ライフサイエンスコーパス: actinomycin

1 beta-D-ribofuranosylbenzimidazole (DRB), and actinomycin.

2 Actinomycin ablated the increase in mRNA and protein see

3 th chemotherapy based on either vincristine, actinomycin, and cyclophosphamide or vincristine, actino

4 omycin, and cyclophosphamide or vincristine, actinomycin, and ifosfamide-based chemotherapy and proto

5 The nonvital DNA dye 7-amino-actinomycin D (7-AAD) is added to distinguish late apopt

6 es, such as propidium iodide (PI) or 7-amino-actinomycin D (7-AAD), are themselves cytotoxic, they ar

7 in the number of annexin V-positive, 7-amino-actinomycin D (7-AAD)-negative cells upon TA knockdown,

8 Actinomycin D (Act D), a clinically used agent and trans

9 tigated the effects of a DNA damaging agent, actinomycin D (Act D), on the function of sphingosine ki

10 ls was markedly enhanced when TNF-alpha plus actinomycin D (act-D) was coapplied with N,N,N',N'-tetra

11 tophagy in tumor necrosis factor (TNF)-alpha/actinomycin D (ActD) and lipopolysaccharide/D-galactosam

12 s on d(CGTCGTCG) had led to the finding that actinomycin D (ACTD) binds strongly to d(TGTCATTG) of ap

13 Earlier studies by others had indicated that actinomycin D (ACTD) binds well to d(AACCATAG) and the e

14 Actinomycin D (ACTD) has been shown to bind weakly to th

15 Actinomycin D (ActD) is a small molecule with strong ant

16 Actinomycin D (ActD) is a transcription inhibitor and ha

17 We also described the effects of actinomycin D (actD) on the interactions of HuR with bet

18 TGTCATTG) has been found to bind strongly to actinomycin D (ACTD) with 1:1 drug to strand binding sto

19 Injections of actinomycin D (an RNA synthesis inhibitor) or cyclohexim

20 d the mobility of RCC1 as did high levels of actinomycin D (to inhibit RNA polymerases I, II, and III

21 insulin mRNA and pre-mRNAs after addition of actinomycin D (to stop transcription).

22 age by more than fourfold in the presence of Actinomycin D (with a half life between 4 and 8 h post-i

23 15, 17, 18, 20, 21, 23, 24, 26, and 27, plus actinomycin D 45 mug/kg every 3 weeks from week 2, eithe

24 The addition of actinomycin D abolished the cAMP-mediated increase in AQ

25 Inclusion of actinomycin D abolishes both basal and ADR-induced RAD6B

26 Addition of actinomycin D abrogated the IL-4- and IL-13-induced incr

27 Actinomycin D accelerated induction of apoptosis of HeLa

28 lso treated with the transcription inhibitor actinomycin D after resistin treatment or with the NF-ka

29 Actinomycin D alone also enhanced the appearance of DISC

30 alyses of RNA expression show that RG7787 or actinomycin D alone and together increase levels of TNF/

31 oside and then treated for a short time with actinomycin D also suppressed macrophage responses, indi

32 abrogated by the transcriptional inhibitors actinomycin D and alpha-amanitin and requires the kinase

33 s blocked by the transcriptional inhibitors, actinomycin D and alpha-amanitin.

34 prevented by actinomycin D, suggesting that actinomycin D and Bis IX have similar mechanisms of inte

35 In addition, we found that actinomycin D and Bis IX induced caspase activity to the

36 O(2)) for 1 hour in the presence of 5 mug/mL actinomycin D and compared with untreated cells.

37 Actinomycin D and cycloheximide could only partially blo

38 nd de novo protein synthesis, as addition of actinomycin D and cycloheximide eliminated the induction

39 Inhibitors of transcription and translation, actinomycin D and cycloheximide, partially cancelled thi

40 nd surface antigens were examined by 7-amino-actinomycin D and flow cytometric analysis.

41 chieved by treatment with the p53 activators actinomycin D and nutlin-3, the increases in p53 and p21

42 very effectively abrogated by treatment with actinomycin D and other transcription inhibitors, which

43 rent affinities of P-gp for anticancer drugs actinomycin D and paclitaxel are approximately 4,000 and

44 ed by sodium nitroprusside and TNFalpha plus actinomycin D and prevented sGAG loss induced by IL-1alp

45 sensitivity to the transcriptional inhibitor actinomycin D and reduced amounts of rRNA.

46 We report here that actinomycin D and RG7787 act synergistically to kill man

47 diate-early gene response that is blocked by actinomycin D and tetrodotoxin, by inhibitors of ionotro

48 AR mediated IL-6 production and secretion by actinomycin D and the increase of intracellular IL-6 lev

49 LPS pre-stimulation, cells were treated with actinomycin D and then exposed to NO* without or with th

50 GC-specific intercalator actinomycin D and three minor groove-binders, chromomyci

51 ated with apoptotic agents staurosporine and actinomycin D and with necrosis inducer ionomycin.

52 ly), whereas both forms, when complexed with actinomycin D are stabilized with melting temperatures o

53 ced TRAF1 mRNA expression; pretreatment with actinomycin D blocked PMA-mediated TRAF1 expression sugg

54 Actinomycin D blocked the increase in P450R poly(A) tail

55 e-treatment with the transcription inhibitor actinomycin D blocked the inducible but not the constitu

56 Actinomycin D blocked transcription, and cycloheximide a

57 The inclusion of the sensitizing agent actinomycin D both accelerated and amplified the appeara

58 oid induction of TTP mRNA is also blocked by actinomycin D but not by cycloheximide, suggesting a tra

59 was blocked by pretreating THP-1 cells with actinomycin D but not by cycloheximide.

60 L23 with MDM2 was enhanced by treatment with actinomycin D but not by gamma-irradiation, leading to p

61 e step in the biosynthesis of the antibiotic actinomycin D by Streptomyces antibioticus.

62 nce is the fact that antitumor drugs such as Actinomycin D can selectively bind DNA hairpins over ful

63 Actinomycin D caused only minor changes in angiogenic as

64 Actinomycin D chase experiments showed that fluasterone

65 Actinomycin D chase experiments showed that hypoxic indu

66 of the small E2E RNAs estimated by using the actinomycin D chase method appear to account for their l

67 Treatment of HKC-8 cells with actinomycin D completely abolished HGF-mediated SnoN ind

68 heximide superinduces the Act1 mRNA, whereas actinomycin D completely abolishes the Act1 mRNA, indica

69 Actinomycin D completely blocked the induction of IRF-1

70 Actinomycin D decreased the rapidly moving fraction, sug

71 d oocytes with the transcriptional inhibitor actinomycin D did not prevent the appearance of these P-

72 Actinomycin D experiments revealed that enhanced express

73 Inhibition of DNA transcription with actinomycin D failed to block calcineurin activation, bu

74 protein level, RNA synthesis inhibition with actinomycin D failed to do so.

75 tomography and ex vivo by annexin V/7-amino actinomycin D flow cytometry, terminal deoxynucleotidylt

76 macrophages is therefore due to exposure to actinomycin D from apoptotic cells and is not the result

77 Higher concentrations of actinomycin D globally repressed transcription.

78 Actinomycin D had no effect on dexamethasone-independent

79 e addition of wild-type SBDS complements the actinomycin D hypersensitivity of SDS patient cells.

80 sed rapidly after culture in the presence of actinomycin D in concordance with effector caspase activ

81 t the interesting and unexpected result that actinomycin D increased the expression of FADD protein,

82 Incubation of 786-O with actinomycin D increased the expression of the death-indu

83 Inhibition of de novo transcription by actinomycin D increased the stability of IGF-1R mRNA in

84 indicating that suppression was mediated by actinomycin D independent of the mechanism of cell death

85 Actinomycin D inhibited all NSCLC VEGF secretion, and VE

86 Actinomycin D inhibited LNO(2) induction of HO-1 in huma

87 in the cytoplasm as well as cycloheximide or actinomycin D inhibited Tat- or TNF-mediated kappaB tran

88 Treatment with actinomycin D inhibits Vdr mRNA synthesis, indicating th

89 roximately 24 h is optimal for induction but actinomycin D injection before dexamethasone priming pre

90 njecting Fas antibody (Ab) or TNF-alpha plus actinomycin D into mice that overexpress wild-type (WT)

91 Actinomycin D is a potent transcription inhibitor that i

92 bosomal biogenesis by a low concentration of actinomycin D is associated with an increased L11-HDM2 i

93 es may indicate that the phenoxazone ring of actinomycin D is stacked on the G-tetrad rather than int

94 TEC apoptosis induced with anti-Fas or actinomycin D is substantially greater in IL-15-/- than

95 caspase pathways by M protein versus that by actinomycin D or 5,6-dichlorobenzimidazole riboside (DRB

96 lls with the ribosomal stress-inducing agent actinomycin D or 5-fluorouracil significantly decreased

97 eatment with ribosomal stress-inducing agent actinomycin D or 5-fluorouracil.

98 nduction of HO-1 by ER stress was blocked by actinomycin D or cycloheximide and was independent of an

99 bition of FAAH activity potentiates, whereas actinomycin D or cycloheximide blocks the LPS-induced in

100 These effects were abolished by actinomycin D or cycloheximide or by the AhR antagonists

101 Finally, actinomycin D or cycloheximide prevented the anti-apopto

102 itors of transcription or protein synthesis (actinomycin D or cycloheximide).

103 by FGF-1 was completely inhibited by either actinomycin D or cycloheximide, selective inhibitors of

104 d onset of apoptosis, which was prevented by actinomycin D or cycloheximide.

105 of HO-1 expression by serum was inhibited by actinomycin D or cycloheximide.

106 eolus and reveal redistribution of NuMA upon actinomycin D or doxorubicin-induced nucleolar stress.

107 aspase-9-like enzymes, as did treatment with actinomycin D or DRB.

108 The increase in cytoplasmic FADD protein by actinomycin D or FADD overexpression alone both correlat

109 was induced upon ribosomal stress caused by actinomycin D or mycophenolic acid.

110 , and blockade of MKP induction using either actinomycin D or Ro-31-8220 significantly decreased loss

111 h inhibitory conditions, such as low dose of actinomycin D or serum depletion, can be significantly a

112 by the treatment of cells with a low dose of actinomycin D or serum starvation, L11 binding to these

113 In cell-based assays, low concentrations of actinomycin D preferentially blocked EWS-FLI1 binding to

114 These results demonstrate that actinomycin D preferentially disrupts EWS-FLI1 binding t

115 6 h in cultured cTALH, which was blocked by actinomycin D pretreatment, suggesting transcriptional r

116 i) Addition of the transcriptional inhibitor actinomycin D prevented death factor processing upon inf

117 Actinomycin D prevented lovastatin-dependent increases i

118 cells with Nutlin-3 or low concentrations of actinomycin D resulted in a strong elevation of CerS6 mR

119 Complex formation with actinomycin D results in changes to both the Na(+) or K(

120 he addition of the transcriptional inhibitor actinomycin D revealed increased IL-8 mRNA stability in

121 Treatment of cells with alpha-amanitin or actinomycin D revealed that extension of B2 RNA by Pol I

122 Actinomycin D sensitized TRAIL-resistant cells through u

123 porine and hypersensitivity to etoposide and actinomycin D show that Top1, in addition to being the t

124 de novo protein synthesis, and studies with actinomycin D showed that DMSO did not alter the half-li

125 ranscriptional inhibitors alpha-amanitin and actinomycin D specifically disrupt the symmetry and orie

126 Actinomycin D studies revealed that Hcy stabilized HMGCR

127 -thaw and cell lysis experiments, along with actinomycin D studies, suggested that CCL20 and TNF-alph

128 strate that Jurkat cells induced to die with actinomycin D suppressed inflammatory cytokine productio

129 exposure of cells to a low concentration of actinomycin D that selectively inhibits rRNA synthesis h

130 0 and mouse NIH 3T3 fibroblasts treated with actinomycin D to block de novo transcription, microarray

131 GF and heregulin-beta1, and experiments with actinomycin D to block new mRNA synthesis showed that AR

132 tic cells act as "Trojan horses," delivering actinomycin D to engulfing macrophages.

133 ranscriptional mechanisms as the addition of actinomycin D to IL-2- and IL-12-treated NK92 slightly a

134 CR of p53 mRNA from cultures with or without actinomycin D to monitor mRNA transcription/stability, a

135 f transcripts present in leaves treated with actinomycin D to prevent continued transcription of the

136 The method is based on the use of actinomycin D to render the nuclear genome transcription

137 The binding of actinomycin D to the G-quadruplex DNAs is characterized

138 ich do not have AREs, were more stable after actinomycin D treatment and were not altered with oxidat

139 Actinomycin D treatment blocked, and high dose salicylat

140 e-mRNA levels in a time-dependent manner and actinomycin D treatment can abolish stimulatory effect o

141 Apoptosis induced by TNF-alpha and actinomycin D treatment is increased upon expression of

142 Tumor necrosis factor-alpha (TNF-alpha) and actinomycin D treatment results in accelerated TRAF2 deg

143 Actinomycin D treatment suggests that doxycycline decrea

144 ACF relocates to the cytoplasm after actinomycin D treatment, an effect blocked by the CRM1 i

145 After tumor necrosis factor alpha/actinomycin D treatment, caspase 2 activity increased se

146 When decay rates were analyzed after actinomycin D treatment, only 4,992 (9.1%) of probe set-

147 oteasomal degradation of S27a in response to actinomycin D treatment, thus forming a mutual-regulator

148 Following actinomycin D treatment, we observed that CsA increased,

149 RNA stability was determined after actinomycin D treatment.

150 0 mimics decreased luciferase activity after actinomycin D treatment.

151 ty and increased apoptosis when subjected to actinomycin D treatment.

152 ent decay rates, after serum stimulation and actinomycin D treatment.

153 lso decreased HIV-1 mRNA stability following actinomycin D treatment.

154 r1 transcripts as rapidly and effectively as actinomycin D treatment.

155 toplasm and that this binding is enhanced by actinomycin D treatment.

156 Actinomycin D was added to arrest transcription, and tot

157 expression was indeed recent transcription, Actinomycin D was administered immediately after explora

158 riptional level, the transcription inhibitor actinomycin D was employed.

159 In contrast, actinomycin D was found to preferentially disrupt EWS-FL

160 duced by the antineoplastics doxorubicin and actinomycin D was partially or completely abrogated by c

161 GATA-4 transcript levels in the presence of actinomycin D was unaltered by anthracyclines, indicatin

162 he rate of transcript degradation studied by actinomycin D were documented for only a subset of trans

163 The co-administration of actinomycin D with NGF negated both neutrophil accumulat

164 tin, 5-fluorouracil, hydroxyurea, Taxol, and actinomycin D) for their effect on viral DNA replication

165 incubation with inhibitors of transcription (actinomycin D) or translation (cycloheximide), suggestin

166 gs (palbociclib, gemcitabine, paclitaxel and actinomycin D) to illustrate potential applications of t

167 (10 mum) or by inhibition of transcription (actinomycin D, 4 mum) or protein biosynthesis (cyclohexi

168 nt, 1 mum), and inhibition of transcription (actinomycin D, 5 mug ml-1) or translation (cycloheximide

169 Disruption of transcription by actinomycin D, 5,6-dichloro-1-beta-D-ribofuranosyl-benzi

170 other primary sites of action (methotrexate, actinomycin D, 5-azacytidine, 8-thioguanosine).

171 ells with nucleolar stress inducers, such as actinomycin D, 5-fluorouridine, or doxorubicin, induced

172 ated with MECM in the absence or presence of actinomycin D, a general transcription inhibitor.

173 Actinomycin D, a transcriptional inhibitor, did not bloc

174 emotherapy using etoposide, methotrexate and actinomycin D, alternating with cyclophosphamide and onc

175 Actinomycin D, an inhibitor of gene transcription, abrog

176 an anemia are hypersensitive to low doses of actinomycin D, an inhibitor of rRNA transcription.

177 Bath application of actinomycin D, an irreversible RNA synthesis inhibitor,

178 fection and inhibition of transcription with actinomycin D, analysis of mRNA turnover failed to revea

179 Induction of apoptosis by M protein, actinomycin D, and DRB was inhibited in stably transfect

180 lished by cycloheximide but was abolished by actinomycin D, and in transfected granulosa cells activi

181 tumor necrosis factor alpha (TNFalpha) plus actinomycin D, and the proinflammatory cytokine interleu

182 using Org 34116, the transcription inhibitor actinomycin D, and the protein synthesis inhibitor cyclo

183 rM51R-M virus) in the presence or absence of actinomycin D, another inhibitor of host gene expression

184 e of CB-184 was combined with doxorubicin or actinomycin D, both in drug-sensitive (MCF-7) and drug-r

185 to the chemotherapeutic compounds, Taxol and Actinomycin D, but higher susceptibility to the CSC-sele

186 Induction was blocked by actinomycin D, but not cycloheximide, suggesting that pr

187 T3 cells with the transcriptional inhibitor, actinomycin D, completely blocked TSA mediated repressio

188 mainly of topoisomerase II inhibitors (i.e., actinomycin D, doxorubicin, and etoposide) and antimicro

189 Treatment of cells with actinomycin D, DRB, or alpha-amanitin, specific inhibito

190 ed and was not prevented by cycloheximide or actinomycin D, eliminating several potential transcripti

191 eriments using the transcriptional inhibitor actinomycin D, eotaxin mRNA half-life was significantly

192 Apoptosis was induced by exposure to actinomycin D, etoposide, or tunicamycin, with each agen

193 In cells treated with actinomycin D, FADD levels were elevated homogeneously i

194 eosinophils with a transcription inhibitor, actinomycin D, for 8 hours completely depletes intracell

195 e work presented here, the anticancer agent, actinomycin D, is demonstrated to bind to and induce cha

196 easomes upon inhibition of Pol I activity by actinomycin D, L5 and L11 accumulate in the ribosome-fre

197 ed that four DNA-damaging agents (cisplatin, actinomycin D, MMS, and etoposide), but not the cisplati

198 inhibit induction of apoptosis by M protein, actinomycin D, or DRB.

199 SB, BRCA1, or BRCA2 function, treatment with actinomycin D, or overexpression of the tetrameric p53 C

200 After blocking transcription by actinomycin D, R38X appeared to accelerate the degradati

201 lation or transcription by cycloheximide and actinomycin D, respectively, elicits the eIF2alpha phosp

202 of slices with the transcription inhibitor, actinomycin D, resulted in a reduction of sustained pote

203 Upon infection in the presence of actinomycin D, spliced mRNAs were much less sensitive to

204 minutes, and this effect is not inhibited by actinomycin D, suggesting a nongenomic effect of aldoste

205 y 15d-PGJ2 is prevented by cycloheximide and actinomycin D, suggesting a requirement of new protein s

206 or okadaic acid or transcriptional inhibitor actinomycin D, suggesting P-gp regulation is CAR-depende

207 binding activity of Bis IX was prevented by actinomycin D, suggesting that actinomycin D and Bis IX

208 sensitive to cycloheximide but resistant to actinomycin D, suggesting that dsRNA is a viral product.

209 nduced induction of FPN1 mRNA was blocked by actinomycin D, suggesting that transcriptional control w

210 eximide, to inhibit protein synthesis, or of actinomycin D, to inhibit RNA synthesis.

211 Using the transcriptional inhibitor actinomycin D, we determined that treatment with Stx1 or

212 By blocking transcription with actinomycin D, we found that almost 40% of these genes w

213 Knockdown of MDMX increases sensitivity to actinomycin D, whereas MDMX overexpression abrogates p53

214 In contrast, actinomycin D, which both intercalates and binds in the

215 Neither Doxorubicin nor Actinomycin D, which cause the release of nucleostemin f

216 we have combined the emetine treatment with actinomycin D, which effectively prevents the upregulati

217 inhibited by low doses of UV irradiation or actinomycin D, which induce CTD kinase activity, and tha

218 By using actinomycin D, which inhibits new RNA synthesis, we show

219 Consistent with this idea, pretreatment with actinomycin D, which inhibits transcription, decreased t

220 Treatment of CrPV(R146A)-infected cells with actinomycin D, which represses transcription, restores S

221 transition (MPT) 5 hours after rhTRAIL plus actinomycin D, which was followed by cytochrome c releas

222 r the absence of tumor necrosis factor alpha/actinomycin D, while a reduction of SirT1 by siRNA led t

223 o induce mRNA degradation in the presence of actinomycin D, while degradation induced by Delta20R was

224 The induced CD signals observed for the actinomycin D-G-quadruplex complexes may indicate that t

225 Actinomycin D-induced apoptosis was blocked by proteasom

226 sis, whereas overexpression of Mcl-1 delayed actinomycin D-induced apoptosis with kinetics that corre

227 anced cellular sensitivity to viral or dsRNA/actinomycin D-induced apoptosis, typified by enhanced cy

228 the nucleus and then to the cytoplasm during actinomycin D-induced apoptosis.

229 ls overexpressing MDMX are less sensitive to actinomycin D-induced growth arrest due to formation of

230 hmania donovani to protect their "home" from actinomycin D-induced mitochondria-dependent apoptosis.

231 Actinomycin D-induced p53 was inhibited by small interfe

232 by inhibitors of stress kinases but also by actinomycin D-inhibitor of transcription.

233 However, it was abrogated by actinomycin D-mediated inhibition of gene transcription.

234 SP600125 rescued actinomycin D-pretreated hepatocytes and hepatocytes exp

235 r to GA treatment, heat shock resulted in an actinomycin D-sensitive elevation of phagocytosis, which

236 ociated with the vascular endothelium) by an actinomycin D-sensitive signalling mechanism (i.e. trans

237 Furthermore, PNR significantly boosted actinomycin D-stimulated p53 acetylation.

238 Finally, phagocytosis of actinomycin D-treated cells caused apoptosis in macropha

239 This immune repression mediated by actinomycin D-treated cells did not require phagocytosis

240 Conditioning of actinomycin D-treated cells with LPS resulted in no chan

241 ons and cosegregate within nucleolar caps of actinomycin d-treated HeLa cells.

242 nificant attenuation of apoptosis induced by actinomycin D.

243 d cells, in both the presence and absence of actinomycin D.

244 fection or mock infection in the presence of actinomycin D.

245 degraded in vivo during apoptosis induced by actinomycin D.

246 factors, and COX-2 induction was blocked by actinomycin D.

247 ting weekly with etoposide, methotrexate and actinomycin D.

248 n, but not by the transcriptional inhibitor, actinomycin D.

249 the transcriptional level and is blocked by actinomycin D.

250 translated upon infection in the presence of actinomycin D.

251 s completely abolished with cyclohexamide or actinomycin D.

252 n impairing cell cycle arrest in response to Actinomycin D.

253 and H9 following transcriptional arrest with actinomycin D.

254 dle7777 by using tumor necrosis factor alpha/actinomycin D.

255 t alone in cells synchronized by exposure to actinomycin D.

256 n of HAMP mRNA expression was not blocked by actinomycin D.

257 asured following transcriptional arrest with actinomycin D.

258 ion by the therapeutic drugs doxorubicin and actinomycin D.

259 lso enhanced by treatment with a low dose of actinomycin D.

260 s of UbcH5B/C are reduced by doxorubicin and actinomycin D.

261 comparable RNA degradation in the absence of actinomycin D.

262 eoperative chemotherapy with vincristine and actinomycin D.

263 proximately 30% of the cell death induced by actinomycin D.

264 se, but not by the transcriptional inhibitor actinomycin D.

265 d Beas-2B cells and a complete inhibition by actinomycin D.

266 esence or absence of either cycloheximide or actinomycin D.

267 lls in the presence of cycloheximide but not actinomycin D.

268 insensitive to the transcriptional inhibitor actinomycin D.

269 orferi following transcriptional arrest with actinomycin D.

270 n but not degradation of mRNAs is blocked by actinomycin D.

271 cells (CPC) upon exposure to doxorubicin or actinomycin D.

272 induced SGK-1 mRNA expression was blocked by actinomycin D.

273 hairpins by a fluorescent analog of the drug Actinomycin D.

274 tely sensitive to culture in the presence of actinomycin D: caspase activation occurred within 3 hour

275 We identified the antibiotics actinomycins D, X2 and X0beta, produced by the bacterium

276 nt of cells with the RNA synthesis inhibitor actinomycin-D (0.5 microg ml(-1)), the protein synthesis

277 tion and dissociation intercalation rates of actinomycin-D (ACTD) to and from double-stranded 5'-TGCT

278 1 binding with markers of apoptosis (7-amino-actinomycin-D and caspase-3).

279 tiation at a rate comparable with that after actinomycin-D application.

280 on of emetine or the RNA synthesis inhibitor actinomycin-D before delivery of HFS to MF input also ca

281 of association and dissociation kinetics of actinomycin-D binding to a low-density doubled-stranded

282 Further, actinomycin-D blocked LY37's effects, suggesting a trans

283 Notably, actinomycin-D completely abrogated the ability of AF to

284 i-CD3 stimulation of IELs in the presence of actinomycin-D did not inhibit FasL expression, suggestin

285 eated with translational inhibitors, whereas actinomycin-D had no effect.

286 Actinomycin-D treatment of fibroblast cultures indicated

287 ments in which the transcriptional inhibitor actinomycin-D was used.

288 Cycloheximide, but not actinomycin-D, abrogated increased laminin-beta1 synthes

289 er drugs, including paclitaxel, doxorubicin, actinomycin-D, and rapamycin, which are also P-gp substr

290 the effects of the mRNA synthesis inhibitor, actinomycin-D, and the protein synthesis inhibitor, cycl

291 ining different drugs including echinomycin, actinomycin-D, ethidium bromide, Hoechst 33342, and cis-

292 rprisingly, Bak and not Bax is essential for actinomycin-D-induced apoptosis in human embryonic stem

293 o found that E2 modulated PELP1 levels in an actinomycin-D-sensitive manner, suggesting transcription

294 duced by TGF-beta1 was completely blocked by actinomycin-D.

295 rapamycin) or the transcriptional inhibitor actinomycin-D.

296 Netropsin, ethidium, daunorubicin and actinomycin, ligands with known sequence preferences, we

297 imeric form and a hexameric form, with older actinomycin-producing cultures containing predominately

298 Using actinomycin to inhibit transcription, we found that Tat

299 TALH were incubated in low salt for 2 h, and actinomycin was then added with or without SB203580.

300 This is the first report of elaiophylins, actinomycin X0beta and shearinines in the fungus-growing