ライフサイエンスコーパス: cytochalasin D

1 n by forces of 2 or 4 pN and were removed by cytochalasin D).

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

3 ter inhibition of actin polymerization using cytochalasin D.

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

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

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

7 effect was also inhibited by phalloidin and cytochalasin D.

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

9 markers were not affected by treatment with cytochalasin D.

10 nnin and attenuated in cells pretreated with cytochalasin D.

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

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

13 Lengthening was blocked by 100 nM cytochalasin D.

14 actin filaments against depolymerization by cytochalasin D.

15 with the inhibitor of actin polymerization, cytochalasin D.

16 tment with the cytoskeletal-disrupting agent cytochalasin D.

17 r treatment with the actin-disrupting agent, cytochalasin D.

18 osis was blocked by preincubation of DC with cytochalasin D.

19 ic domain tyrosines and was not inhibited by cytochalasin D.

20 ct was less pronounced in roots treated with cytochalasin D.

21 uced changes in actin and was not blocked by cytochalasin D.

22 ptor increases upon actin destabilization by cytochalasin D.

23 by disruption of the actin cytoskeleton with cytochalasin D.

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

25 -incubations with the antioxidant ebselen or cytochalasin D.

26 filamentous actin formation was inhibited by cytochalasin D.

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

28 r disassembly of the actin cytoskeleton with cytochalasin D.

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

30 Cytochalasin D, a drug blocking tachyzoite invasion of,

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

32 Pretreatment of macrophages with cytochalasin D, a phagocytosis inhibitor, yielded compar

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

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

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

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

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

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

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

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

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

42 Collagenase, integrin-binding peptides, and cytochalasin D also block ATP release, indicating that e

43 ton, the downstream target of Rho-kinase, by cytochalasin D also upregulated eNOS expression.

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

45 A second inhibitor of endocytosis, cytochalasin D, also blocked insulin-dependent MAPK phos

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

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

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

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

50 Cytochalasin D, an actin depolymerizing agent, inhibited

51 Cytochalasin D, an actin destabilizer, dramatically rest

52 dosed with three different concentrations of cytochalasin D, an actin-depolymerizing toxin.

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

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

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

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

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

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

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

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

61 ; uptake was nearly completely eliminated by cytochalasin D and genistein.

62 Using cytochalasin D and jasplakinolide to selectively inhibit

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

64 s are altered by pharmacological treatments (Cytochalasin D and Jasplakinolide) or genetic disruption

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

66 Cytochalasin D and latrunculin A cause an increase in si

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

68 margin of these holes, and drug studies with cytochalasin D and latrunculin A indicated that actin po

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

70 Cytochalasin D and latrunculin A treatments, which are k

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

72 roteins and FGFR expression was inhibited by cytochalasin D and latrunculin A, suggesting a role for

73 Cytochalasin D and latrunculin A, which block actin poly

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

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

76 Cytochalasin D and latrunculin B, inhibitors of actin po

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

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

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

80 Cytochalasin D and latrunculin-B permitted all events ex

81 ents less sensitive to disruption by LatB or Cytochalasin D and led to increased actin filament skewn

82 he endosome-associated NHE3 was decreased by cytochalasin D and MbetaCD treatment.

83 In contrast, cytochalasin D and nocodazole did not affect the increas

84 Cytochalasin D and nocodazole inhibited the uptake by He

85 Cytochalasin D and nocodazole pretreatment also prevente

86 lular actin microfilament and microtubule by cytochalasin D and nocodazole, respectively, had no effe

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

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

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

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

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

92 of SK-1 is constitutive and is inhibited by cytochalasin D and treatment at 4 degrees C but not by b

93 in (F-actin) and NPA-binding activity, while cytochalasin D and Tris decreased both F-actin and NPA-b

94 Cytochalasin D and vinblastine, actin and microtubule in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 Cytochalasin D blocked recruitment of actin and alpha-ac

112 Cytochalasin D blocked the Francisella internalization a

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

114 and an organized actin cytoskeleton because cytochalasin D blocks the recruitment.

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

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

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

118 Cytochalasin D can restore the polarity in cells express

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

120 osure of TSHR(GFP/Myc) cells to forskolin or cytochalasin D caused no change in the FRET index, confi

121 Cytochalasin D caused stereocilia to shorten at rates ma

122 nhibitor (ML-7) or the actin-disrupting drug cytochalasin D causes an expansion of the MT array and p

123 4) Depolymerization of F-actin with cytochalasin D causes VSM relaxation and increased G-act

124 Cytochalasin D (CCD) exerted opposite effects.

125 cytoskeleton, as discerned by treatment with cytochalasin D (CCD).

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

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

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

129 Cytochalasin D (CD) that depolymerizes actin also enhanc

130 age of cultured epithelial cells, we applied cytochalasin D (CD), a known inhibitor of cytokinesis [4

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

132 Cytochalasin D, colchicine, and 17-demethoxygeldanamycin

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

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

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

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

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

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

139 d with an inhibitor of actin polymerization (cytochalasin D [CytoD]).

140 es, including Rho kinase inhibitor (Y27632), Cytochalasin D, Dasatinib, and Lysophosphatidic acid to

141 atment of etiolated zucchini hypocotyls with cytochalasin D decreased the amount of auxin transport a

142 or destabilizing the actin cytoskeleton with cytochalasin D decreased the amount of NHE3 in early end

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

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

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

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

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

148 Cytochalasin D did not affect the staining pattern, but

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

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

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

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

153 Cytochalasin D disruption of these actin structures resu

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

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

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

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

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

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

160 ion into GluT1 while cytochalasin B (but not cytochalasin D) enhances [gamma-32P]azidoATP photoincorp

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

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

163 Conversely, actin breakdown with cytochalasin D facilitated Ca(2+) signaling while decrea

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

165 hen cytoskeletal tension was disrupted using cytochalasin D, FRET increased, indicating refolding of

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

167 Amastigotes entered CHO cells by a cytochalasin D, genistein, wortmannin, and 2,3-butanedio

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

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

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

171 Cytochalasin D had no impact on cytokine production in c

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

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

174 ith the actin-binding drugs latrunculin B or cytochalasin D, has corresponding effects on Rac GTP loa

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

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

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

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

179 Cytochalasin D increased the number of rolling cells, th

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

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

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

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

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

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

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

187 However, cytochalasin D-induced inhibition of CD8(+) cytoskeletal

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

189 Cytochalasin D inhibited DEP-induced superoxide producti

190 Further, cytochalasin D inhibited FAK phosphorylation and cleavag

191 Treatment of microglia with cytochalasin D inhibited internalization of C. neoforman

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

193 Cytochalasin D inhibited the adhesion of cells expressin

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

195 Cytochalasin-D inhibition of barbed-end exchange reduces

196 occurred in the presence of latrunculin A or cytochalasin D, inhibitors of actin polymerization.

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

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

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

200 Treatment of HeLa cells with cytochalasin D markedly inhibited the internalization of

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

202 agents nocodazole (microtubule specific) or cytochalasin D (microfilament specific) prevented the ef

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

204 s inhibited by treatment of glial cells with cytochalasin D, nocodazole, and acrylamide, whereas SV40

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

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

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

208 Neither cytochalasin D nor nocodazole altered the distribution o

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

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

211 os in Ca2+-free medium, or medium containing cytochalasin D or aphidicolin, respectively.

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

213 and was prevented by pre-treating cells with cytochalasin D or latrunculin A to inhibit actin polymer

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

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

216 bitor PP2 or the actin-depolymerizing agents cytochalasin D or latrunculin.

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

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

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

220 Pretreatment of cells with cytochalasin D or staurosporine did not affect Trp3 but

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

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

223 Perturbation of actin filaments by either cytochalasin-D or conditional Cofilin expression resulte

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

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

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

227 The actin polymerization inhibitor cytochalasin D partially reversed the inhibition of CCE

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

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

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

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

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

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

234 Cytochalasin D reduced cytokine induction, but not to th

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

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

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

238 Application of cytochalasin B or cytochalasin D resulted in extensive disruption of MFs i

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

240 ted by structural components on the EBs, and cytochalasin D sensitive.

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

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

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

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

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

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

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

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

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

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

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

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

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

254 either nocodazole to disrupt microtubules or cytochalasin D to disassemble microfilaments simplifies

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

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

257 ptry-derived secretory vesicles, we utilized cytochalasin D to prevent invasion, leading to accumulat

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

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

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

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

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

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

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

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

266 Cytochalasin D treatment did not reduce F-actin formatio

267 Cytochalasin D treatment impaired T cell activation by c

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

269 Cytochalasin D treatment of these polarized cells reveal

270 Sustained cytochalasin D treatment of undifferentiated lens epithe

271 Cytochalasin D treatment revealed that internalization o

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

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

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

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

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

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

278 mically induced cytoskeletal disruption with cytochalasin-D treatment.

279 e I injections, as well as latrunculin B and cytochalasin D treatments, under quantitatively controll

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

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

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

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

284 the cytoskeleton inhibitors blebbistatin and cytochalasin D, we show that cell migration is a key dri

285 Cells treated with cytochalasin D were more deformable, further resisted de

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

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

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

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

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

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

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

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

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

295 However, in the presence of cytochalasin D, which inhibits membrane actin repair mec

296 Microglial uptake of A beta was blocked by cytochalasin D, which inhibits phagocytosis.

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

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

299 PP2, a Src family kinase inhibitor, or cytochalasin D, which selectively disrupts the network o

300 ng griseofulvin, dechlorogriseofulvin, epoxy/cytochalasin D, zygosporin E, hirsutatin A, cyclic penta