ライフサイエンスコーパス: Triton X-100

1 pon the addition of nonionic detergent (0.1% Triton X-100).

2 of Jurkat cells in the presence of the agent Triton X-100).

3 +), O 2, alpha-ketoglutarate, ascorbate, and Triton X-100.

4 olubilized from frozen RBC by addition of 1% Triton X-100.

5 t is extracted from low density fractions by Triton X-100.

6 nel is reversibly inhibited by the detergent Triton X-100.

7 ective to facilitate CeO2-NPs transport than Triton X-100.

8 the presence of a sublethal concentration of Triton X-100.

9 s reactive on extraction of the protein into Triton X-100.

10 acrylate combined with a nonionic surfactant Triton X-100.

11 microdomains (DRMs) were extracted with cold Triton X-100.

12 GPI(+) PrP-sen resisted extraction with cold Triton X-100.

13 ral elasticity and resists solubilization by Triton X-100.

14 d resistance of the patches to extraction by Triton X-100.

15 n levels if cultured in the presence of 0.1% Triton X-100.

16 be reversed or prevented by the addition of Triton X-100.

17 ions of the host cell and was extractable by Triton X-100.

18 nce of high levels of salt and the detergent Triton X-100.

19 g of the GEM domains and their resistance to Triton X-100.

20 constructs for resistance to extraction with Triton X-100.

21 at pH 8 and is inhibited by 0.01% (or more) Triton X-100.

22 s, which were isolated in the presence of 1% Triton X-100.

23 f cell monolayers or tissue homogenates with Triton X-100.

24 ed iron oxidation, and was also sensitive to Triton X-100.

25 ut are disrupted in harsh detergents such as Triton X-100.

26 teinase K only when exosomes were exposed to Triton X-100.

27 e removed effectively by nonionic surfactant Triton X-100.

28 H 7), aqueous, micellar solutions of reduced Triton-X 100.

29 ase activity required Mg(2+) ions (8 mm) and Triton X-100 (0.25 mm) at pH 5.0.

30 Maximum PAP activity was dependent on Triton X-100 (20 mm), PA (2 mm), Mg(2+) (0.5 mm), and 2-

31 r the homogenization of the oil samples with Triton X-100, 200 muL of methanol was added to facilitat

32 les composed of 10% anionic phospholipids in Triton X-100 a monodisperse protein-lipid complex is for

33 When 0.1% reduced Triton X-100, a detergent that more closely simulates th

34 Conversely pre-extraction in Triton X-100, a treatment that promotes SNARE complexes

35 We utilize purified Triton-X 100, a nonionic surfactant, to make soap bubble

36 of urothelial plaques with 0.02-0.1 % (v/v) Triton X-100 allowed the stain to penetrate into the mem

37 Triton X-100 also thickens Lo domains, but partitions to

38 g in methanol, we report that the surfactant Triton-X 100 also yields a large absorbance or fluoresce

39 The protein was solubilized with 1% Triton X-100 and 0.5 M sodium chloride and then purified

40 of these observations, we used a mixture of Triton X-100 and 1-butanol and observed that water-solub

41 ne/HCl, pH 7, buffer containing 0.025% (w/v) Triton X-100 and 15 mM MgCl(2) provided optimum conditio

42 hR, were obtained for samples solubilized in Triton X-100 and assayed by use of a sinapinic acid matr

43 % or 1% sodium dodecyl sulfate (SDS) or 0.1% Triton X-100 and assayed for clinical chemistry and mala

44 The subsequent introduction of Triton X-100 and CoQ10 causes the MLs lysis and the cres

45 amprenavir, and the Envs were solubilized in Triton X-100 and isolated by sedimentation in a sucrose

46 h medium and hypersensitive to the detergent Triton X-100 and multiple antibiotics.

47 Milk sample slurries were prepared using Triton X-100 and nitric acid for direct analysis of Pb u

48 mide; and importantly, low concentrations of Triton X-100 and other non-ionic detergents were strongl

49 anced autolysis and increased sensitivity to Triton X-100 and penicillin, attributable in part to inc

50 The sarV mutant was more resistant to Triton X-100 and penicillin-induced lysis compared to th

51 emicellar aggregation of the DiC(6)SNPE with Triton X-100 and PLA(2).

52 The protein was solubilized with Triton X-100 and purified to near-homogeneity.

53 en perfused with PBS, followed by successive Triton X-100 and SDS solutions in saline buffer.

54 In Triton X-100 and sodium cholate solutions, the aggregate

55 SDS, Brij-35, Brij-58, Triton X-100 and Span-40 were explored for the extractio

56 s dependent on the presence of the detergent Triton X-100 and the methyldonor S-adenosylmethionine.

57 d on a single cryo-cooled crystal grown with Triton X-100 and the structure was solved by molecular r

58 KCl solution containing nonionic surfactant Triton X-100 and their translocation was studied at diff

59 In aqueous solution of nonionic surfactants (Triton X-100 and Tween 20) arrays from the second series

60 d from HeLa-Cx43(His)(6)/Cx45 cells by using Triton X-100 and were applied to a Ni(2+)-NTA column, wh

61 s (donor ages, 69-84 years) and treated with Triton X-100 and/or coated with a mixture of laminin (33

62 onorhamnolipid was compared to that of SDBS, Triton X-100, and ethanol.

63 ocked with cis-Golgi, were solubilized in 2% Triton X-100, and proteins were immunoprecipitated using

64 pilQ also resulted in reduced entry of heme, Triton X-100, and some antibiotics.

65 moderate concentrations, the activity of the Triton X-100- and octylglucoside-solubilized material co

66 gh concentrations of inorganic ions, using a Triton X-100 aqueous solution to dilute the sample durin

67 ted as detergent concentrations (Tween 80 or Triton X-100) are increased up to their critical micelle

68 ap the interface of the Bax oligomer we used Triton X-100 as a membrane surrogate and performed site-

69 duction of micellar organised media by using Triton X-100 as an extraction solvent.

70 nd basolateral plasma membrane domains using Triton X-100 as detergent, and characterized their lipid

71 the CPD transmembrane domain was soluble in Triton X-100 as was endogenous palmitoylated CPD, indica

72 Bovine ROS membranes were incubated with 1% Triton X-100 at 4 degrees C and subjected to density gra

73 After lysis with Triton X-100 at 4 degrees C and sucrose linear-density c

74 on of cells expressing the F protein with 1% Triton X-100 at 4 degrees C, ca. 40% of total, cell-asso

75 insolubility in nonionic detergents such as Triton X-100 at 4 degrees C.

76 e are solubilized by lower concentrations of Triton X-100, at least within certain temperature ranges

77 ondrial membranes contains up to 120 nmol of Triton X-100 bound per nanomole of the enzyme.

78 Removal of Triton X-100 bound to bovine cytochrome bc(1) was accomp

79 el resistance to HAs (e.g., erythromycin and Triton X-100) but only a twofold increase in resistance

80 rmediates are disrupted by solubilization in Triton X-100, but chemical cross-linking stabilizes a pu

81 s was more easily perturbed by the detergent Triton X-100, but not other non-ionic detergents.

82 by dilute buffer, high salt concentrations, Triton X-100, Ca(2+)-dipicolinic acid, dithiothreitol, o

83 (pH 7.6) containing 0.1 M NaCl and 1% (v/v) Triton X-100 caused liberation of the Ru(bpy)32+ from th

84 sucrose gradient ultracentrifugation of cold Triton X-100 cell lysates yielded both CD36 and caveolin

85 Western blot analysis of Triton X-100 cold-extracted membrane fractions confirmed

86 e complexation and extraction (pH, DDTC, and Triton X-100 concentration, vortex agitation time and co

87 dependent binding of cytoplasmic proteins to Triton X-100 cytoskeletons of L-929 cells grown on colla

88 , these GPC microdomains are soluble in cold Triton X-100 detergent and are thus distinct from conven

89 WT beta2 subunits are resistant to live cell Triton X-100 detergent extraction from the hippocampal a

90 activity by approximately 70% and abolished Triton X-100 detergent inhibition of Ca-dependent nucleo

91 sites maintained 'lipid rafts' as defined by Triton X-100 detergent resistant membrane formation.

92 glycosylation status, expression level, and Triton X-100 detergent sensitivity.

93 ions containing BIG/TIR3 and partitions into Triton X-100 detergent-resistant membrane (DRM) fraction

94 e Nephrin and Podocin, Neph1 was enriched in Triton X-100 detergent-resistant membrane fractions.

95 A protocol to prepare Triton X-100 detergent-resistant membranes (DRMs) was de

96 that of monomeric BR solubilized in reduced Triton X-100 detergent.

97 nfirmed by TEM, treatment of sperm with 0.2% Triton X-100 disrupted the plasma, acrosomal, and inner

98 We demonstrated that Triton X-100 dissociated the heptameric complex into thr

99 ECM by detergent decellularization methods (Triton X-100, DOC and SDS are compared).

100 Treatment of blood samples with 0.1% SDS or Triton X-100 does not inactivate EBOV.

101 ced in the presence of low concentrations of Triton X-100 either by brief exposure to 80 degrees C or

102 nol gave slightly better results than when a Triton X-100-ethanol solution was used for dilution.

103 all TM layers, but not in tissues killed by Triton X-100 exposure.

104 liposomes generated from a flippase-enriched Triton X-100 extract of ER can flip analogues of phospha

105 By using cold Triton X-100 extractability of different lipids as a cri

106 Triton X-100 extracted approximately 10% of the cellular

107 phalloidin staining and Western blotting of Triton X-100 extracted cell lysate.

108 O flipping in proteoliposomes generated from Triton X-100-extracted Saccharomyces cerevisiae microsom

109 was found to be largely insoluble following Triton X-100 extraction and cofractionationed with bioch

110 r localization of CLIC-5A was retained after Triton X-100 extraction and was disrupted by treatment w

111 S disk membrane was found to be resistant to Triton X-100 extraction at 4 degrees C.

112 this fraction was resistant to high salt and Triton X-100 extraction at pH 6.5.

113 Experiments using Triton X-100 extraction followed by OptiPrep density gra

114 is showed that full-length LEDGF/p75 resists Triton X-100 extraction from chromatin.

115 We now demonstrate by Triton X-100 extraction immunoprecipitation and in vitro

116 Triton X-100 extraction of cardiac muscle fibers promote

117 with CKI-7, and Cx43 content was analyzed by Triton X-100 extraction, cell-surface biotinylation, and

118 ng the cell membrane and soluble proteins by Triton X-100 extraction, we found that the remaining com

119 teins CD4, CXCR4, and CCR5, as determined by Triton X-100 extraction.

120 t disrupted by hypotonic treatment and brief Triton X-100 extraction.

121 d, at least at 4 degrees C, are resistant to Triton X-100 extraction.

122 We observed that Triton X-100 extracts of N. gonorrhoeae strain F62 conta

123 rast to assays utilizing intact membranes or Triton X-100 extracts, assays using CHAPS- or tDOC-washe

124 l membranes were extracted sequentially with Triton X-100, followed by DNase I or potassium iodide to

125 Permeabilization with Triton X-100 for 60 min also abolished hypoxic relaxatio

126 The resulting Triton X-100-free cytochrome bc(1) retained nearly full

127 rthermore, GPC was more readily extracted by Triton X-100 from adenosine triphosphate (ATP)-depleted

128 ure, buffered at pH 7.8 and containing Tris, Triton X-100, glucose-6-phosphate, nicotinamide adenine

129 to protein extraction and reconstitution in Triton X-100/glycerol-permeabilized smooth muscle fibers

130 to a butyl Sepharose column and eluted in a Triton X-100 gradient.

131 ta activity was abolished by the denaturants triton X-100, Gua-HCl, Gua-thiocyanate, SDS and urea in

132 ed IC50 values of three cytotoxic chemicals, Triton X-100, H2O2, and cadmium chloride, as model compo

133 A mixture of phospholipids and Triton X-100 in a molar ratio of 5:1 forms well-aligned

134 turing detergent perfluoro-octanoic acid and Triton X-100 in combination with gel filtration, sucrose

135 s largely relieved by the inclusion of 0.01% Triton X-100 in the assay solutions, which has been sugg

136 by sodium dodecyl sulfate, Nonidet P-40, or Triton X-100 in the mass spectrometry analysis.

137 is opposite to the observed orientation for Triton X-100 in the SCP-2-like domain from the peroxisom

138 e neuroglian is resistant to extraction with Triton X-100 in the sorting zone and nerve layer, possib

139 mphiphiles, sodium dodecyl sulfate (SDS) and Triton X-100, in addition to a similar synthesized dendr

140 TcGP63 is soluble in cold Triton X-100, in contrast to Leishmania GP63, which is d

141 tion of cardiac myocytes with saponin and/or Triton X-100 increased NAADP synthesis, indicating that

142 erythrocytes were more easily extractable by Triton X-100, indicating weaker association to the cytos

143 of USA300 was found to be more resistant to Triton X-100-induced autolysis and also to lysis by lyso

144 on of gcp expression can effectively inhibit Triton X-100-induced lysis, eliminate penicillin- and va

145 otidase activities while greatly attenuating Triton X-100 inhibition of Mg-dependent nucleotidase act

146 mple dilution with an OIS and the surfactant Triton X-100 (inorganic media) or ethanol (organic media

147 pid raft association, using as the criterion Triton X-100 insolubility, loss of raft association did

148 ls; like HMW2, HMW2Deltamid exhibited marked Triton X-100 insolubility.

149 with the actin cytoskeleton, we isolated the Triton X-100 insoluble actin cytoskeleton from platelets

150 We also found similar Triton X-100 insoluble forms of alpha-synuclein in an al

151 isfolded and aggregated alpha-synuclein in a Triton X-100 insoluble fraction as well as a high molecu

152 IL-11 induced a shift of hsp25 to Triton x-100 insoluble fractions containing cytoskeletal

153 cking the N-terminal domain, was detected in Triton X-100 insoluble fractions in Western blot analysi

154 istribution was characterized by analysis of Triton x-100 insoluble fractions, 2-D isoelectric focusi

155 lted in a redistribution of PrP(C) away from Triton X-100 insoluble lipid rafts.

156 was associated almost exclusively with 0.1% Triton X-100 insoluble material, consistent with its sig

157 ibited by DP-S2849G-GFP in the cytoskeletal (Triton X-100 insoluble) fraction, and keratin filament r

158 lated (activated) EGFR was found only in the Triton X-100-insoluble (lipid raft) fraction, whereas to

159 butes to the edge of the lamellae and to the Triton X-100-insoluble actin cytoskeleton of activated W

160 ither WTsyn or A53Tsyn led to a reduction in Triton X-100-insoluble aggregates and an increase in pro

161 Expression of 16 kDa also resulted in a Triton X-100-insoluble aggregation of an unusual 87-kDa

162 localized in Triton X-100-soluble as well as Triton X-100-insoluble cell fractions.

163 Flightless-I targets caspase-11 to the Triton X-100-insoluble cytoskeleton fraction and the cel

164 Triton X-100-insoluble cytoskeletons were stretched by 1

165 tin and moesin and was found enriched in the Triton X-100-insoluble fraction along with p67(phox) and

166 searched for Dyrk1A binding proteins in the Triton X-100-insoluble fraction extracted with urea and

167 ome isoforms being enriched primarily in the Triton X-100-insoluble fraction in lens tissue.

168 ounts of all three proteins increased in the Triton X-100-insoluble fraction of cell lysates and decr

169 GFP-CFTR localized to low density Triton X-100-insoluble fractions in lysates of Madin-Dar

170 The Triton X-100-insoluble fractions of M. penetrans and M.

171 Both receptors were excluded from Triton X-100-insoluble lipid rafts, and at high agonist

172 brain NgR1 and NgR2 are strongly enriched in Triton X-100-insoluble lipid rafts.

173 c tail abrogated the association of BHA with Triton X-100-insoluble lipid rafts.

174 re spermatozoa, caveolin-1 was enriched in a Triton X-100-insoluble membrane fraction, as well as in

175 fts, Triton X-100-soluble fractions, and the Triton X-100-insoluble pellet following apical infection

176 Flotation of the cold Triton X-100-insoluble portion of membranes on sucrose g

177 post-translationally converted into a 20-kDa Triton X-100-insoluble proteasome substrate.

178 The amount of endogenous p130Cas in the Triton X-100-insoluble protein fraction, and fibronectin

179 redistribution of Kir2.1 and Kv2.1 from the Triton X-100-insoluble to the Triton X-100-soluble membr

180 Triton X-100 is employed at finely tuned concentrations

181 ether dodecyl maltoside, decyl maltoside, or Triton X-100 is the primary solubilizing detergent or th

182 t when the apposed bilayers are dissolved in Triton X-100; it is also observed during fusion of isola

183 to nonionic micelles in the running buffer (Triton X-100), linking the tagged DNA to the micellar dr

184 Density gradient centrifugation of Triton X-100 lysates from B lymphocytes demonstrated tha

185 radient analysis of plasma membrane-labeled, Triton X-100-lysed cells shows that proximity measured b

186 non-detergent or detergent-based (saponin or Triton X-100) methods.

187 t interact in the hetero-complex formed in a Triton X-100 micelle as a membrane surrogate.

188 ha (>15-fold) with a K(a) of 2.4 mol % C-1-P/Triton X-100 micelle.

189 We also show that smaller Triton X-100 micelles give a read length of 103 bases in

190 Arabidopsis SphK with Sph presented in mixed Triton X-100 micelles indicated that SphK associates wit

191 zyme activity in a cell-free system using PA/Triton X-100 mixed micelles as substrate, analyzing it i

192 Binding of DiC(6)SNPE when presented as Triton X-100 mixed micelles saturated at 0.93 binding si

193 centrations at all surface concentrations in Triton X-100 mixed micelles.

194 hange in the lipin 1beta affinity for the PA/Triton X-100 mixed micelles.

195 The nonionic detergents Triton X-100, Nonidet P-40, Brij, Tween, and octylglucos

196 mbrane expressing CFTR in detergents such as Triton X-100, Nonidet P-40, deoxycholate, and SDS tended

197 o]-1-propanesulfonate (CHAPS, zwitterionic), Triton X-100 (nonionic), sodium dodecyl sulfate (SDS, an

198 d point temperature of non-ionic surfactant, Triton X-100 occurred and complex was entrapped in surfa

199 in a highly purified plant PSII preparation (Triton X-100, octylthioglucoside).

200 We have studied the solubilization by Triton X-100 of binary mixtures composed of egg sphingom

201 ticity because the micelle-forming detergent Triton X-100 only minimally affects TRPV1 properties.

202 LpxE activity is dependent upon Triton X-100, optimal near pH 6.5, and Mg2+-independent.

203 omere-binding activity () was solubilized by Triton X-100 or micrococcal nuclease extraction, whereas

204 Perturbations caused by Triton X-100 or mutations convert faster to slower forms

205 were obtained if extraction media contained Triton X-100 or sodium dodecyl sulfate.

206 les (e.g., diheptanoylphosphatidylcholine or Triton X-100) or 0.1-0.2 M inorganic salts.

207 %, but it was not inhibited by Nonidet P-40, Triton X-100, or octyl glucoside, even at concentrations

208 Analysis of surface dilution kinetics with Triton X-100/PA-mixed micelles yielded constants for sur

209 of 4.2, 4.5, and 4.3 mol %, respectively) in Triton X-100/PA-mixed micelles.

210 Confocal microscopy of Triton X-100 permeabilized neutrophils showed that a sma

211 Triton X-100-permeabilized proplatelets containing dynei

212 In this study, a Triton X-100/phosphatidylcholine (PC) mixed micelle assa

213 centration of substrate phospholipids in the Triton X-100/phospholipid mixed micelles.

214 Platelet-derived FV/Va, purified from Triton X-100 platelet lysates was composed of a mixture

215 The effects of the nonionic surfactant Triton X-100 (poly(ethylene glycol) tert-octylphenyl eth

216 When lipid vesicles were disrupted by Triton X-100, PrP aggregation was necessary to maintain

217 inner and outer leaflet lipids, whereas the Triton X-100 rafts contained a preponderance of outer le

218 lin than did the non-EGF receptor-containing Triton X-100 rafts.

219 The Triton X-100 releases the cytoplasmic contents into the

220 opy, SCD overexpression led to a decrease of Triton X-100-resistant domains in the plasma membrane, i

221 Analysis of proteins associated with the Triton X-100-resistant fraction showed it to be enriched

222 Biochemical analysis of the Triton X-100-resistant fraction showed it to be enriched

223 ll of the Cx43 in G0 cells is assembled into Triton X-100-resistant junctions, Cx43-ZO-1 interaction

224 orts the isolation and characterization of a Triton X-100-resistant membrane fraction from homogenate

225 t with EGCG caused a marked reduction in the Triton X-100-resistant membrane fraction.

226 to cellular membranes but are not present in Triton X-100-resistant membrane rafts.

227 The Triton X-100-resistant membranes described herein did no

228 class V myosin isoforms are associated with Triton X-100-resistant membranes isolated from mouse for

229 When the Triton X-100-resistant membranes were treated with methy

230 The lipid profiles of the Triton X-100-resistant membranes were virtually identica

231 (QRD(194-196)) is required for strong (i.e., Triton X-100-resistant) alpha 3 beta 1 association and f

232 d Brij 98-resistant) and those that did not (Triton X-100-resistant), we used multidimensional electr

233 7-s incubation times were 290 and 250 microM Triton X-100, respectively.

234 was diluted and homogenised by n-hexane and Triton X-100, respectively.

235 ation of transfected cells with digitonin or Triton X-100, respectively.

236 Addition of submicellar amounts of Triton X-100 resulted in a linear nonsaturating response

237 derivatives in aqueous solutions of reduced Triton X-100 (RTX-100) were determined by measurements o

238 th itself, integrins, or other tetraspanins (Triton X-100-sensitive but Brij 96-resistant) were indep

239 sodium dodecyl sulfate (SDS), Lubrol PX, or Triton X-100, separately or in combination with 1-hexano

240 Binding of DiC(6)SNPC with 2.0 mM Triton X-100 showed positive cooperativity (Hill coeffic

241 c(1) is fully active; however, protein-bound Triton X-100 significantly interferes with structural st

242 Triton X-100 solubility assays demonstrate that mutant D

243 First, we did cold Triton X-100 solubility assays.

244 ve compound, did not significantly alter the Triton X-100 solubility properties of the membrane.

245 both by fluorescence microscopy and by actin Triton X-100 solubility.

246 anol were microdissected and subjected to 1% Triton X-100 solubilization at 4 degrees C.

247 -48 h) certain mixtures were not amenable to Triton X-100 solubilization at one or more temperatures.

248 ne sphingolipids, for enabling resistance to Triton X-100 solubilization, and for interacting with sp

249 rol are colocalized and are resistant to the Triton X-100 solubilization.

250 amounts of soluble CD44S in POAG aqueous and Triton X-100-solubilized CD44H characterized POAG in the

251 Sucrose gradient analysis of Triton X-100-solubilized connexins showed that either Cx

252 uced using nonspecific alkaline phosphatase, Triton X-100-solubilized membranes from DGK1-overexpress

253 Cytochrome bc(1) isolated from Triton X-100-solubilized mitochondrial membranes contain

254 Using proteoliposomes reconstituted from Triton X-100-solubilized rat liver ER membrane proteins,

255 osomes prepared from phosphatidylcholine and Triton X-100-solubilized rat liver ER-membrane proteins.

256 minally truncated HMW2 derivative was partly Triton X-100 soluble and incapable of restoring HMW1, HM

257 TJ proteins were redistributed/localized in Triton X-100-soluble as well as Triton X-100-insoluble c

258 ereas total cellular EGFR was present in the Triton X-100-soluble fraction.

259 Dimers and oligomers were found in Triton X-100-soluble fractions from adenovirus-mediated

260 hyperphosphorylated occludin in lipid rafts, Triton X-100-soluble fractions, and the Triton X-100-ins

261 Claudin-4 was localized to Triton X-100-soluble gradient fractions of control or CP

262 in normal astrocytes exists primarily in the Triton X-100-soluble membrane fraction, distinct from th

263 Kv2.1 from the Triton X-100-insoluble to the Triton X-100-soluble membrane fraction.

264 raction of cell lysates and decreased in the Triton X-100-soluble pool.

265 Ubr1 function leads slGFP to accumulate in a Triton X-100-soluble state with slGFP degradation interm

266 quantitatively removed using injection of 5% Triton X-100 solution, generating a fresh surface for ea

267 ively removed using a cleaning method of 0.5%Triton X-100 sonication plus 1 N nitric acid sonication.

268 e inner membrane fraction was solubilized by Triton X-100, suggesting that GerD is a lipoprotein, and

269 Interestingly, CHAPS and Triton X-100, thanks to similar surface binding preferen

270 ional channels, even without the presence of Triton X-100 that has been found necessary for in vitro-

271 When extracted with Triton X-100, the isolated Ndi1 did not contain Q.

272 Some tissues were exposed to Triton X-100 to establish dead tissue controls.

273 ndorff-perfused mouse hearts were treated by triton X-100 to produce endothelial dysfunction and subs

274 can be stimulated 35-fold by the addition of Triton X-100 to the reaction mixture.

275 function during reperfusion was impaired in triton X-100 treated hearts compared with vehicle-treate

276 y by affinity isolation using native but not Triton X-100-treated budded vesicles.

277 Triton X-100 treatment of transgenic mouse cardiac myofi

278 erently on native gels both before and after Triton X-100 treatment.

279 l sulfate (SDS), sodium deoxycholate, Chaps, Triton X-100, Triton X-114, NP-40, Brij-35, octyl glucos

280 llows: n-octyl glucoside, dodecyl maltoside, Triton X-100, Tween 20, 3-[(3-cholamidopropyl)dimethylam

281 xperiments in which neutral additives (e.g., Triton X-100, Tween 20, poly(ethylene glycol)) are remov

282 ort, we confirm that TRAF2 translocates to a Triton X-100 (TX)-insoluble compartment upon TNF-R2 enga

283 month-old mice by intranasal irrigation with Triton X-100 (TX).

284 by using extraction with the mild detergent Triton X-100 (TX-100) followed by a sucrose gradient flo

285 (OLs) in culture MOG is not raft associated [Triton X-100 (TX-100) soluble, 4 degrees C].

286 rlin resists solubilization by the detergent Triton X-100 (TX-100), a property commonly attributed to

287 majority of CEACAMs were solubilized by cold Triton X-100 (TX-100), indicating their absence from lip

288 s the tegument was resistant to removal with Triton X-100 (TX-100), whereas it was lost nearly comple

289 e demonstrated that Gs alpha migrates from a Triton X-100 (TX-100)-insoluble membrane domain (lipid r

290 otein expression by Western blot analysis of Triton X-100 (TX-100)-soluble and TX-100-insoluble cell

291 (erythro-GUVs) when exposed to the detergent Triton X-100 (TX-100).

292 ity, and viability caused by the presence of Triton X-100 (TX100), a nonionic surfactant, were studie

293 exhibit differential functional stability in Triton X-100 versus dodecyl maltoside.

294 Sucrose gradient analysis of Triton X-100 virus lysates showed that Gag and envelope

295 In one assay, insolubility in Triton X-100 was assessed in bilayers composed of sterol

296 s of IPC synthase activity solubilized in 2% Triton X-100 was between 1.5 x 10(6) and 20 x 10(6) Da,

297 An average LC50 value of 138 microM for Triton X-100 was obtained for an incubation period of 7-

298 The presence of a nonionic detergent, Triton X-100, was found essential to produce a multilaye

299 from beta(2)m upon exposure to the detergent Triton X-100, whereas a mutant expressing only glycan 2

300 Combining the use of Triton X-100 with the newly introduced UPLC method, we w