
125 his blue shift disappeared after exposure to methyl-beta-cyclodextrin (m beta CD), which disrupts lip
126 ith BKV and the cholesterol-depleting agents methyl beta cyclodextrin (MBCD) and nystatin (Nys), drug
130 epletion of plasma membrane cholesterol with methyl-beta-cyclodextrin (MbetaCD) caused activation of
131 tment of cells with the raft disrupting drug methyl-beta-cyclodextrin (MbetaCD) caused activation of
134 atment with the cholesterol-extracting agent methyl-beta-cyclodextrin (MbetaCD) not only disrupted th
135 t of peripheral blood lymphocytes (PBL) with methyl-beta-cyclodextrin (MbetaCD) or cytochalasin reduc
136 rupting rafts by removal of cholesterol with methyl-beta-cyclodextrin (MbetaCD) or destabilizing the
137 epletion of plasma membrane cholesterol with methyl-beta-cyclodextrin (MbetaCD) relocalized raft-resi
141 gated the effect of cholesterol depletion by methyl-beta-cyclodextrin (MbetaCD) treatment on influenz
142 eceptor mediates this signaling specificity, methyl-beta-cyclodextrin (MbetaCD) treatment was used to
145 ntum chagasi promastigotes were treated with methyl-beta-cyclodextrin (MbetaCD), a sterol-chelating r
146 mbrane cholesterol levels were reduced using methyl-beta-cyclodextrin (mbetaCD), as confirmed by Ampl
147 he cells with the caveolae-disrupting agent, methyl-beta-cyclodextrin (mbetaCD), selectively inhibite
151 Acute depletion of cholesterol with 5 mm methyl-beta-cyclodextrin (MCD) caused a substantial incr
153 sly shown that depletion of cholesterol with methyl-beta-cyclodextrin (MCD) disrupts caveolar microdo
154 atment with the cholesterol depleting agent, methyl-beta-cyclodextrin (MCD), significantly inhibited
155 STARD4 with that of a simple sterol carrier, methyl-beta-cyclodextrin (MCD), when STARD4 and MCD were
157 us laevis oocytes with cholesterol-depleting methyl-beta-cyclodextrin (MebetaCD) stimulates phosphory
160 e, cholesterol depletion of macrophages with methyl-beta-cyclodextrin normalized FC content between t
162 minated by disruption of caveolae with 10 mM methyl beta-cyclodextrin or by small interfering RNA dir
163 Finally, depletion of either cholesterol by methyl beta-cyclodextrin or caveolin-1 by siRNA signific
164 We showed that cholesterol depletion by methyl beta-cyclodextrin or filipin did not affect virus
165 e current study, cholesterol, solubilized by methyl- beta-cyclodextrin or ethanol, was added to the c
167 ither short-term cholesterol chelation using methyl-beta-cyclodextrin or by stable knockdown of caveo
171 henomena, we used growth media enriched with methyl-beta-cyclodextrin or cholesterol to reduce or ele
172 e microdomains by acute exposure of cells to methyl-beta-cyclodextrin or chronic exposure to differen
174 ontent was depleted by exposing the cells to methyl-beta-cyclodextrin or enriched by exposing the cel
176 disrupted by pretreatment of the cells with methyl-beta-cyclodextrin or Filipin III, hence implicati
178 th agents that deplete membrane cholesterol (methyl-beta-cyclodextrin or lovastatin) disrupted caveol
180 rthermore, pretreatment of the bacteria with methyl-beta-cyclodextrin or NBD-cholesterol deprived the
181 with cholesterol-sequestering drugs such as methyl-beta-cyclodextrin or nystatin and then exposed to
183 icient toxoids or pretreatment of cells with methyl-beta-cyclodextrin) or osmotic protection of targe
184 urthermore, cholesterol lowering by statins, methyl-beta-cyclodextrin, or filipin also activates PKA
185 ced either in vitro, by treatment with 25 mM methyl-beta-cyclodextrin, or in vivo, by subjecting anim
189 pid ratio from intact cells does not reflect methyl-beta-cyclodextrin plasma membrane extraction prop
190 e dynamin (K44A) or cholesterol depletion by methyl-beta-cyclodextrin prevented EGFR internalization.
193 ecryption of tissue factor was achieved with methyl-beta-cyclodextrin prior to complete disruption of
194 ng either m1 or m3 muscarinic receptors with methyl-beta-cyclodextrin produced a loss of localization
195 ate to inhibit IP(3)Rs negated the effect of methyl-beta-cyclodextrin, providing further support that
198 holesterol in human fibroblasts (WI-38) with methyl-beta-cyclodextrin-reduced TF activity at the cell
200 This contrasts with the inhibitory effect of methyl-beta-cyclodextrin reported for other P2X subtypes
201 r cholesterol levels by brief treatment with methyl-beta-cyclodextrin resulted in a 100-fold reductio
202 th lipid rafts, yet disruption of rafts with methyl-beta-cyclodextrin resulted in a 3-fold stimulatio
203 of mouse brain plasma membrane vesicles with methyl-beta-cyclodextrin resulted in a significant reduc
204 letion of cellular cholesterol with the drug methyl-beta-cyclodextrin resulted in inhibition of palmi
206 h the cholesterol-binding agents filipin and methyl-beta-cyclodextrin resulted in the inhibition of s
207 these domains by cholesterol extraction with methyl-beta-cyclodextrin resulted in the release of viri
208 Treatment of plasma membrane vesicles with methyl-beta-cyclodextrin resulting in 75% cholesterol de
209 ol with 2-hydroxypropyl beta-cyclodextrin or methyl beta-cyclodextrin reversibly inhibited CT-induced
210 Cholesterol depletion and repletion with methyl-beta-cyclodextrin reversibly altered PI4KIIalpha
211 dextrin or enriched by exposing the cells to methyl-beta-cyclodextrin saturated with cholesterol.
212 al region that is palmitoylated and mediates methyl-beta-cyclodextrin-sensitive self-association of p
213 ys (amiloride, cytochalasin D, nystatin, and methyl-beta-cyclodextrin) showed that hCTR1 degradation
215 sterol-binding agents filipin, nystatin and methyl beta-cyclodextrin specifically block FimH-mediate
216 ly, acute cholesterol depletion induced with methyl-beta-cyclodextrin stimulated relocation of NPC1L1
217 We find that cholesterol depletion with methyl-beta-cyclodextrin substantially reduces stimulate
218 s by extraction of cellular cholesterol with methyl-beta-cyclodextrin suffers from various adverse ef
219 asma membrane cholesterol is extracted using methyl beta-cyclodextrin, suggesting that lipid raft mic
220 inhibited by the cholesterol-depleting drug, methyl beta-cyclodextrin, suggesting that the physiologi
221 rnalization as does disruption of rafts with methyl-beta-cyclodextrin, suggesting raft exit enables i
222 dispersed after cholesterol extraction with methyl-beta-cyclodextrin, suggesting that the majority o
223 ion of membrane cholesterol by treating with methyl-beta-cyclodextrin suppressed deoxycholic acid (DC
224 cells with the cholesterol chelating agent, methyl-beta-cyclodextrin, that is thought to disrupt lip
225 cholesterol-sequestering drugs nystatin and methyl-beta-cyclodextrin, the dynamin-specific inhibitor
228 ment of cells co-expressing CPM and B1R with methyl-beta-cyclodextrin to disrupt lipid rafts reduced
229 We have overcome these limitations using methyl-beta-cyclodextrin to solubilize VLCFA for rapid d
231 ycin A1, hypertonic sucrose) or lipid rafts (methyl-beta-cyclodextrin) to treat restrictive cells and
232 ntinuous sucrose density gradients, and that methyl-beta-cyclodextrin treatment causes a redistributi
234 e found that depleting endogenous 7-DHC with methyl-beta-cyclodextrin treatment enhances Hedgehog act
235 ing sucrose gradient ultracentrifugation and methyl-beta-cyclodextrin treatment that CLEC-2 transloca
236 and increased to approximately 79 pN/mum by methyl-beta-cyclodextrin treatment to sequester membrane
241 r VIIa/tissue factor activity decrypted with methyl-beta-cyclodextrin was quantitatively similar to t
243 -soluble cholesterol (cholesterol mixed with methyl-beta-cyclodextrin), we observed an increase in DA
245 which sequesters cholesterol) had no effect, methyl-beta-cyclodextrin (which extracts cholesterol) re
247 VECs treated with hypertonic medium and with methyl-beta-cyclodextrin, which disrupts lipid rafts.
248 ission, we treated hippocampal cultures with methyl-beta-cyclodextrin, which reversibly binds cholest
251 LTCC antagonist or disrupting caveolae with methyl-beta-cyclodextrin, with an associated approximate
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