ライフサイエンスコーパス: cytochalasin

1 We used cytochalasin and latrunculin to investigate participatio

2 tructural component varies widely within the cytochalasins and seems to play an important role in the

3 The cytochalasins are structurally complex natural products

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 Cytochalasin B prevented haemolysis.

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

28 with formylmethionylleucylphenylalanine plus cytochalasin B stimulation.

29 Likewise, cytochalasin B treatment abolished the dominant inhibito

30 Cytochalasin B treatment of neutrophils decreased the se

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

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

33 lostery (uptake stimulation by subsaturating cytochalasin B).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 ell as by blocking actin polymerization with cytochalasin B.

53 resence of the GLUT2 inhibitors phloretin or cytochalasin B.

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

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

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

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

58 E) stimulation in the absence or presence of cytochalasin D (3 x 10(-7)m) and nocodazole (3 x 10(-6)m

59 colocalization, and studying the effects of cytochalasin D (actin depolymerizing agent) exposure, a

60 Both cytochalasin D (an inhibitor of actin polymerization) an

61 ities of the MCF-7 cells upon treatment with cytochalasin D (an inhibitor of actin-filament dynamics)

62 Cytochalasin D (CCD) exerted opposite effects.

63 Depolymerization of actin with cytochalasin D (CD) and latrunculin B (latB) failed to b

64 chicine (Colch) or actin microfilaments with cytochalasin D (CD) dramatically reduced the amount of c

65 The fungal toxin cytochalasin D (CD) interferes with the normal dynamics

66 Disrupting the actin cytoskeleton with cytochalasin D (Cyto D) selectively decreased basal and

67 sue stress and stiffness, both attenuated by cytochalasin D (CytoD) and PP2, inhibitors of actin poly

68 Cytochalasin D (CytoD) disrupts actin filaments, thus pr

69 CapZ and cytochalasin D (CytoD), a barbed-end capping drug, stron

70 ing microglial phagocytosis by adding either cytochalasin D (to block actin polymerization) or cyclo(

71 odonaphthalene-1-sulfonyl homopiperazine and cytochalasin D abolished the effects of ZASP1-D117N on N

72 Inhibition of phagocytosis with cytochalasin D abolished the IL-1beta stimulatory activi

73 nal antibodies, PI3-K inhibitors, as well as cytochalasin D abrogate IGF-I-induced MM cell transmigra

74 We also show that high concentrations of cytochalasin D accelerate ATP turnover by actin but thro

75 her insulin nor depolymerization of actin by cytochalasin D affected this interaction.

76 Depolymerization of actin with cytochalasin D allows receptors to aggregate and restore

77 Inhibitors of MPC, Cytochalasin D and amiloride, decreased P27-mediated upt

78 ffect abolished by the actomyosin inhibitors cytochalasin D and blebbistatin.

79 n of parasite cytoskeleton polymerization by cytochalasin D and colchicine and the depletion of intra

80 parasite actin and tubulin polymerization by cytochalasin D and colchicines, respectively, inhibited

81 Inhibition of BAD1 uptake with cytochalasin D and FcR-redirected delivery of soluble BA

82 Using cytochalasin D and jasplakinolide to selectively inhibit

83 Agents that modulate the actin cytoskeleton (cytochalasin D and jasplakinolide) altered the plasma me

84 Cytoplasmic rod formation is inhibited by cytochalasin D and jasplakinolide.

85 actin thickening and ROS production, whereas cytochalasin D and latrunculin A enhanced basal and hype

86 Treatment of HTM cells with cytochalasin D and latrunculin A led to significant acti

87 Cytochalasin D and latrunculin A treatments, which are k

88 und that inhibitors of actin polymerization (cytochalasin D and latrunculin A) cause a similar, but m

89 sruption of nonsarcomeric actin filaments by cytochalasin D and latrunculin B decreased this differen

90 otubules (thiabendazole) and microfilaments (cytochalasin D and latrunculin B) of the rod photorecept

91 F4 and the actin cytoskeleton destabilizers, cytochalasin D and latrunculin B.

92 pidly by the actin filament-disrupting drugs cytochalasin D and latrunculin B.

93 ly (2 h) with the actin-depolymerizing drugs cytochalasin D and latrunculin B.

94 Cytochalasin D and latrunculin-B permitted all events ex

95 Cytochalasin D and nocodazole inhibited the uptake by He

96 rofessional phagocytic cells is inhibited by cytochalasin D and nocodazole, suggesting that both the

97 ytoskeleton, as indicated by inhibition with cytochalasin D and nocodazole.

98 alization of B. burgdorferi was inhibited by cytochalasin D and PP2, suggesting that B. burgdorferi i

99 with (6 of 6, 100%) or without (4 of 6, 67%) cytochalasin D and significantly reduced inducibility.

100 letely blocked by the cytoskeletal disruptor cytochalasin D and the phosphatidylinositol 3-kinase inh

101 Cytochalasin D and vinblastine, actin and microtubule in

102 isrupting agents nocodazole, colchicine, and cytochalasin D are able to revert the suppression of c-F

103 ce of soluble cyclicRGD as a competitor, and cytochalasin D as inhibitor of cell spreading.

104 In addition, local application of cytochalasin D at the tip inhibited frontal extension wi

105 adiol-induced beta-actin polymerization with cytochalasin D attenuated lordosis behavior, indicating

106 Preincubation with Y-27632 or cytochalasin D blocked both the initial contractile and

107 We found that macropinocytosis inhibitor cytochalasin D blocked rAAV transduction of HeLa cells (

108 Cytochalasin D blocked recruitment of actin and alpha-ac

109 Cytochalasin D blocked the Francisella internalization a

110 Disrupting actin by cytochalasin D blocks the FSS-induced changes in NHE3 an

111 Cytochalasin D can restore the polarity in cells express

112 mazine, phorbol 12-myristate 13-acetate, and cytochalasin D caused a reduction in the total number of

113 Cytochalasin D caused stereocilia to shorten at rates ma

114 Treatment of midstage gametocytes with cytochalasin D decreases the vertical coupling and incre

115 Treatment of epithelial cells with cytochalasin D depolymerized actin filaments and increas

116 owever, gelsolin, gelsolin-actin complex, or cytochalasin D did not enhance disassembly by ADF/cofili

117 perturbed the localization of AtMAP70-1 but cytochalasin D did not.

118 ate have demonstrated that very low doses of cytochalasin D disconnect beta2-integrins from their cyt

119 Viable tissues treated by hyaluronidase and cytochalasin D displayed targeted disruption of matrix a

120 Cytochalasin D disruption of these actin structures resu

121 ent of the NHERF-1-assembled complex because cytochalasin D disrupts apical localization of both NHER

122 In contrast, cytochalasin D disrupts only the short actin filament si

123 endent of bacterial internalization, because cytochalasin D does not affect presentation.

124 Inhibiting F-actin assembly with cytochalasin D enhanced secretion in WT platelets and fu

125 olymerization (latrunculin A for G-actin and cytochalasin D for actin filament-free barbed ends) or s

126 Treatment with cytochalasin D had little noticeable effect on either th

127 Cytochalasin D had no effect on DeltaV1, while DeltaV1 w

128 ctin polymerization-dependent mechanisms, as cytochalasin D had no effect on this early response.

129 Cytochalasin D had no impact on cytokine production in c

130 ared to 2D, and actin network disruption via Cytochalasin D has a more pronounced effect on internal

131 ical disruption of the actin cytoskeleton by cytochalasin D in control cardiomyocytes mirrored the al

132 nalysis of membrane compartments showed that cytochalasin D increased [14C]dextran association with a

133 e by disrupting the actin cytoskeleton using cytochalasin D increased the amount of IIF.

134 Cytochalasin D increased the number of rolling cells, th

135 ation site with human cofilin (HsCOF1) using cytochalasin D increases its severing rate.

136 utilizing latrunculin B, cytochalasin B, and cytochalasin D indicate that SHFV does not hijack the ac

137 ess fibers, or the actin depolymerizing drug cytochalasin D induced expression of lens cell different

138 tegrin monoclonal antibody, RGD peptide, and cytochalasin D inhibit IGF-I-induced cell adhesion to FN

139 Cytochalasin D inhibited DEP-induced superoxide producti

140 Further, cytochalasin D inhibited FAK phosphorylation and cleavag

141 Actin disruption with Cytochalasin D inhibited peptide entry in both cell line

142 ement as demonstrated by Pertussis toxin and cytochalasin D inhibition.

143 ts only the short actin filament signal, and cytochalasin D neither inhibits GLUT4 translocation nor

144 Neither cytochalasin D nor colchicine blocked DEX-induced or RU4

145 However, neither cytochalasin D nor GM6001 affected translocation of CD40

146 ycosylated HIV-1 gp120 envelope protein, and cytochalasin D on the uptake of strains and on the immun

147 inhibit podosome formation is unaffected by cytochalasin D or jasplakinolide, whereas its ability to

148 at cultured hippocampal neurons treated with cytochalasin D or latrunculin B contained dense accumula

149 Application of cytochalasin D or latrunculin B to disrupt the microfila

150 uption of actin-containing microfilaments by cytochalasin D or microtubules by nocodazole had no effe

151 d endocytosis that was either inhibitable by cytochalasin D or not inhibitable, depending upon aggreg

152 f internalization of OspA via treatment with cytochalasin D or of the lipohexapeptide via serum starv

153 F-actin intermediates during this process by cytochalasin D or syndapin SH3 domains impairs endocytos

154 vents are inhibited in cells pretreated with cytochalasin D or with Clostridium difficile toxin B.

155 us application of the actin-disrupting agent cytochalasin D partially rescued the Atadf4 mutant in th

156 In LMN myocytes, cytochalasin D prevented inhibition of cAMP/PKA from enh

157 tment with the actin microfilament disrupter cytochalasin D prevented iNOS recruitment to latex bead

158 Treatment with EDTA and cytochalasin D prevented PIM-induced T cell adhesion.

159 Abrogation of phagocytosis with cytochalasin D prevented the death response.

160 noncoupled sites, but the F-actin disruptor cytochalasin D prevented the specific modulation of coup

161 scence and electron microscopy revealed that cytochalasin D promoted apical accumulation of clathrin,

162 Cytochalasin D reduced cytokine induction, but not to th

163 y, the enhanced virion production induced by cytochalasin D required a functional late (L) domain, ei

164 of filamentous actin using latrunculin B or cytochalasin D restored wild-type stomatal sensitivity t

165 The inhibition of actin polymerization by cytochalasin D resulted in extended intracellular bacter

166 cells with the actin-depolymerizing compound cytochalasin D resulted in reversible flagellar shorteni

167 Blockage of H. ducreyi uptake by cytochalasin D significantly reduced the amount of secre

168 also repeated our screen in the presence of cytochalasin D that inhibits actin polymerization.

169 cortical actin filament network resistant to cytochalasin D that inhibits fast barbed end actin assem

170 Addition of the actin-depolymerizing drug cytochalasin D to cells transfected or infected with BAC

171 Treatment with low doses of cytochalasin D to disrupt F-actin assembly led to filopo

172 ing lipopolysachharide (LPS) to activate and cytochalasin D to inhibit phagocytosis.

173 Addition of cytochalasin D to TLR2(-/-) BMDM inhibited inflammatory

174 Cytochalasin D treatment did not reduce F-actin formatio

175 Cytochalasin D treatment impaired T cell activation by c

176 Consistent with these observations, cytochalasin D treatment of infected cells resulted in s

177 Sustained cytochalasin D treatment of undifferentiated lens epithe

178 Cytochalasin D treatment revealed that internalization o

179 e) in all particle sizes except 50 nm, while cytochalasin D treatment significantly reduced the cellu

180 ntly decreased to approximately 29 pN/mum by cytochalasin D treatment to disrupt actin cytoskeleton a

181 Cells were subject to Cytochalasin D treatment to provoke a drastic change in

182 sensitivity phenotype of hsr3 was rescued by cytochalasin D treatment, suggesting that the aberrant s

183 and size, and these changes are inhibited by cytochalasin D treatment, suggesting that the morphogene

184 is is independent of cAMP or not affected by cytochalasin D treatment.

185 in stress fibers in lens epithelial cells by cytochalasin D was sufficient to signal lens cell differ

186 When cytochalasin D was used to block phagocytosis of live B.

187 Cells treated with cytochalasin D were used for analysis of cargo movement

188 ipitation, and the actin depolymerizing drug cytochalasin D were used to evaluate uPAR's interaction

189 An actin nucleation inhibitor (cytochalasin D) and an N-WASP inhibitor (wiskostatin) bo

190 reated or inhibitor-treated (bafilomycin and cytochalasin D) human monocyte-derived dendritic cells (

191 ing cells in response to agents that soften (cytochalasin D) or stiffen (paraformaldehyde) the cytosk

192 diverse actin disruptors (latrunculin A and cytochalasin D).

193 Additionally, pretreatment of cells with cytochalasin D, a known actin filament disruptor, produc

194 Before mechanical testing, cytochalasin D, acrylamide, or colchicine was used to di

195 We show that nocodazole, but not cytochalasin D, affected the distribution of N and reduc

196 contain actin and disperse upon exposure to cytochalasin D, an actin depolymerizer.

197 Pretreatment with 3 micromol/L cytochalasin D, an actin depolymerizing agent, abrogated

198 Cytochalasin D, an actin depolymerizing agent, inhibited

199 Cytochalasin D, an actin destabilizer, dramatically rest

200 CFTR endocytosis was decreased by cytochalasin D, an actin-filament depolymerizing agent.

201 s gastrulation commences, and find that both Cytochalasin D, an inhibitor of actin polymerization, an

202 on and migration with microsources releasing cytochalasin D, an inhibitor of actin polymerization.

203 cytoskeleton reorganization since BAPTA AM, cytochalasin D, and inhibitors of Rho and myosin light c

204 XCL1 endocytosis was inhibited by amiloride, cytochalasin D, and the PKC inhibitor Go6976 whereas Pla

205 This pattern was abolished by cytochalasin D, and was not observed in cells treated wi

206 ith the actin filament depolymerizing agent, cytochalasin D, as well as knockdown of LIM kinase by sh

207 We investigated the effect of cytochalasin D, at concentrations that increase integrin

208 Interestingly, disassembly of MFs with cytochalasin D, at early stage of PIXV replication cycle

209 s also seen in macrophage cells treated with cytochalasin D, both with and without a subsequent expos

210 nhibited by the cytoskeleton-disrupting drug cytochalasin D, but persisted in the presence of the mic

211 bition of MMP-induced IFN-alpha secretion by cytochalasin D, chloroquine, and an inhibitory G-rich ol

212 Cytochalasin D, colchicine, and 17-demethoxygeldanamycin

213 Disruption of these projections with cytochalasin D, colchicine, or BAPTA-AM had no affect on

214 astrocytes was inhibited by vinblastine and cytochalasin D, demonstrating that this mobility depends

215 oduction were both normal in the presence of cytochalasin D, despite defective internalization of bet

216 orozoites was prevented by latrunculin B and cytochalasin D, drugs that depolymerize the parasite act

217 ated by MyD88, TLR9, and IRF1 and blocked by cytochalasin D, dynasore, and chloroquine.

218 host cell cytoskeleton and was inhibited by cytochalasin D, even in host cells that were resistant t

219 e treated with the actin-depolymerizing drug cytochalasin D, exhibiting stunted branches but dramatic

220 d a "splash"-type response, was decreased by cytochalasin D, genistein, colchicine, and wortmannin, a

221 actin depolymerizing agents, latrunculin or cytochalasin D, had no effect on epsilon, but increased

222 d by treatment with nocodazole, colcemid, or cytochalasin D, indicating it is dependent on both micro

223 TR1 degradation was blocked by amiloride and cytochalasin D, indicating that hCTR1 was internalized p

224 filament function, including cytochalasin B, cytochalasin D, latrunculin A, and jasplakinolide, also

225 n cytoskeleton-interfering agents, including cytochalasin D, latrunculin A, ethacrynic acid (ECA), a

226 ment turnover is impeded by incubations with cytochalasin D, latrunculin B, 8-bromo-cGMP, or formylme

227 cytic redistribution process is abolished by cytochalasin D, nocodazole, or anti-DYRK3 (dual specific

228 rs of various endosomal pathways (amiloride, cytochalasin D, nystatin, and methyl-beta-cyclodextrin)

229 ytes if grown in alginate, in monolayer with cytochalasin D, or with specific inhibition of the RhoA

230 d when epithelial cells were pretreated with cytochalasin D, staurosporine, or cycloheximide.

231 f amygdala is blocked by the actin inhibitor cytochalasin D, suggesting that 5-HT stimulates a cytosk

232 ved upon stimulation, which was inhibited by cytochalasin D, suggesting that actin polymerization con

233 s sensitive to propyzamid and insensitive to cytochalasin D, suggesting that DRP1A is associated with

234 , as well as by an inhibitor of endocytosis, cytochalasin D, suggesting that MD-2 phosphorylation occ

235 mimicked in subconfluent cells treated with cytochalasin D, suggesting that the shift results from m

236 centrations of the actin-destabilizing agent cytochalasin D, the cortical cytoskeleton network is thi

237 ride] and rottlerin [C(30)H(28)O(8)]) and by cytochalasin D, which affects actin polymerization.

238 Cytochalasin D, which allows assembly-disassembly, but o

239 e infected with parasites in the presence of cytochalasin D, which allows rhoptry secretion but preve

240 was substantially reduced in the presence of cytochalasin D, which antagonizes actin-mediated interna

241 was experimentally confirmed with the use of Cytochalasin D, which caps growing actin filaments.

242 SMCs on denatured collagen were treated with cytochalasin D, which decreased SMC spreading and activa

243 ng of N in cells treated with nocodazole and cytochalasin D, which depolymerize microtubules and acti

244 Cytochalasin D, which led to dissolution of the PAMR, al

245 atment of SS RBCs with low concentrations of cytochalasin D, which may release alpha4beta1 from cytos

246 These studies indicate that cytochalasin D- and latrunculin A-induced alteration of

247 cer cell lines that became more sensitive to cytochalasin D- and paclitaxel-induced apoptosis followi

248 ved macrophages are able to engulf NETs in a cytochalasin D-dependent manner, indicating that this is

249 y oversized outer segment disks resembling a cytochalasin D-induced defect and have a more severe dis

250 both adult and fetal middle cerebral artery, cytochalasin D-induced inhibition of actin polymerizatio

251 ide facing the flow, which was enhanced by a cytochalasin D-mediated disruption of actin filaments bu

252 tion that DP incorporation into junctions is cytochalasin D-sensitive, here we ask whether PKP2 may a

253 tiple experiments, showing that receptor and cytochalasin D-stimulated changes in DRM lipid compositi

254 In cytochalasin D-treated cells ezrin localized to a subapi

255 y taxol treatment did not stop elongation of cytochalasin d-treated neurites.

256 ed TCR/CD28-stimulated signaling pathways in cytochalasin D-treated T cells to determine the cytoskel

257 hCG as do LH receptors on cells treated with cytochalasin D.

258 r disassembly of the actin cytoskeleton with cytochalasin D.

259 ter inhibition of actin polymerization using cytochalasin D.

260 were abrogated by the actin-disrupting drug, cytochalasin D.

261 e also resistant to cell rounding induced by cytochalasin D.

262 re reduced by 60 +/- 8% (n = 8, P < 0.01) by cytochalasin D.

263 effect was also inhibited by phalloidin and cytochalasin D.

264 unable to phagocytose due to the presence of cytochalasin D.

265 markers were not affected by treatment with cytochalasin D.

266 nnin and attenuated in cells pretreated with cytochalasin D.

267 cesses formed by S2 cells in the presence of cytochalasin D.

268 pletion but was inhibited in the presence of cytochalasin D.

269 by disruption of the actin cytoskeleton with cytochalasin D.

270 Lengthening was blocked by 100 nM cytochalasin D.

271 cysteine residues and by co-incubations with cytochalasin D.

272 -incubations with the antioxidant ebselen or cytochalasin D.

273 filamentous actin formation was inhibited by cytochalasin D.

274 etreated with the actin-depolymerizing drug, cytochalasin D. uPAR was found also in focal adhesions,

275 Actin cytoskeletal disruption with cytochalasin-D also prevented stretch from increasing nu

276 ssembly in Arpc2(-/-) cells was resistant to cytochalasin-D and was highly dependent on profilin-1 an

277 Cytochalasin-D inhibition of barbed-end exchange reduces

278 AGP-1 were treated with amiprophosmethyl and cytochalasin-D to disrupt MTs and F-actin, and effects o

279 mically induced cytoskeletal disruption with cytochalasin-D treatment.

280 Similarly, amiprophosmethyl and cytochalasin-D treatments resulted in relocalization of

281 Inhibition of actin polymerization with cytochalasin-D, but not inhibition of Rho kinase with Y2

282 Erythroblasts treated with NSC23766, cytochalasin-D, colchicine, ML7, or filipin that inhibit

283 Pretreatment with either Mab13 or Cytochalasin-D, to inhibit beta-integrin or actin polyme

284 l dimension was inhibited in nocodazole- and cytochalasin-D-treated neural precursor cells in large-f

285 ve assessed the effects of latrunculin A and cytochalasin E on granule secretion.

286 ent of the wild-type Arabidopsis plants with cytochalasin E, an inhibitor of actin microfilament poly

287 Knowledge of acid sensitivity within the cytochalasin family provides a valuable cautionary lesso

288 Five rounds of approximately 30% cytochalasin-induced cleavage failure in untransformed h

289 ior PM in hearts with (N=6) or without (N=6) cytochalasin infusion, the LV lateral epicardium (Epi gr

290 homopsis sp. (CMB-M0042F), yielded the known cytochalasins J (1) and H (2), together with five new an

291 and H (2), together with five new analogues, cytochalasins J1-J3 (3-5) and H1 and H2 (6 and 7).

292 aments) and the 11-membered macrocarbocyclic cytochalasin L-696,474 (2, an inhibitor of HIV protease)

293 lization of rAdpF was inhibited by nystatin, cytochalasin, latrunculin, nocodazole, and wortmannin, i

294 isruption of the actin/myosin machinery with cytochalasin or blebbistatin disrupts polarization of Pk

295 Wash out of cytochalasin restored Pk polarization, but not if done i

296 icles after as little as 15 min; and (3) the cytochalasin-sensitive translocation of cytoplasmic part

297 and enantioselective synthetic route to the cytochalasins that allows for the late-stage introductio

298 Using 10 microM cytochalasin to block cleavage, we confirm that most bin

299 r localization of both was compromised after cytochalasin treatment.

300 However, when we use lower concentrations of cytochalasin, we find that binucleate cells undergo DNA