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1 he use of inhibitors of translation (notably cycloheximide).
2 totoxic agents such as TRAIL, etoposide, and cycloheximide.
3 nd is blocked with the translation inhibitor cycloheximide.
4 findings were seen in cells co-treated with cycloheximide.
5 treated with the mRNA translation inhibitor cycloheximide.
6 reducing translation of wild-type yeast with cycloheximide.
7 nduce its expression even in the presence of cycloheximide.
8 eaction was inhibited by aminoglycosides and cycloheximide.
9 presence of the protein synthesis inhibitor cycloheximide.
10 TNFalpha-induced apoptosis in the absence of cycloheximide.
11 th either a JAK-3 inhibitor, brefeldin A, or cycloheximide.
12 c concentrations but is markedly enhanced by cycloheximide.
13 tiated apoptosis elicited by Fas ligand plus cycloheximide.
14 the presence of protein synthesis inhibitor cycloheximide.
15 to mRNA surveillance was investigated using cycloheximide.
16 the eukaryotic protein synthesis inhibitor, cycloheximide.
17 ession blocked apoptosis induced by TNF plus cycloheximide.
18 sis was blocked by the translation inhibitor cycloheximide.
19 mRNA when protein synthesis was inhibited by cycloheximide.
20 imetic but dispensable for that triggered by cycloheximide.
21 seen when protein synthesis was inhibited by cycloheximide.
22 eatment with tumor necrosis factor-alpha and cycloheximide.
23 ng THP-1 cells with actinomycin D but not by cycloheximide.
24 when translation elongation is inhibited by cycloheximide.
25 nt on protein synthesis and were reversed by cycloheximide.
26 uitin turnover, rendering yeast resistant to cycloheximide.
27 bation with the global translation inhibitor cycloheximide.
28 presence of the protein synthesis inhibitor cycloheximide.
29 silencing pathway but which is alleviated by cycloheximide.
30 e 8, and caspase 9 induced by TNFalpha or by cycloheximide.
31 presence of the protein-synthesis inhibitor cycloheximide.
32 ked and reversed by the elongation inhibitor cycloheximide.
33 eatment with the protein-synthesis inhibitor cycloheximide.
34 is when NF-kappaB activation is inhibited by cycloheximide.
35 assays that lack a reference and/or involve cycloheximide.
36 ss), and both in the presence and absence of cycloheximide.
37 HeLa 229 cells incubated with TNF-alpha and cycloheximide.
38 ein synthesis inhibitors, such as saporin or cycloheximide.
39 seen when protein synthesis is inhibited by cycloheximide.
40 esence of the protein biosynthesis inhibitor cycloheximide.
41 e male pronucleus of the zygote treated with cycloheximide.
42 ppearance after translation was stopped with cycloheximide.
43 r treatment with the translational inhibitor cycloheximide.
44 , localization, motility, and sensitivity to cycloheximide.
45 lational inhibition of secondary feedback by cycloheximide.
46 mples treated with the translation inhibitor cycloheximide.
47 ons of the translation elongation inhibitors cycloheximide (0.7-70 nM) and anisomycin (7.5-750 nM), i
48 e blocked by the protein synthesis inhibitor cycloheximide (1.0 muM), a known inhibitor of delayed is
49 KCl (50 mm) or a mixture of taste compounds (cycloheximide, 10 microm; saccharin, 2 mm; denatonium, 1
52 ctinomycin D (an RNA synthesis inhibitor) or cycloheximide (a protein synthesis inhibitor) blocked ga
55 in an osteoblast cell line by treatment with cycloheximide, a protein synthesis inhibitor, showing th
57 with the length of darkness preceding the NB Cycloheximide abolished the NB up-regulation of PPD1, su
58 locking protein synthesis in the presence of cycloheximide abolished the PDGF effect, but not in the
59 njections of the protein synthesis inhibitor cycloheximide, administered after inhibitory avoidance t
60 ynthesis was blocked by either anisomycin or cycloheximide after the representation of a conditioning
61 istration of the protein synthesis inhibitor cycloheximide after training blocked the long-term effec
62 ion of internalized hCTR1 in the presence of cycloheximide after up to 2 h of exposure to 0-100 micro
63 n addition, the coordinated use of GuHCl and cycloheximide allowed us to demonstrate that MRV dsRNA s
67 d decrease in ETR2 levels is not affected by cycloheximide, an inhibitor of protein biosynthesis, but
68 slational mechanism, which is insensitive to cycloheximide, an inhibitor of protein biosynthesis.
69 ss granules in a manner that is prevented by cycloheximide, an inhibitor of translational elongation.
71 :C-induced IDO and HLA-G expression, whereas cycloheximide and a TLR3-neutralizing antibody had no ef
72 ll death induced by 15d-PGJ2 is prevented by cycloheximide and actinomycin D, suggesting a requiremen
73 application of protein synthesis inhibitors cycloheximide and emetine to acute rat hippocampal slice
76 tive to inhibition of protein synthesis with cycloheximide and extend protein turnover assays to long
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
83 ypersensitivity to the translation inhibitor cycloheximide and yields synthetic "sickness" in cells w
84 nce of primaquine, concanamycin A, monensin, cycloheximide, and an inhibitor of microsomal triglyceri
85 sive to the bitter taste stimuli quinine and cycloheximide, and aversive concentrations of sodium, co
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
90 retreatment with protein synthesis inhibitor cycloheximide antagonized BBR-induced beta-catenin reduc
91 A translation was inhibited by rapamycin and cycloheximide as well as by RNA interference-mediated kn
92 nges in protein half-life were tested with a cycloheximide assay; gene expression was examined by rea
93 Pharmacologic inhibition of translation with cycloheximide attenuated Cited2 down-regulation by TGF-b
94 Actinomycin D blocked transcription, and cycloheximide attenuated synthesis of MTs in the presenc
97 chondrocytes with a JAK-3 inhibitor or with cycloheximide blocked the IL-7-mediated secretion of S10
99 tion inhibition by some antibiotics, such as cycloheximide, both in ribosome run-off assays and in in
102 ne transcription, as it was not abolished by cycloheximide but was abolished by actinomycin D, and in
103 fear to S2 was unaffected by the infusion of cycloheximide but was disrupted by the DNA methyltransfe
106 hology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpressi
109 ed the protein stability of KLF5 as shown by cycloheximide chase assay, indicating that SMURF2 specif
115 2) decrease protein stability estimated from cycloheximide chase assays; and 3) prevent the CaValpha2
123 nce of heat shock, sodium arsenite (NaAsO2), cycloheximide (CHX) and Lipofectamine 2000-mediated tran
124 te of Tat protein degradation as measured by cycloheximide (CHX) chase assay was increased in the pre
128 FP due to inhibition of ribosome activity by cycloheximide (CHX) was quantified with real-time quanti
130 coded DAP5 (eIF4G2/p97) mRNA is resistant to cycloheximide (CHX), a translation inhibitor that severe
131 m either virus was reduced by treatment with cycloheximide (CHX), an inhibitor of protein synthesis.
132 ability following UVB that was alleviated by cycloheximide (CHX), indicating that translation repress
133 nce to tumor necrosis factor (TNF)-alpha and cycloheximide (CHX)-induced apoptosis, and NF-kappaB act
138 dopsis plants with the translation inhibitor cycloheximide, cleavage events accumulate 13 to 14 nucle
139 ere, we investigate the influence of ranging cycloheximide concentrations on ribosome profiles in Sac
140 creased ABCB4 and ABCB19 protein levels when cycloheximide concomitantly inhibited new protein synthe
141 The reduction in TH mRNA was blocked by cycloheximide consistent with a protein-dependent mechan
142 y induces Cebpa mRNA in these cells, even in cycloheximide, consistent with direct gene regulation.
143 f c-Myc by OA or protein synthesis inhibitor cycloheximide contributed to HBC growth inhibition and t
145 ter inhibition of new protein synthesis with cycloheximide, CX50fs disappeared much more rapidly than
146 were injected subcutaneously with saline or cycloheximide (CXM; 1 mg/kg) and returned to their home
148 ical protection of CA1 ischemic neurons with cycloheximide decreased the formation of SGs and restore
149 ntly with TLR ligands and in the presence of cycloheximide, demonstrating that they act independently
154 sms, as inhibition of protein synthesis with cycloheximide did not completely prevent the protective
158 e blockage of de novo protein synthesis with cycloheximide failed to reverse the KSHV-induced disrupt
160 ed with translation inhibitor (anisomycin or cycloheximide), group I mGluRs elicited a sustained decr
163 up-regulation of foxj1a was not inhibited by cycloheximide, identifying foxj1a as a primary response
164 infusion of the protein synthesis inhibitor, cycloheximide, immediately after the S2-S1-shock session
165 hen de novo protein synthesis was blocked by cycloheximide in OLA1-knockdown cells, they continued to
166 Functional hyaluronan cables were induced by cycloheximide in the confirmed absence of protein synthe
167 se of global translation inhibitors, such as cycloheximide, in protein degradation assays may result
168 y of FKBP12, including FK506, rapamycin, and cycloheximide, increase steady-state palmitoylation.
175 amptothecin-, or tumor necrosis factor alpha/cycloheximide-induced apoptosis and caspase-3-8, and cas
177 Bak, downstream targets of Mcl-1, inhibited cycloheximide-induced apoptosis, as did knockdown of Bax
179 both H(2)O(2)-induced necrosis and TNF-alpha/cycloheximide-induced apoptosis; the S1P(2)R agonist had
181 c protein Bcl-X(L) were resistant to LPS and cycloheximide-induced death and that the proapoptotic Bc
188 ons, the commonly used translation inhibitor cycloheximide induces rapid transcriptional upregulation
190 racellular pools was followed by late (24 h) cycloheximide-inhibitable secretion requiring new protei
191 and the general protein synthesis inhibitor cycloheximide inhibited both the LPS and TNF-alpha sensi
192 pping enzyme knockdown, apoptosis induced by cycloheximide inhibition of protein synthesis required B
194 Moreover, qRT-PCR analyses coupled with cycloheximide inhibition studies suggest that the underl
195 ere a direct effect of hepcidin, as shown by cycloheximide insensitivity, and dependent on the presen
197 e to TNF or LPS and a translation inhibitor, cycloheximide, leads to prolonged NF-kappaB activation a
198 f cells with the protein synthesis inhibitor cycloheximide led to an almost instantaneous loss of unm
199 presence of the protein synthesis inhibitor cycloheximide, LPS primarily induces caspase-dependent a
200 is, GLX had a greater effect on quinine than cycloheximide (mean shift of 1.02 vs. 0.27 log10 units).
203 not affected by protein synthesis inhibitor cycloheximide nor protein transport inhibitor monensin,
204 egradation was strongly inhibited by feeding cycloheximide or amino acids to detached leaves, while S
206 e effects were abolished by actinomycin D or cycloheximide or by the AhR antagonists resveratrol and
208 1 and HDAC3, markedly increased stability in cycloheximide or in the presence of co-expressed Cdh1, a
209 ty of influenza A viruses in the presence of cycloheximide or nucleoprotein (NP) small interfering RN
210 poptosis was induced by exposure to TNFalpha/cycloheximide or other apoptotic signaling molecules, th
211 ermore, inhibition of protein synthesis with cycloheximide or overexpression of dominant negative hea
212 Moreover, ectopic expression followed by cycloheximide or pulse-chase treatment demonstrated that
213 eatment with the protein synthesis inhibitor cycloheximide or RNA interference-mediated knockdown of
216 reatment with a protein synthesis inhibitor, cycloheximide, or Smac mimetic, a small molecule mimic o
221 scription and translation, actinomycin D and cycloheximide, partially cancelled this process, suggest
223 ibitor of metalloproteinases 3 (TIMP-3), and cycloheximide pretreatment were used to identify ADAMTS
224 Although inhibiting protein synthesis with cycloheximide prevented H(2)O(2) from elevating Nrf2 pro
226 Because blocking protein synthesis with cycloheximide prevented the buildup of SUMOylated protei
227 n of the cytoplasmic translational inhibitor cycloheximide prevents S deprivation-triggered accumulat
228 that inhibition of protein biosynthesis with cycloheximide prior to 3-AP and 3-AP-Me treatment leads
230 In isolated cardiomyocytes, experiments with cycloheximide, proteasome inhibitor MG-132, and siBVR su
231 rformed with the protein synthesis inhibitor cycloheximide provided evidence that JAZs, MYC2, and gen
232 in the presence of the translation inhibitor cycloheximide, providing evidence that CTCF partitions t
233 her than GLX alone for every stimulus except cycloheximide (ps < .03), suggesting that the GSP nerve
234 nce of translational inhibitors (anisomycin, cycloheximide, rapamycin) or the transcriptional inhibit
235 on, while macrophage-like cells treated with cycloheximide remained viable and showed transient activ
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
241 ment of cells with the translation inhibitor cycloheximide revealed that control of NT1 expression oc
243 ibition of protein synthesis in COS cells by cycloheximide reveals remarkably rapid turnover of expre
244 e inhibition of ubiquitination also caused a cycloheximide-sensitive decrease in a distinct set of SU
245 t macrophage activation with C1q resulted in cycloheximide-sensitive enhanced engulfment, indicating
247 ubiquitination inhibition underwent similar cycloheximide-sensitive increases or decreases upon prot
249 Turnover measurements in the presence of cycloheximide show that, whereas 4E-BP1 is normally a ve
250 JNJ16259685 and protein synthesis inhibitor cycloheximide significantly attenuated or blocked the ac
251 y after inhibition of protein synthesis with cycloheximide, so we searched for interacting proteins t
252 al signaling pathways (UV radiation, TNF and cycloheximide, staurosporine, thapsigargin and tunicamyc
253 induced by tumor necrosis factor alpha plus cycloheximide, suggesting a unique mitochondrial pathway
254 eral hours after translation is stopped with cycloheximide, suggesting that the beta(2) subunit under
255 vity to the translation elongation inhibitor cycloheximide, suggesting that VIG1 may have a nonessent
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
266 imary transcription, even in the presence of cycloheximide to block genome replication and secondary
272 g features accumulated in the fry2-1 mutant, cycloheximide-treated wild type, and upf3 mutant plants,
277 The loss of Synpo protein after Stattic or cycloheximide treatment did not occur when podocytes wer
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
292 d in vivo by the protein synthesis inhibitor cycloheximide, validating TePhe as a translation reporte
294 or omitting translation inhibitors, such as cycloheximide, was noted as it markedly affected ribosom
295 Using the reversible translational inhibitor cycloheximide, we show that this signal memory requires
296 est expression of these genes was blocked by cycloheximide when the EBV lytic cycle was induced by hi
297 treated with the protein synthesis inhibitor cycloheximide, whereas overexpression of WT OTUB1, but n
298 ession of Mcl-1 blocked apoptosis induced by cycloheximide, whereas RNA interference knockdown of Mcl
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