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 n impairing cell cycle arrest in response to Actinomycin D.

11 s completely abolished with cyclohexamide or actinomycin D.

12 and H9 following transcriptional arrest with actinomycin D.

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

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

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

16 asured following transcriptional arrest with actinomycin D.

17 ion by the therapeutic drugs doxorubicin and actinomycin D.

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

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

20 eoperative chemotherapy with vincristine and actinomycin D.

21 comparable RNA degradation in the absence of actinomycin D.

22 proximately 30% of the cell death induced by 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 t was partially blocked by KT5823 but not by actinomycin D.

28 fold, and this was confirmed with the use of actinomycin D.

29 insensitive to the transcriptional inhibitor actinomycin D.

30 orferi following transcriptional arrest with actinomycin D.

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

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

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

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

35 rapamycin) or the transcriptional inhibitor actinomycin-D.

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

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

38 (10 mum) or by inhibition of transcription (actinomycin D, 4 mum) or protein biosynthesis (cyclohexi

39 15, 17, 18, 20, 21, 23, 24, 26, and 27, plus actinomycin D 45 mug/kg every 3 weeks from week 2, eithe

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

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

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

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

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 The potent anticancer drug actinomycin D (ActD) acts by binding to DNA, thereby int

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

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

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

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

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

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

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

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

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

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

68 Actinomycin D alone also enhanced the appearance of DISC

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

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

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

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

73 Actinomycin D, an inhibitor of gene transcription, abrog

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

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

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

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

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

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

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

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

82 Actinomycin D and cycloheximide could only partially blo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 1 binding with markers of apoptosis (7-amino-actinomycin-D and caspase-3).

98 was blocked by a transcriptional inhibitor, actinomycin D, and does require de novo protein synthesi

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 cer drugs, such as vinblastine, doxorubicin, actinomycin-D, and cisplatin, that are also substrates f

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 Actinomycin D experiments suggested that this effect was

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

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

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

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

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

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

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

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

156 Higher concentrations of actinomycin D globally repressed transcription.

157 Actinomycin D had no effect on dexamethasone-independent

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

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

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

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

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

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

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

165 Actinomycin D-induced apoptosis was blocked by proteasom

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

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

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

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

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

171 Actinomycin D-induced p53 was inhibited by small interfe

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

173 Actinomycin D inhibited all NSCLC VEGF secretion, and VE

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

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

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

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

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

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

180 Actinomycin D is a potent transcription inhibitor that i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 SP600125 rescued actinomycin D-pretreated hepatocytes and hepatocytes exp

212 6 h in cultured cTALH, which was blocked by actinomycin D pretreatment, suggesting transcriptional r

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

214 Actinomycin D prevented lovastatin-dependent increases i

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

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

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

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

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

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

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

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

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

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

225 Actinomycin D sensitized TRAIL-resistant cells through u

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

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

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

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

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

231 Actinomycin D studies revealed that Hcy stabilized HMGCR

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

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

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

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

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

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

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

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

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

241 0 and mouse NIH 3T3 fibroblasts treated with actinomycin D to block de novo transcription, microarray

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Brief actinomycin D treatment of conjugating cells blocked M-e

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

263 Actinomycin D treatment suggests that doxycycline decrea

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

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

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

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

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

269 RNA stability was determined after actinomycin D treatment.

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

271 0 mimics decreased luciferase activity after actinomycin D treatment.

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

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

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

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

276 Actinomycin-D treatment of fibroblast cultures indicated

277 Actinomycin D was added to arrest transcription, and tot

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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