ライフサイエンスコーパス: cytochalasin B

1 lostery (uptake stimulation by subsaturating cytochalasin B).

2 ell as by blocking actin polymerization with cytochalasin B.

3 y altered affinity of sugar export sites for cytochalasin B.

4 te, 2-deoxyglucose, gadolinium chloride, and cytochalasin B.

5 blocked by the microfilament-disrupting drug cytochalasin B.

6 tation of the particulate Ag is inhibited by cytochalasin B.

7 resence of the GLUT2 inhibitors phloretin or cytochalasin B.

8 ng in vitro of purified GLUT1 to glucose and cytochalasin B.

9 the microfilament assembly was inhibited by cytochalasin B.

10 codazole but was fully additive with that of cytochalasin B.

11 he activated cell in a reaction sensitive to cytochalasin B.

12 cultured with the cytokinesis-blocking agent cytochalasin B.

13 ibitor of poly(ADP-ribosyl) polymerase], and cytochalasin B.

14 sport mediated by GLUT9 was not inhibited by cytochalasin B.

15 inophils activated with formyl-Met-Leu-Phe + cytochalasin B.

16 timulated by ATP and by the exit site ligand cytochalasin B.

17 s similar to that observed with the alkaloid cytochalasin B.

18 lso inhibited by MyoX knockdown and low-dose cytochalasin-B.

19 ained from the relationship: kobs = k-1 + k1[cytochalasin B].

20 nching increases in a saturable manner with [cytochalasin B].

21 (concentration 2 x 10(6)/ml) and primed with cytochalasin B (1 ng/ml) and tumor necrosis factor alpha

22 he synthesis of the 14-membered macrolactone cytochalasin B (1, an inhibitor of the formation of acti

23 Platelets exposed to cytochalasin B (1.01 +/- 0.31) or to hypertonic conditio

24 nuclease type 1 (DNase 1; 50 microg ml-1) or cytochalasin B (10 microM) to intact cells or inside-out

25 Cytochalasin B (10 microM), another actin filament disru

26 rystallized with three different inhibitors: cytochalasin B, a nine-membered bicyclic ring fused to a

27 actin polymerization with latrunculin A and cytochalasin B abolishes long-term increase of presynapt

28 An inhibitor of phagocytosis, cytochalasin B, abrogated the induction of TNF-alpha in

29 However, in cells treated with cytochalasin B alpha3beta1-TM4SF protein complexes are r

30 this question by analysis of binding of [3H]cytochalasin B (an export conformer ligand) to the human

31 Cytochalasin B, an agent that blocks new actin filament

32 Further, cytochalasin B, an agent which depolymerizes actin, reve

33 Fourth, cytochalasin B, an inhibitor of actin polymerization, co

34 of platelets to hypertonic conditions or to cytochalasin-B, an agent that prevents assembly of actin

35 Cytochalasin D (a cytochalasin B analogue that does not interact with GluT

36 re multiple classes of binding sites for [3H]cytochalasin B and a percentage of these sites were comp

37 Cytochalasin B and ATP binding are synergistic.

38 on into Percoll gradients in the presence of cytochalasin B and ATP.

39 Remarkably, the cytoskeleton inhibitors cytochalasin B and blebbistatin blocked not only PMA-ind

40 pting the cytoskeleton and microtubules with cytochalasin B and colchicine had no effect on the activ

41 Cytochalasin B and cytochalasin D, but not nocodazole, d

42 Treatments with cytochalasin B and D, ethanol, and nocodazole affect the

43 Trypsin-digested GLUT1 retained cytochalasin B and d-glucose binding capacity and releas

44 ransport of both substrates was inhibited by cytochalasin B and displayed saturable kinetics.

45 inhibitions of 3-O-methylglucose uniport by cytochalasin B and forskolin (sugar export site ligands)

46 transfected RE700A, including inhibition by cytochalasin B and high-affinity transport of the nonmet

47 The effects of cytochalasin B and histamine on IK(BA) were not additive

48 encountered in 20% of the patients receiving cytochalasin B and in 38% of the patients receiving plac

49 ort is mediated by a simple-carrier and that cytochalasin B and intracellular D-glucose binding sites

50 hat decreased cellular ATP levels, including cytochalasin B and iodoacetic acid.

51 aled rapid disassembly of actin filaments by cytochalasin B and leptin, the latter action being preve

52 nt on intact cytoskeleton, as treatment with cytochalasin B and nocodazole blocked this activity.

53 ts of the cytoskeleton, since treatment with cytochalasin B and nocodazole did not affect cytoplasmic

54 red cell membrane proteins upon addition of cytochalasin B and phloretin and (2) the d-glucose inhib

55 taining the inhibitors of glucose transport, cytochalasin B and phloretin.

56 transport differed regarding sensitivity to cytochalasin B and showed different relative kinetics fo

57 These aspects are inhibited by cytochalasin B and, therefore, are dependent on actin.

58 Cytochalasins B and D and latrunculin-A, agents that dis

59 Cytochalasins B and D were each a potent inhibitor of MM

60 hibition of actin polymerization by 1 microM cytochalasins B and D, but was not affected by 10 microM

61 presence of microfilament-disrupting agents cytochalasins B and D.

62 r (genistein), by a microfilament inhibitor (cytochalasin B), and by incubation at 4 degrees C.

63 e and in the presence of the GLUT1 inhibitor cytochalasin B, and by comparing their anticancer activi

64 owed a t1/2 < 15 min, limited sensitivity to cytochalasin B, and complete insensitivity to genistein.

65 Experiments utilizing latrunculin B, cytochalasin B, and cytochalasin D indicate that SHFV do

66 Cytochalasin D, cytochalasin B, and latrunculin A all impaired the maint

67 hannel activity could be induced by 1 microM cytochalasin B, applied either through the patch pipette

68 GLUT9 did not bind cytochalasin B as shown by a cytochalasin B binding assa

69 facial site next to the channel opening; and cytochalasin B at a positively charged endofacial pocket

70 feasibility and outcome of local delivery of cytochalasin B at the site of coronary angioplasty.

71 ear demonstration in which the substrate and cytochalasin B binding activities of GLUT1 are different

72 ooperativity between sites and K(d(app)) for cytochalasin B binding are reduced in the presence of in

73 T9 did not bind cytochalasin B as shown by a cytochalasin B binding assay, indicating a similar behav

74 r D-glucose (a transported sugar) stimulates cytochalasin B binding at low D-glucose concentrations (

75 ational change in GLUT1 that interferes with cytochalasin B binding but enhances substrate binding.

76 phloretin and (2) the d-glucose inhibitable cytochalasin B binding capacity of red cell membranes.

77 The cytochalasin B binding data are consistent with both sym

78 se binding sites are mutually exclusive, the cytochalasin B binding data are explained only if transp

79 Maltose modulation of cytochalasin B binding is mediated by altered affinity o

80 Rate constants for cytochalasin B binding to GLUT1 (k1) and dissociation fr

81 Cadmium inhibited cytochalasin B binding to GLUT1 competitively by reducin

82 Phloretin-inhibitable cytochalasin B binding to human red blood cells, to huma

83 concentrations of maltose (1-100 mM) inhibit cytochalasin B binding to human red cells.

84 Phloretin-inhibitable cytochalasin B binding to intact red cells is unaffected

85 We approached this question by analysis of cytochalasin B binding to the human erythrocyte sugar ex

86 Cytochalasin B binding to the purified, human erythrocyt

87 analysis of the rapid kinetics of reversible cytochalasin B binding to the sugar export site in the p

88 ffects of intra- and extracellular sugars on cytochalasin B binding to the sugar export site.

89 The rank potency and IC50 values for [3H]cytochalasin B binding were: 2-deoxy-D-glucose (4.5 mM)

90 transporter concentration, as determined by cytochalasin B binding, were 2-fold greater in the lumin

91 00 microM) increase the level of erythrocyte cytochalasin B binding.

92 Intracellular D-glucose inhibits cytochalasin B binding.

93 ansmembrane helix 8 release did not abrogate cytochalasin B binding.

94 However, D-glucose displaced cytochalasin B bound to GLUT1 as effectively in the pres

95 evels is inhibited by high concentrations of cytochalasin B but is stimulated by lower (<20 nM) conce

96 alasin B photoincorporation into GluT1 while cytochalasin B (but not cytochalasin D) enhances [gamma-

97 eased full-length transmembrane helix 8 upon cytochalasin B (but not D-glucose) binding.

98 The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cot

99 Cytochalasin B can be safely administered by local deliv

100 Cytochalasin B (CB) is a reversible, noncompetitive inhi

101 , collagenase, in response to agents such as cytochalasin B (CB) or phorbol myristate acetate (PMA),

102 oes not affect inhibition of sugar uptake by cytochalasin B (CB), indicating that it does not compete

103 Disruption of the actin cytoskeleton with cytochalasin B (CB), which mimics changes in shape that

104 d activated with formyl-met-leu-phe (FMLP) + cytochalasin B (CB).

105 IN) to inhibit monocarboxylate transport and cytochalasin B (CCB) to inhibit glucose transport, we ex

106 ibitors of actin/microtubule polymerization (cytochalasin B, colchicine, or nocodozole) or serine/thr

107 ion of filopodia with a low concentration of cytochalasin B completely abolished the turning response

108 o GLUT1 (k1) and dissociation from the GLUT1.cytochalasin B complex (k-1) are obtained from the relat

109 t impaired microfilament function, including cytochalasin B, cytochalasin D, latrunculin A, and jaspl

110 Only catalase and cytochalasin B decreased fiber uptake.

111 of actin polymerization in lymphocytes using cytochalasin B did not accelerate apoptosis in these cel

112 Iodine-125 HPP-forskolin and [3H]cytochalasin B did not localize in LX-1 tumors, indicati

113 Iodine-125 HPP-forskolin and [3H]cytochalasin B did not localize in LX-1 tumors.

114 Cytochalasin B did not prevent the tyrosine phosphorylat

115 Cytochalasin B did not produce cellular contraction.

116 Treatment of stage VI oocytes with cytochalasin B disrupted the organization of both cortic

117 Blockade of circus activity with cytochalasin B does not prevent neuronal differentiation

118 Treatment of a cytoskeletal pellet with cytochalasin B doubled NPA binding activity in the resul

119 ngly, pretreatment of tonsillar B cells with cytochalasin B dramatically reduced both integrin- and B

120 of R. rickettsii, since treatment of EC with cytochalasin B during infection to block entry inhibited

121 Treatment with cytochalasin-B eliminated the anisotropy in the spreadin

122 Finally, cytochalasin B enhanced CD44DL, but not ADCC, indicating

123 Further genistein and cytochalasin B failed to inhibit eosinophil degranulatio

124 h epithelial cells were stimulated with FMLP/cytochalasin B (FMLP/B) and/or endothelin-1 (ET-1) befor

125 ivity and degranulation of PMNs treated with cytochalasin B followed by FMLP, and DiC10 restored func

126 cells made compliant with latrunculin A and cytochalasin B further demonstrate that travel time is i

127 phloridzin were 0.94 and 0.95, respectively; cytochalasin B gave 0.95.

128 Cytochalasin-B had a stronger inhibitory effect on PC-co

129 n hydrodynamic shear flow by disruption with cytochalasin B, hypotonic swelling, and chilling.

130 ic and hypoxic cultures with mitomycin C and cytochalasin B indicated that in this system wound closu

131 Inhibition of GLUTs by using cytochalasin B indicated that infected cells utilize GLU

132 ot to the microfilament-depolymerizing agent cytochalasin B, indicating that intact microtubules were

133 s decreased by prior treatment of cells with cytochalasin B, indicating that this process was at leas

134 transport was inhibited by deoxyglucose and cytochalasin B, indicating the direct participation of f

135 Despite the cytochalasin B-induced depolymerization of MFs, gravicur

136 Insulin-stimulated glucose uptake (which was cytochalasin B inhibitable) varied according to MHC isof

137 with a approximately 10-fold stimulation of cytochalasin B-inhibitable 3-O-methyl-D-glucose transpor

138 as glucose-sensitive, temperature-dependent, cytochalasin B-inhibitable, modestly stereoselective for

139 bolism and protein kinase C but nevertheless cytochalasin B-inhibitable; (b) dependent upon proline-r

140 n high stress perfusions with phloridzin and cytochalasin B inhibited absorption by 92 +/- 7 %; non-c

141 Intravitreal injection of cytochalasin B inhibited NF axonal transport in optic ax

142 elet cytoskeleton via actin-binding protein, cytochalasin B inhibited the ADP/epinephrine-, cathepsin

143 Cytochalasin B inhibited this 3-DAG flux in a dose-depen

144 The actin depolymerizing agent cytochalasin B inhibited this KLEIP recruitment around E

145 n of filamentous actin in NB2a/d1 cells with cytochalasin B inhibited translocation of subunits into

146 Cytochalasin B inhibits intrapodial elongation and remov

147 Cytochalasin B inhibits the polymerization of actin and

148 ars increase k-1(app) and reduce k1(app) for cytochalasin B interaction with GLUT1.

149 hich priming with the nonphysiological agent cytochalasin B is necessary to obtain elastase release i

150 However, cytochalasin B, known to reduce cortical tension in neut

151 displays positive cooperativity at very low cytochalasin B levels.

152 Very low concentrations of cytochalasin B (< 2 microM) induced a slight enhancement

153 hrocyte sugar transporter and by analysis of cytochalasin B modulation of human red blood cell sugar

154 The effects of cytochalasin B, of patch excision, or of histamine on NP

155 Cytochalasin B only marginally reduced microvilli number

156 on was inhibited by pretreatment of DCs with cytochalasin B or brefeldin A, indicating a phagosome/en

157 mV when the K+ conductance was increased by cytochalasin B or by histamine.

158 ially inhibited by ATP depletion, but not by cytochalasin B or chloroquine.

159 Treatment with the actin-disrupting agents cytochalasin B or cytochalasin D prevented the glutamate

160 Application of cytochalasin B or cytochalasin D resulted in extensive d

161 he actin cytoskeleton, we treated cells with cytochalasin B or D and found that the tether lengths in

162 el, or the microfilament-destabilizing drugs cytochalasin B or D, did not exert these effects.

163 eatment of cells on day 3 after passage with cytochalasins B or D caused a reversion to the rapid kin

164 , multicenter, randomized, controlled trial, cytochalasin B (or matching placebo) was administered to

165 th ethacrynic acid, colchicine, vinblastine, cytochalasin B, or 1-(5-isoquinolinylsulfonyl)-2-methylp

166 ed by the human glucose transport inhibitors cytochalasin B, phloretin, and forskolin.

167 ATP (but not AMP) enhances [3H]cytochalasin B photoincorporation into GluT1 while cytoc

168 Disruption of the actin cytoskeleton with cytochalasin B precluded the formation of membrane protr

169 Cytochalasin B prevented haemolysis.

170 hibits intrapodial elongation and removal of cytochalasin B produced a burst of intrapodial activity.

171 Cytochalasin B produced actin disassembly and resulted i

172 ed affinity for the sugar export site ligand cytochalasin B, prolonged substrate occlusion, reduced n

173 inant-negative vimentin mutant or actin with cytochalasin B reduced correlation of behavior of indivi

174 Cytochalasin B selectively triggered the secretion of TN

175 est whether the interaction of CD80 with the cytochalasin B-sensitive cytoskeleton was necessary for

176 stimulated and N-formyl-Met-Leu-Phe (fMLF) + cytochalasin B-stimulated neutrophils or their membrane

177 S; 2) kinases/phosphatases activated in fMLF/cytochalasin B-stimulated neutrophils produce multiple C

178 orms of Ala(323)-Lys(350) only in the fMLF + cytochalasin B-stimulated sample.

179 s were identified in unstimulated and fMLF + cytochalasin B-stimulated samples.

180 with formylmethionylleucylphenylalanine plus cytochalasin B stimulation.

181 lar (maltose or phloretin) or intracellular (cytochalasin B) sugar-transport inhibitors.

182 biotinylated beta-amyloid in the presence of cytochalasin B, suggesting that beta-amyloid binding to

183 nonadherence was mimicked by treatment with cytochalasin B, suggesting that the loss of cytoskeletal

184 The glucose transporter inhibitor cytochalasin B, the aldose reductase inhibitor alrestati

185 in inhibited glucose-displaceable binding of cytochalasin B to GLUT1 in erythrocyte ghosts in a compe

186 blocked the glucose-displaceable binding of cytochalasin B to GLUT1 in erythrocyte ghosts.

187 rmalin fixation, or incubation of cells with cytochalasin B to prevent entry resulted in marked inhib

188 he fusion reaction at 37 degrees C by adding cytochalasin B to the medium.

189 ed PMNs stimulated by FMLP and by 30-fold in cytochalasin B-treated PMNs stimulated by FMLP.

190 vation of the PLD pathway in primed PMNs and cytochalasin B-treated PMNs.

191 PKC-alpha to the plasma membrane in G-CSF or cytochalasin B-treated, FMLP-activated PMNs.

192 Likewise, cytochalasin B treatment abolished the dominant inhibito

193 ls in which particle uptake was inhibited by cytochalasin B treatment before exposure to immune compl

194 Cytochalasin B treatment of neutrophils decreased the se

195 ced the resistance of the actin filaments to cytochalasin B treatment.

196 A new technique involving cytochalasin-B treatment was used to disrupt the intrace

197 regation of E710.2.3, which was inhibited by cytochalasin B, trifluoperazine, a combination of sodium

198 The effect of cytochalasin B was reversible.

199 Phloretin or cytochalasin B was used to inhibit GLUT2 and phloridzin

200 Inhibition by the endofacial inhibitor, cytochalasin B, was non-competitive and inhibition by th

201 dc42) and the filopodial disrupter, low-dose cytochalasin-B, we demonstrate here a requirement for fi

202 cetyl-forskolin([125I]HPP forskolin) and [3H]cytochalasin B, were studied in a tumor model which over

203 The inhibitor of actin filament formation cytochalasin B, when added to the patch pipette in the a

204 he presence of FGF-2 of the modulated cells, cytochalasin B, which did not revert the modulated cell

205 and identical dose-response sensitivities to cytochalasin B, which disrupts microfilaments, and to ge

206 Cytochalasin B, which inhibited pinocytosis by 65% and p

207 In contrast, cytochalasin B, which interferes with actin polymerizati

208 clear cell phagocytosis since treatment with cytochalasin B, which prevents actin polymerization, inh

209 l proliferation in contrast to the effect of cytochalasin B, which slightly decreased the FGF-2 actio

210 scence decay (kobs) increases linearly with [cytochalasin B] while the extent of fluorescence quenchi

211 w temperature, isolated SECs were exposed to cytochalasin B with or without pretreatment with phalloi