ライフサイエンスコーパス: cycloheximide

1 he use of inhibitors of translation (notably cycloheximide).

2 assays that lack a reference and/or involve cycloheximide.

3 nduce its expression even in the presence of cycloheximide.

4 ss), and both in the presence and absence of cycloheximide.

5 eaction was inhibited by aminoglycosides and cycloheximide.

6 TNFalpha-induced apoptosis in the absence of cycloheximide.

7 th either a JAK-3 inhibitor, brefeldin A, or cycloheximide.

8 c concentrations but is markedly enhanced by cycloheximide.

9 tiated apoptosis elicited by Fas ligand plus cycloheximide.

10 the presence of protein synthesis inhibitor cycloheximide.

11 to mRNA surveillance was investigated using cycloheximide.

12 the eukaryotic protein synthesis inhibitor, cycloheximide.

13 ession blocked apoptosis induced by TNF plus cycloheximide.

14 sis was blocked by the translation inhibitor cycloheximide.

15 mRNA when protein synthesis was inhibited by cycloheximide.

16 imetic but dispensable for that triggered by cycloheximide.

17 seen when protein synthesis was inhibited by cycloheximide.

18 eatment with tumor necrosis factor-alpha and cycloheximide.

19 ng THP-1 cells with actinomycin D but not by cycloheximide.

20 when translation elongation is inhibited by cycloheximide.

21 nt on protein synthesis and were reversed by cycloheximide.

22 uitin turnover, rendering yeast resistant to cycloheximide.

23 bation with the global translation inhibitor cycloheximide.

24 presence of the protein synthesis inhibitor cycloheximide.

25 silencing pathway but which is alleviated by cycloheximide.

26 HeLa 229 cells incubated with TNF-alpha and cycloheximide.

27 e 8, and caspase 9 induced by TNFalpha or by cycloheximide.

28 presence of the protein-synthesis inhibitor cycloheximide.

29 ked and reversed by the elongation inhibitor cycloheximide.

30 eatment with the protein-synthesis inhibitor cycloheximide.

31 also supported the superinduction of SOX9 by cycloheximide.

32 7 cells) was induced with either TNFalpha or cycloheximide.

33 ein synthesis inhibitors, such as saporin or cycloheximide.

34 ydroxytamoxifen treatment in the presence of cycloheximide.

35 seen when protein synthesis is inhibited by cycloheximide.

36 esence of the protein biosynthesis inhibitor cycloheximide.

37 e male pronucleus of the zygote treated with cycloheximide.

38 ppearance after translation was stopped with cycloheximide.

39 is when NF-kappaB activation is inhibited by cycloheximide.

40 r treatment with the translational inhibitor cycloheximide.

41 , localization, motility, and sensitivity to cycloheximide.

42 lational inhibition of secondary feedback by cycloheximide.

43 mples treated with the translation inhibitor cycloheximide.

44 totoxic agents such as TRAIL, etoposide, and cycloheximide.

45 nd is blocked with the translation inhibitor cycloheximide.

46 findings were seen in cells co-treated with cycloheximide.

47 reducing translation of wild-type yeast with cycloheximide.

48 ons of the translation elongation inhibitors cycloheximide (0.7-70 nM) and anisomycin (7.5-750 nM), i

49 microM), or the protein synthesis inhibitor cycloheximide (1 microM) failed to reduce the significan

50 e blocked by the protein synthesis inhibitor cycloheximide (1.0 muM), a known inhibitor of delayed is

51 wild-type strain increased its resistance to cycloheximide, 1,10-phenanthroline, 4-NQO, and fluconazo

52 KCl (50 mm) or a mixture of taste compounds (cycloheximide, 10 microm; saccharin, 2 mm; denatonium, 1

53 (actinomycin D, 5 mug ml-1) or translation (cycloheximide, 20 mug ml-1).

54 tinomycin D, 4 mum) or protein biosynthesis (cycloheximide, 70 mum).

55 ctinomycin D (an RNA synthesis inhibitor) or cycloheximide (a protein synthesis inhibitor) blocked ga

56 When the HepG2 cells were treated with cycloheximide, a general inhibitor of protein synthesis,

57 We found that both cycloheximide, a general protein synthesis inhibitor, an

58 in an osteoblast cell line by treatment with cycloheximide, a protein synthesis inhibitor, showing th

59 Cycloheximide, a translation elongation inhibitor known

60 with the length of darkness preceding the NB Cycloheximide abolished the NB up-regulation of PPD1, su

61 locking protein synthesis in the presence of cycloheximide abolished the PDGF effect, but not in the

62 njections of the protein synthesis inhibitor cycloheximide, administered after inhibitory avoidance t

63 ynthesis was blocked by either anisomycin or cycloheximide after the representation of a conditioning

64 istration of the protein synthesis inhibitor cycloheximide after training blocked the long-term effec

65 ion of internalized hCTR1 in the presence of cycloheximide after up to 2 h of exposure to 0-100 micro

66 n addition, the coordinated use of GuHCl and cycloheximide allowed us to demonstrate that MRV dsRNA s

67 Cycloheximide also ameliorated proteotoxic stress via a

68 Another elongation inhibitor, cycloheximide, also prevented eEF2/ATP-dependent splitti

69 d decrease in ETR2 levels is not affected by cycloheximide, an inhibitor of protein biosynthesis, but

70 slational mechanism, which is insensitive to cycloheximide, an inhibitor of protein biosynthesis.

71 ss granules in a manner that is prevented by cycloheximide, an inhibitor of translational elongation.

72 d by supplying culture medium with 0.1 mg/mL cycloheximide and 10 nM phorbol myristate acetate.

73 ll death induced by 15d-PGJ2 is prevented by cycloheximide and actinomycin D, suggesting a requiremen

74 application of protein synthesis inhibitors cycloheximide and emetine to acute rat hippocampal slice

75 TIA-1-mediated decay is inhibited by cycloheximide and emetine, drugs that stabilize polysome

76 Results from cycloheximide and endosomal Cys protease inhibitor E-64d

77 Here, we show that translocation inhibitors cycloheximide and lactimidomycin inhibited all three rea

78 a greater effect on behavioral avoidance of cycloheximide and PROP than quinine and denatonium, whic

79 s, axons grew for 24-48 h in the presence of cycloheximide and responded to negative and positive cue

80 to growth in the presence of brefeldin A and cycloheximide and resulted in new synthesis of ergostero

81 P:TGBp2 or pRTL2-GFP:TGBp2 were treated with cycloheximide and the decline of GFP fluorescence was gr

82 lial HEp-2 cells from apoptosis triggered by cycloheximide and tumor necrosis factor alpha.

83 Cells lacking Hpm1p are resistant to cycloheximide and verrucarin A and have decreased transl

84 ypersensitivity to the translation inhibitor cycloheximide and yields synthetic "sickness" in cells w

85 nce of primaquine, concanamycin A, monensin, cycloheximide, and an inhibitor of microsomal triglyceri

86 y injecting the protein synthesis inhibitor, cycloheximide, and the afferent nerve blocker, capsaicin

87 olished by inhibiting protein synthesis with cycloheximide, and Trim21 expression could not be induce

88 ssed if the synthesis of REST was blocked by cycloheximide; and (c) histone deacetylase inhibitors re

89 y autoradiography and was also observed with cycloheximide, another translational inhibitor.

90 A translation was inhibited by rapamycin and cycloheximide as well as by RNA interference-mediated kn

91 nges in protein half-life were tested with a cycloheximide assay; gene expression was examined by rea

92 Pharmacologic inhibition of translation with cycloheximide attenuated Cited2 down-regulation by TGF-b

93 Actinomycin D blocked transcription, and cycloheximide attenuated synthesis of MTs in the presenc

94 The cycloheximide-based protein degradation analysis indicat

95 The impact of cycloheximide becomes apparent after the first peak of n

96 dogenous IL-10 nor the translation inhibitor cycloheximide blocked SOCS1/SOCS3 induction by B. burgdo

97 chondrocytes with a JAK-3 inhibitor or with cycloheximide blocked the IL-7-mediated secretion of S10

98 The protein synthesis inhibitor, cycloheximide, blocked the appearance of Mos, blocked Me

99 tion inhibition by some antibiotics, such as cycloheximide, both in ribosome run-off assays and in in

100 Cycloheximide, brefeldin A, ionic composition of the med

101 Production of dsRNA was sensitive to cycloheximide but resistant to actinomycin D, suggesting

102 ne transcription, as it was not abolished by cycloheximide but was abolished by actinomycin D, and in

103 Cycloheximide, but not actinomycin-D, abrogated increase

104 d HBC cell viabilities when exposed to OA or cycloheximide, but not by Taxol.

105 hology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpressi

106 Cycloheximide chase assay showed a decrease in the half-

107 ed the protein stability of KLF5 as shown by cycloheximide chase assay, indicating that SMURF2 specif

108 erve as a reporter of protein stability in a cycloheximide chase assay.

109 Cycloheximide chase assays revealed a shortening of APP

110 As measured by pulse-chase and cycloheximide chase assays, a major binding site Nedd4-2

111 By cycloheximide chase assays, we found that KLF5 decreases

112 2) decrease protein stability estimated from cycloheximide chase assays; and 3) prevent the CaValpha2

113 Cycloheximide chase experiments showed that Ecm7 was sta

114 ubiquitin-binding entity precipitations and cycloheximide chase experiments.

115 uced COX-2 protein stability as confirmed by cycloheximide chase experiments.

116 Pulse-chase and cycloheximide-chase assays demonstrated that the marked

117 Inducible cell line and cycloheximide-chase experiments indicate that these drug

118 nce of heat shock, sodium arsenite (NaAsO2), cycloheximide (CHX) and Lipofectamine 2000-mediated tran

119 se cells to camptothecin (CPT) or TNF-alpha/ cycloheximide (CHX) failed to induce apoptosis.

120 Medium was replaced, cycloheximide (CHX) was added to inhibit synthesis of ne

121 FP due to inhibition of ribosome activity by cycloheximide (CHX) was quantified with real-time quanti

122 ndothelial cells (HMEC) need the presence of cycloheximide (CHX) with LPS to induce apoptosis.

123 m either virus was reduced by treatment with cycloheximide (CHX), an inhibitor of protein synthesis.

124 ability following UVB that was alleviated by cycloheximide (CHX), indicating that translation repress

125 nce to tumor necrosis factor (TNF)-alpha and cycloheximide (CHX)-induced apoptosis, and NF-kappaB act

126 These P-bodies were also preset in cycloheximide (CHX)-treated cells but not in either trea

127 re treated with an inhibitor of translation, cycloheximide (CHX).

128 with tumor necrosis factor (TNF)-alpha plus cycloheximide (CHX).

129 to tumor necrosis factor-alpha (TNFalpha) + cycloheximide (CHX).

130 dopsis plants with the translation inhibitor cycloheximide, cleavage events accumulate 13 to 14 nucle

131 ere, we investigate the influence of ranging cycloheximide concentrations on ribosome profiles in Sac

132 creased ABCB4 and ABCB19 protein levels when cycloheximide concomitantly inhibited new protein synthe

133 The reduction in TH mRNA was blocked by cycloheximide consistent with a protein-dependent mechan

134 y induces Cebpa mRNA in these cells, even in cycloheximide, consistent with direct gene regulation.

135 f c-Myc by OA or protein synthesis inhibitor cycloheximide contributed to HBC growth inhibition and t

136 Actinomycin D and cycloheximide could only partially block androgen-induce

137 ter inhibition of new protein synthesis with cycloheximide, CX50fs disappeared much more rapidly than

138 were injected subcutaneously with saline or cycloheximide (CXM; 1 mg/kg) and returned to their home

139 Cycloheximide decreased basal Y1R mRNA expression; howev

140 ical protection of CA1 ischemic neurons with cycloheximide decreased the formation of SGs and restore

141 ntly with TLR ligands and in the presence of cycloheximide, demonstrating that they act independently

142 ation on the 5' side of coding sequences was cycloheximide-dependent.

143 Inhibition of IE protein synthesis by cycloheximide did not affect histone occupancy on most I

144 Cycloheximide did not affect resensitization, but bafilo

145 sms, as inhibition of protein synthesis with cycloheximide did not completely prevent the protective

146 Cycloheximide did not inhibit 9-cis retinoic acid-induce

147 A was not increased by TGFbeta treatment and cycloheximide did not inhibit syndecan-1 induction by TG

148 Our results demonstrate that cycloheximide does influence some of the results of ribo

149 for degradation of PIF1, as the presence of cycloheximide does not prevent degradation of PIF1 in th

150 Treatment of cells with cycloheximide does not reduce the internalization of BL2

151 Cycloheximide experiments show that Delta264 CFTR is deg

152 e blockage of de novo protein synthesis with cycloheximide failed to reverse the KSHV-induced disrupt

153 treated with the protein synthesis inhibitor cycloheximide followed by fluprostenol or IL-1 for 1.5 h

154 BI-D1870 also inhibited transformation from cycloheximide-generated blebbishields.

155 ed with translation inhibitor (anisomycin or cycloheximide), group I mGluRs elicited a sustained decr

156 Cycloheximide had minor effects on overall ribosome dens

157 or suppressors that eliminated Pdr5-mediated cycloheximide hyper-resistance.

158 up-regulation of foxj1a was not inhibited by cycloheximide, identifying foxj1a as a primary response

159 hen de novo protein synthesis was blocked by cycloheximide in OLA1-knockdown cells, they continued to

160 Functional hyaluronan cables were induced by cycloheximide in the confirmed absence of protein synthe

161 se of global translation inhibitors, such as cycloheximide, in protein degradation assays may result

162 y of FKBP12, including FK506, rapamycin, and cycloheximide, increase steady-state palmitoylation.

163 esensitized 4-8-fold faster than NK(1)Rwt by cycloheximide-independent mechanisms.

164 Early (< or = 60 min), cycloheximide-independent secretion from preformed intra

165 Pulse-labeling in the presence of cycloheximide indicated that chloroplast protein synthes

166 Insensitivity to cycloheximide indicated that IL-33 was a direct target o

167 In addition, cycloheximide induced rapid activation of Bak and Bax, w

168 aF/3 cells with TNF-alpha in the presence of cycloheximide, induced apoptosis in both cases.

169 amptothecin-, or tumor necrosis factor alpha/cycloheximide-induced apoptosis and caspase-3-8, and cas

170 Both Bim and Mcl-1 levels decreased in cycloheximide-induced apoptosis while Bik levels were un

171 Bak, downstream targets of Mcl-1, inhibited cycloheximide-induced apoptosis, as did knockdown of Bax

172 ition and overexpression of Bcl-x(L) blocked cycloheximide-induced apoptosis.

173 both H(2)O(2)-induced necrosis and TNF-alpha/cycloheximide-induced apoptosis; the S1P(2)R agonist had

174 We sought to determine whether LPS and cycloheximide-induced cell death in human lung microvasc

175 c protein Bcl-X(L) were resistant to LPS and cycloheximide-induced death and that the proapoptotic Bc

176 We conclude that LPS and cycloheximide-induced death in HmVECs requires the intri

177 rho(0) cells) were protected against LPS and cycloheximide-induced death.

178 occurred, as indicated by PLD resistance to cycloheximide-induced EGFR protein degradation.

179 Moreover the cycloheximide-induced increase in mTORC1 signaling was s

180 not tumor necrosis factor alpha (TNF-alpha)/cycloheximide-induced, apoptosis.

181 d overexpression of NFIL3 in the presence of cycloheximide induces GLepsilon transcripts.

182 ons in the initial studies are the result of cycloheximide-inflicted artifacts.

183 racellular pools was followed by late (24 h) cycloheximide-inhibitable secretion requiring new protei

184 and the general protein synthesis inhibitor cycloheximide inhibited both the LPS and TNF-alpha sensi

185 pping enzyme knockdown, apoptosis induced by cycloheximide inhibition of protein synthesis required B

186 In experiments with cycloheximide inhibition of protein synthesis, the time

187 Moreover, qRT-PCR analyses coupled with cycloheximide inhibition studies suggest that the underl

188 ere a direct effect of hepcidin, as shown by cycloheximide insensitivity, and dependent on the presen

189 ere a direct effect of hepcidin, as shown by cycloheximide insensitivity, and dependent on the presen

190 Cycloheximide is a non-competitive inhibitor of both eEF

191 e to TNF or LPS and a translation inhibitor, cycloheximide, leads to prolonged NF-kappaB activation a

192 f cells with the protein synthesis inhibitor cycloheximide led to an almost instantaneous loss of unm

193 Inhibition of protein synthesis with cycloheximide led to intracellular depletion of the glyc

194 is of putative trans imprinting factors with cycloheximide led to loss of IGF2 imprinting in normal c

195 presence of the protein synthesis inhibitor cycloheximide, LPS primarily induces caspase-dependent a

196 is, GLX had a greater effect on quinine than cycloheximide (mean shift of 1.02 vs. 0.27 log10 units).

197 reases the sensitivity of HUVECs to LPS plus cycloheximide-mediated death.

198 ition of peptide ligand generation following cycloheximide-mediated inhibition of protein synthesis.

199 aracterized the mechanisms by which PatA and cycloheximide modulate NMD.

200 not affected by protein synthesis inhibitor cycloheximide nor protein transport inhibitor monensin,

201 egradation was strongly inhibited by feeding cycloheximide or amino acids to detached leaves, while S

202 In the presence of cycloheximide or anisomycin, ephrin-A2, slit-3, and sema

203 e effects were abolished by actinomycin D or cycloheximide or by the AhR antagonists resveratrol and

204 Cycloheximide or Chk2 inhibitor pretreatment abrogated n

205 1 and HDAC3, markedly increased stability in cycloheximide or in the presence of co-expressed Cdh1, a

206 ty of influenza A viruses in the presence of cycloheximide or nucleoprotein (NP) small interfering RN

207 poptosis was induced by exposure to TNFalpha/cycloheximide or other apoptotic signaling molecules, th

208 ermore, inhibition of protein synthesis with cycloheximide or overexpression of dominant negative hea

209 Moreover, ectopic expression followed by cycloheximide or pulse-chase treatment demonstrated that

210 eatment with the protein synthesis inhibitor cycloheximide or RNA interference-mediated knockdown of

211 e slices with the mRNA translation inhibitor cycloheximide or the mammalian target of rapamycin (mTOR

212 itors for phospholipases (PL) (-C or -D), or cycloheximide, or brefeldin A.

213 omyl, diamide, and menadione, but not 4-NQO, cycloheximide, or fluconazole.

214 Partial inhibition of translation by cycloheximide, or of autophagy by lithium chloride, resc

215 reatment with a protein synthesis inhibitor, cycloheximide, or Smac mimetic, a small molecule mimic o

216 OA, cycloheximide, or the chemotherapeutic drug Taxol suppre

217 mild ER stress, are protected from H(2)O(2), cycloheximide- or ultraviolet-induced cell death.

218 However, we also noted that cycloheximide partially inhibits R5020 induction of E2F1

219 inhibitor-treated embryos with low doses of cycloheximide partially rescued viability.

220 scription and translation, actinomycin D and cycloheximide, partially cancelled this process, suggest

221 ibitor of metalloproteinases 3 (TIMP-3), and cycloheximide pretreatment were used to identify ADAMTS

222 Although inhibiting protein synthesis with cycloheximide prevented H(2)O(2) from elevating Nrf2 pro

223 In contrast, cycloheximide prevented lovastatin from increasing both

224 Resensitization occurred after 16 h, and cycloheximide prevented resensitization, implicating new

225 Finally, actinomycin D or cycloheximide prevented the anti-apoptotic effect of 1al

226 n of the cytoplasmic translational inhibitor cycloheximide prevents S deprivation-triggered accumulat

227 that inhibition of protein biosynthesis with cycloheximide prior to 3-AP and 3-AP-Me treatment leads

228 Cycloheximide promotes caspase-8 activation by eliminati

229 In isolated cardiomyocytes, experiments with cycloheximide, proteasome inhibitor MG-132, and siBVR su

230 rformed with the protein synthesis inhibitor cycloheximide provided evidence that JAZs, MYC2, and gen

231 in the presence of the translation inhibitor cycloheximide, providing evidence that CTCF partitions t

232 her than GLX alone for every stimulus except cycloheximide (ps < .03), suggesting that the GSP nerve

233 nce of translational inhibitors (anisomycin, cycloheximide, rapamycin) or the transcriptional inhibit

234 eas treatment with the translation inhibitor cycloheximide reduced both kinases, demonstrating that t

235 on, while macrophage-like cells treated with cycloheximide remained viable and showed transient activ

236 r library to confirm known genes that confer cycloheximide resistance in yeast.

237 tage of a previously undescribed, recessive, cycloheximide-resistance mutation.

238 ent, apoptosis and cell growth resulted from cycloheximide-resistant primary IFNgamma signalling.

239 This hypothesis is supported by reports of cycloheximide-responsive cells with GSP-innervated recep

240 Inhibition of protein synthesis with cycloheximide resulted in NET disappearance rates from D

241 Treatment of DC with cycloheximide revealed that bryostatin-1-induced T-bet e

242 ment of cells with the translation inhibitor cycloheximide revealed that control of NT1 expression oc

243 Application of cycloheximide revealed that forskolin enhanced IRS2 prot

244 ibition of protein synthesis in COS cells by cycloheximide reveals remarkably rapid turnover of expre

245 t macrophage activation with C1q resulted in cycloheximide-sensitive enhanced engulfment, indicating

246 To investigate the cycloheximide-sensitive pathway, C1q-elicited macrophage

247 Turnover measurements in the presence of cycloheximide show that, whereas 4E-BP1 is normally a ve

248 the presence of protein synthesis inhibitor cycloheximide, showing that the effect is direct.

249 JNJ16259685 and protein synthesis inhibitor cycloheximide significantly attenuated or blocked the ac

250 y after inhibition of protein synthesis with cycloheximide, so we searched for interacting proteins t

251 al signaling pathways (UV radiation, TNF and cycloheximide, staurosporine, thapsigargin and tunicamyc

252 ranscription (actinomycin D) or translation (cycloheximide), suggesting that gene expression was requ

253 is also blocked by actinomycin D but not by cycloheximide, suggesting a transcriptional mechanism wh

254 induced by tumor necrosis factor alpha plus cycloheximide, suggesting a unique mitochondrial pathway

255 eral hours after translation is stopped with cycloheximide, suggesting that the beta(2) subunit under

256 osinase protein abundance in the presence of cycloheximide, suggestive of increased degradation.

257 arkably rapid as measured in the presence of cycloheximide (t(1/2) = 2 h), but silencing Map4k4 had n

258 rly true for some bitter stimuli like PROP & cycloheximide that stimulate the GL to a far greater ext

259 ed by the use of a chylomicron flow blocker, cycloheximide, that prevented the oral absorption of doc

260 ICP4 protein from E5 cells was inhibited by cycloheximide, the d120 virion-associated ICP4 protein w

261 aversive LTM in that it can be disrupted by cycloheximide, the dCreb2-b transcriptional repressor, a

262 STAT signaling, as indicated by studies with cycloheximide, the JAK inhibitor I, and small interferin

263 nduction of E2F1 activity in the presence of cycloheximide, thus indicating that RhoBTB2 is a direct

264 te translation inhibitors lactimidomycin and cycloheximide to achieve simultaneous detection of both

265 We used the translational inhibitor cycloheximide to analyze turnover and observed that the

266 Using cycloheximide to prevent de novo protein synthesis, palm

267 activity was prevented by addition of either cycloheximide, to inhibit protein synthesis, or of actin

268 pancy showed strong positive correlations in cycloheximide-treated and untreated cells.

269 umulation of ribosomes on 5' leaders in both cycloheximide-treated and untreated cells.

270 ibition of Plk1 increased Mre11 stability in cycloheximide-treated cells.

271 as elevated in the case of the OA-treated or cycloheximide-treated HBC cell nuclear extracts.

272 ic susceptibility testing were performed for cycloheximide-treated HEp-2 cells in 96-well microtiter

273 g features accumulated in the fry2-1 mutant, cycloheximide-treated wild type, and upf3 mutant plants,

274 Cycloheximide treatment also revealed that several of th

275 te that had been cured of virus infection by cycloheximide treatment and hyphal tipping.

276 Cycloheximide treatment before mitosis affected neither

277 Immunofluorescence after cycloheximide treatment demonstrated decreased retention

278 The loss of Synpo protein after Stattic or cycloheximide treatment did not occur when podocytes wer

279 Cycloheximide treatment increased the levels of both tra

280 Additionally, inhibition of translation by cycloheximide treatment rescued IFN-beta induction follo

281 urement of beta-catenin protein stability by cycloheximide treatment showed that Rad6B silencing spec

282 e-mediated decay (NMD); inhibition of NMD by cycloheximide treatment stabilized these transcripts and

283 in cytoplasmic granules was not disrupted by cycloheximide treatment, suggesting that these sites wer

284 and on Pgp stability by immunoblotting after cycloheximide treatment.

285 Dronc-mediated apoptosis upon DIAP1 RNAi or cycloheximide treatment.

286 when other mRNAs are trapped in polysomes by cycloheximide treatment.

287 g in response to tumor necrosis factor-alpha/cycloheximide treatment.

288 ed tRNAs have similar turnover kinetics upon cycloheximide treatment.

289 However, OA or cycloheximide treatments over 6 or 10 h, respectively, i

290 lities after all-trans-retinoic acid (RA) or cycloheximide treatments.

291 Induction of apoptosis by cycloheximide was detected within 2-4 h and blocked by p

292 or omitting translation inhibitors, such as cycloheximide, was noted as it markedly affected ribosom

293 Using the reversible translational inhibitor cycloheximide, we show that this signal memory requires

294 est expression of these genes was blocked by cycloheximide when the EBV lytic cycle was induced by hi

295 treated with the protein synthesis inhibitor cycloheximide, whereas overexpression of WT OTUB1, but n

296 ession of Mcl-1 blocked apoptosis induced by cycloheximide, whereas RNA interference knockdown of Mcl

297 CK4 are all induced by exposure of tissue to cycloheximide, whereas ZmPPCK1 is not.

298 ws a time-dependent decay in the presence of cycloheximide which is not apparent for the cytoplasmic

299 ase was not seen when eggs were activated by cycloheximide, which does not cause a Ca(2+) increase.

300 ment of cells with the translation inhibitor cycloheximide, which relieves ER load, ameliorated this