ライフサイエンスコーパス: actinomycin D

1 nificant attenuation of apoptosis induced by actinomycin D.

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

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

4 degraded in vivo during apoptosis induced by actinomycin D.

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

6 ting weekly with etoposide, methotrexate and actinomycin D.

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

8 the transcriptional level and is blocked by actinomycin D.

9 translated upon infection in the presence of actinomycin D.

10 s completely abolished with cyclohexamide or actinomycin D.

11 and H9 following transcriptional arrest with actinomycin D.

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

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

14 asured following transcriptional arrest with actinomycin D.

15 ion by the therapeutic drugs doxorubicin and actinomycin D.

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

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

18 comparable RNA degradation in the absence of actinomycin D.

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

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

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

22 eoperative chemotherapy with vincristine and actinomycin D.

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

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

25 esence or absence of either cycloheximide or actinomycin D.

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

27 insensitive to the transcriptional inhibitor actinomycin D.

28 orferi following transcriptional arrest with actinomycin D.

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

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

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

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

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

34 rapamycin) or the transcriptional inhibitor actinomycin-D.

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

36 (10 mum) or by inhibition of transcription (actinomycin D, 4 mum) or protein biosynthesis (cyclohexi

37 nt patients (46.7%), hCG was normalized with actinomycin D (42.3%) or combination chemotherapy/surger

38 15, 17, 18, 20, 21, 23, 24, 26, and 27, plus actinomycin D 45 mug/kg every 3 weeks from week 2, eithe

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

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

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

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

43 r treatment included methotrexate (100%) and actinomycin D (7%).

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

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

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

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

48 Actinomycin D, a transcriptional inhibitor, did not bloc

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

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

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

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

53 Actinomycin D accelerated induction of apoptosis of HeLa

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

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

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

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

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

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

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

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

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

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

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

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

66 for binding by the GC-selective intercalator actinomycin D (ActiD).

67 g tumoroid cultures led to identification of Actinomycin D (AD) as a top CSC inhibitor.

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

69 Actinomycin D alone also enhanced the appearance of DISC

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

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

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

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

74 Actinomycin D, an inhibitor of gene transcription, abrog

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

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

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

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

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

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

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

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

83 Actinomycin D and cycloheximide could only partially blo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 1 binding with markers of apoptosis (7-amino-actinomycin-D and caspase-3).

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

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

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

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

103 conventional chemotherapy with vincristine, actinomycin-D, and doxorubicin given singly or in combin

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

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

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

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

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

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

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

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

112 nd the inhibition of gene transcription with actinomycin D blocked the increase in ERalpha with E2.

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

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

115 Actinomycin D blocked transcription, and cycloheximide a

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

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

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

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

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

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

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

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

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

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

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

127 Actinomycin D caused only minor changes in angiogenic as

128 Actinomycin D chase experiments showed that fluasterone

129 Actinomycin D chase experiments showed that hypoxic indu

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

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

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

133 Actinomycin D completely blocked the induction of IRF-1

134 Pretreatment with actinomycin D completely prevents the induced up-regulat

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

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

137 Actinomycin D decreased the rapidly moving fraction, sug

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

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

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

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

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

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

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

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

146 Actinomycin D experiments revealed that enhanced express

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

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

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

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

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

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

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

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

155 Higher concentrations of actinomycin D globally repressed transcription.

156 Actinomycin D had no effect on dexamethasone-independent

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

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

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

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

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

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

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

164 Actinomycin D-induced apoptosis was blocked by proteasom

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

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

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

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

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

170 Actinomycin D-induced p53 was inhibited by small interfe

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

172 Actinomycin D inhibited all NSCLC VEGF secretion, and VE

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

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

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

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

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

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

179 Actinomycin D is a potent transcription inhibitor that i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 SP600125 rescued actinomycin D-pretreated hepatocytes and hepatocytes exp

211 6 h in cultured cTALH, which was blocked by actinomycin D pretreatment, suggesting transcriptional r

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

213 Actinomycin D prevented lovastatin-dependent increases i

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

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

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

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

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

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

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

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

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

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

224 Actinomycin D sensitized TRAIL-resistant cells through u

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

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

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

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

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

230 Actinomycin D studies revealed that Hcy stabilized HMGCR

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

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

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

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

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

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

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

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

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

240 0 and mouse NIH 3T3 fibroblasts treated with actinomycin D to block de novo transcription, microarray

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 to provide intrinsic antiviral protection in actinomycin D-treated cells.

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

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

258 Actinomycin D treatment blocked, and high dose salicylat

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

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

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

262 Actinomycin D treatment suggests that doxycycline decrea

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

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

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

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

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

268 RNA stability was determined after actinomycin D treatment.

269 0 mimics decreased luciferase activity after actinomycin D treatment.

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

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

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

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

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

275 Actinomycin-D treatment of fibroblast cultures indicated

276 Actinomycin D was added to arrest transcription, and tot

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

293 or example, drug screening demonstrated that actinomycin D, which is used for treatment of sarcoma bu

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

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

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

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

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

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

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