ライフサイエンスコーパス: anisomycin

1 as prevented by protein synthesis inhibitor (anisomycin).

2 nt to peptidyl-transferase inhibitors (e.g., anisomycin).

3 e blocked by the protein synthesis inhibitor anisomycin.

4 the protein synthesis inhibitors emetine and anisomycin.

5 T yet fail to antagonize SERT stimulation by anisomycin.

6 infusion of the protein synthesis inhibitor anisomycin.

7 d mimicked by an activator of these kinases, anisomycin.

8 ased for 48 hr and was blocked reversibly by anisomycin.

9 t sensitive to disruption by intra-accumbens anisomycin.

10 voked in the presence of either rapamycin or anisomycin.

11 othiourea abolished the protective effect of anisomycin.

12 irolimus and the protein synthesis inhibitor anisomycin.

13 and by using another translation inhibitor, anisomycin.

14 c-Jun protein were also found with wtVT1 and anisomycin.

15 ng ultraviolet light, hydrogen peroxide, and anisomycin.

16 induction of apoptosis by trichothecenes and anisomycin.

17 oth 12-O-tetradecanoylphorbol-13-acetate and anisomycin.

18 y another ribotoxic stressor, the antibiotic anisomycin.

19 inhibitors of translation, cycloheximide or anisomycin.

20 f apoptosis) of apoptotic trichothecenes and anisomycin.

21 t shock, and the protein synthesis inhibitor anisomycin.

22 inhibited by the protein synthesis inhibitor anisomycin.

23 ypersensitive to the translational inhibitor anisomycin.

24 eled by the selective activation of p38 with anisomycin.

25 tion that was induced by hyperosmolarity and anisomycin.

26 ed ICR mice were treated with p38 activator, anisomycin (0.1 mg/kg IP), or vehicle (5% DMSO).

27 ation of transport by a low concentration of anisomycin (0.3 microM) was transient, peaked at 30-60 m

28 t lasted >1 week and that was not blocked by anisomycin (1 mug/ml).

29 addition, intrahippocampal administration of anisomycin (100 mug/mul), a potent JNKs activator, mimic

30 JNK activator); and hearts treated with both anisomycin (50 ng/mL) and the tyrosine kinase inhibitor

31 Anisomycin (50 ng/ml) prevented the increase in phosphor

32 ion inhibitors cycloheximide (0.7-70 nM) and anisomycin (7.5-750 nM), in contrast to a reporter beari

33 APK activation; hearts treated with 50 ng/mL anisomycin (a p38 MAPK/JNK activator); and hearts treate

34 ollowed immediately by intra-LA infusions of anisomycin (a protein synthesis inhibitor) or Rp-cAMPS (

35 each training session, either a solution of anisomycin (a protein synthesis inhibitor) or vehicle wa

36 detected with both wild-type VT1 (wtVT1) and anisomycin, a 28S rRNA inhibitor.

37 Here we show that anisomycin, a commonly used protein synthesis inhibitor

38 Here, we report that anisomycin, a potent activator of activating transcripti

39 Results indicate that anisomycin, a potent activator of the stress kinase JNK/

40 In contrast, stimulation by anisomycin, a potent Jun-NH2-terminal kinase (JNK) agoni

41 In contrast, bilateral injections of anisomycin, a protein synthesis inhibitor, into BLA did

42 that, in HL-60 cells, the addition of either anisomycin, a protein synthesis inhibitor, or geranylger

43 sis because it is blocked by the presence of anisomycin, a protein synthesis inhibitor.

44 he number of SN varicosities were blocked by anisomycin, a protein synthesis inhibitor.

45 Anisomycin, a strong activator of JNK in these cells, st

46 Anisomycin activated the p38 pathway in fetal hepatocyte

47 ependent on MKK-7 but not on MKK-4; however, anisomycin-activated JNK required both kinases.

48 JNK activity was only MKK-7 dependent, while anisomycin-activated JNK was both MKK-4 and MKK-7 depend

49 In contrast, anisomycin administered after context memory retrieval d

50 e ability of the protein synthesis inhibitor anisomycin administered following a context-only memory

51 eported that the protein synthesis inhibitor anisomycin administered into the hippocampus after conte

52 Mice received injections of anisomycin after either initial acquisition or retrieval

53 ion of protein synthesis within the mPFCv by anisomycin also blocked immunization when administered a

54 Activation of p38 MAPK by anisomycin also increased glucose transport in heart mus

55 h SB 203580 and the p38 MAP kinase activator anisomycin also revealed that p38 MAP kinase negatively

56 t neuronal survival, we investigated whether anisomycin alters neuronal response to hypoxic stress an

57 tial for the stimulating effect of serum and anisomycin although p38 is not directly responsible for

58 However, application of anisomycin, an activator of Jun amino-terminal kinase, r

59 In contrast, anisomycin, an agonist of the recently described MAP kin

60 ed (activated) when KB cells were exposed to anisomycin, an agonist that activates all SAPKs, includi

61 hat make Haloarcula marismortui resistant to anisomycin, an antibiotic that competes with the amino a

62 ic Ca(2+) were partially inhibited by either anisomycin, an inhibitor of passive Ca(2+) leak from the

63 The remaining LTD was reduced by anisomycin, an inhibitor of protein synthesis, by U0126,

64 Furthermore, both anisomycin, an inhibitor of ribosomal protein synthesis,

65 sion and by treatment with the JNK activator anisomycin and Akt pathway inhibitor, wortmannin.

66 Both anisomycin and arsenite activate the JNK pathway and, in

67 in-resistant strains were cross-resistant to anisomycin and chloramphenicol, suggesting that Tcin tar

68 TR chromatin is increased by the p38 agonist anisomycin and decreased by specific p38 inhibition.

69 ion attenuated by the translation inhibitors anisomycin and emetine.

70 pment of succinct approaches to syntheses of anisomycin and epi-cytoxazone.

71 additional translational inhibitors such as anisomycin and hygromycin B, suggesting that ubiquitin d

72 The increase is blocked by anisomycin and is detected by both quantitative immunobl

73 Dominant-negative (DN)-JNK1 can block both anisomycin and latent IL-3 withdrawal-induced Bcl2 phosp

74 activators, including the phorbol ester TPA, anisomycin and MAPK kinase kinase-1 (MEKK1), phosphoryla

75 imulation of protein synthesis is blocked by anisomycin and not observed in untreated neurons.

76 d as these kinases are activated normally by anisomycin and other physicochemical stress.

77 n contrast, the protein synthesis inhibitors anisomycin and puromycin did not activate transcription

78 ministration of protein synthesis inhibitors anisomycin and rapamycin into the hippocampus, but not i

79 Additional experiments showed that anisomycin and Rp-cAMPS interfered with long-term memory

80 ects of two peptidyl-transferase inhibitors, anisomycin and sparsomycin, on ribosomal frameshifting e

81 The synergy between anisomycin and TbRACK1 RNAi suggests that continued tran

82 between the sensitivity of H. marismortui to anisomycin and the affinity of its large ribosomal subun

83 LK7 small interfering RNA completely blocked anisomycin and UV induced but had no effect on interleuk

84 following exposure to stress stimuli such as anisomycin and UV irradiation.

85 of p70/85 S6 kinase (S6K), we observed that anisomycin and UV light stimulated S6K activity, but tha

86 of the stress-activated MAPKs downstream of anisomycin and UV stimulation and that DHP-2 can be used

87 Additionally, the compound blocked anisomycin and UV-induced apoptosis in COS-7 cells.

88 transmitters may mediate amnesia produced by anisomycin and, further, raise important questions about

89 ersensitivity to the translational inhibitor anisomycin and, in specific cases, the ability to enhanc

90 nts it being skipped even in the presence of anisomycin and/or epsilon553del7, indicating that inhere

91 sensitizes melanoma cells to UV-, ribotoxic (anisomycin) and radiomimetic chemicals-induced programme

92 oapoptotic stimuli, including staurosporine, anisomycin, and etoposide.

93 mitosis and apoptosis induced by UV light or anisomycin, and in human psoriatic skin and squamous cel

94 PK and JNK following stimulation with serum, anisomycin, and osmotic stress.

95 sensitive to the protein synthesis inhibitor anisomycin, and relied on the same signaling pathways as

96 nhibited by diphtheria toxin, cycloheximide, anisomycin, and ricin A chain.

97 ated JNK normally in response to heat shock, anisomycin, and ultraviolet irradiation.

98 , BCYE, and selective BCYE with polymyxin B, anisomycin, and vancomycin) and on axenic and monoxenic

99 bilateral intraventricular microinjection of anisomycin (Ani) impairs consolidation of long-term memo

100 ting synapses and motor maps by infusions of anisomycin (ANI) into anatomically reorganized motor, bu

101 n that protein synthesis inhibitors, such as anisomycin (ANI), administered during this consolidation

102 ined with the protein translation inhibitors anisomycin (ANS) and puromycin (PUR).

103 Anisomycin application to the MeA prevented the formatio

104 with one reminder pulse of 5-HT, followed by anisomycin, at 48 hr after the original training.

105 increases and decreases in NE release after anisomycin, attenuated anisomycin-induced amnesia.

106 8 immunoreactivity being upregulated and (2) anisomycin attenuates the increase in phosphorylated p38

107 ol, a third group of hearts was treated with anisomycin before global ischemia, and in these, JNK act

108 Intraamygdala injections of anisomycin before inhibitory avoidance training impaired

109 The aromatic ring of anisomycin binds to the active-site hydrophobic crevice,

110 Anisomycin blocked MF-LTP induction in a dose-dependent

111 otein synthesis inhibitors cycloheximide and anisomycin both in vivo and in vitro, we found that the

112 inhibitors and induced by the p38 activator anisomycin but not by the PKA activator 6-benzoyl-cAMP.

113 ference with Fas/FasL interactions inhibited anisomycin but not UV- or gamma irradiation-induced apop

114 nvironmental stresses (osmotic shock, UV and anisomycin), but not the p38 activation by the cytokine

115 orbol ester phorbol 12-myristate 13-acetate, anisomycin, calyculin A, and insulin.

116 rs of the peptidyltransferase reaction (e.g. anisomycin) can trigger a ribotoxic stress response that

117 The stress-inducing agent, anisomycin, causes activation of JNK, raf, MEK, and ERK

118 Structures of anisomycin, chloramphenicol, sparsomycin, blasticidin S,

119 onal X-ray crystallographic structure of the anisomycin-containing mutant ribosome shows that high co

120 tutive JNK activity with the JNK stimulator, anisomycin, converts the protease mRNA levels from those

121 However, translation inhibitors, such as anisomycin, cycloheximide, emetine, harringtonine, and p

122 Anisomycin, cycloheximide, emetine, puromycin, and purom

123 in the presence of translational inhibitors (anisomycin, cycloheximide, rapamycin) or the transcripti

124 rradiation, osmotic shock, interleukin-1, or anisomycin did not affect this process.

125 p38 MAPK pathway by treatment of cells with anisomycin did not stimulate glucose transport.

126 hesis since translational inhibitors such as anisomycin disrupt subsequent memory when administered i

127 Additional experiments demonstrated that anisomycin does not block the expression of conditioned

128 Here we show that serum and anisomycin enhance the interaction between TSC2 and 14-3

129 In the presence of cycloheximide or anisomycin, ephrin-A2, slit-3, and semaphorin3A still in

130 Here, we determined that UV light, anisomycin, etoposide, and hypoxic stress rapidly induce

131 nhibition of general translation by low-dose anisomycin failed to block hippocampal-dependent memory

132 bitor that competes with trichothecenes (and anisomycin) for ribosome binding, also inhibits the acti

133 Activation of JNK1 by anisomycin further increased Tau phosphorylation, and SP

134 istration of the protein synthesis inhibitor anisomycin generally leads to impairments in memory test

135 or caused by the protein synthesis inhibitor anisomycin given after retrieval are temporary and are t

136 T transport by multiple p38 MAPK activators (anisomycin, H(2)O(2), and UV radiation), in parallel wit

137 presence of the protein synthesis inhibitor anisomycin had no effect on the induction but prevented

138 on of fear conditioning, whereas infusion of anisomycin had no effect.

139 Anisomycin, however, eliminated long-term memory lasting

140 -Jun N-terminal and p38 kinases in vivo with anisomycin, however, was insufficient to activate glycog

141 Post-trial infusions of anisomycin immediately after the first several training

142 Rats receiving 150 mg/kg anisomycin immediately following a 5-min reexposure to t

143 ever, when injected after fear conditioning, anisomycin impaired consolidation of both contextual and

144 raining with the protein synthesis inhibitor anisomycin impaired memory persistence.

145 us findings, intra-hippocampus injections of anisomycin impaired memory tested 48 hr after training y

146 In contrast, intra-amygdala injections of anisomycin impaired memory tested at 0.5, 4, and 48 hr a

147 e, is also transiently (1-2 hr) activated by anisomycin in both normal and cancer cells, checkpoint d

148 or anisomycin in macrophages and TNFalpha or anisomycin in fibroblasts.

149 on of Ser63 and Ser73, in response to LPS or anisomycin in macrophages and TNFalpha or anisomycin in

150 Strikingly, engagement of D1/D5 coupled with anisomycin in primed animals reversed a chronic pain sta

151 We then compared the impact of anisomycin in two conditions: when memory retrieval occu

152 port that intrahippocampal microinfusions of anisomycin in urethane-anesthetized rats at dosages prev

153 f protein synthesis inhibitors (rapamycin or anisomycin) in the amygdala 10 min before memory retriev

154 The same treatment with anisomycin, in the absence of memory reactivation, left

155 that the activation of GLUT1 in response to anisomycin includes two components: a delayed component

156 ted p38 MAPK and activation of p38 MAPK with anisomycin increased the ratio of cholesterol esters ove

157 293 cells expressing dominant-negative Akt, anisomycin-increased JNK activity was not suppressed by

158 and are blocked by the translation inhibitor anisomycin, indicating the need for synthesis of new pro

159 timulation with either fetal bovine serum or anisomycin induced an even stronger activation (eightfol

160 ivation of JNK by subtoxic concentrations of anisomycin induced selective apoptotic killing of Mtb-in

161 This anisomycin-induced amnesia was abolished after cotreatme

162 s in NE release after anisomycin, attenuated anisomycin-induced amnesia.

163 important role of ATF2-FoxP3 pathway in the anisomycin-induced apoptosis of breast cancer cells.

164 MKP-1-deficient MEFs were also sensitive to anisomycin-induced apoptosis.

165 apoptosis but is required for H(2)O(2)- and anisomycin-induced apoptosis.

166 Additionally, both EGF- and anisomycin-induced FGF-BP mRNA was abrogated by inhibiti

167 ntitative single-cell analysis revealed that anisomycin-induced JNK activity exhibited ultrasensitivi

168 Anisomycin-induced NF-kappaB DNA binding activity was in

169 The anisomycin-induced phosphorylation of Ser359 was unaffec

170 e drug, suggesting a ribosomal origin of the anisomycin-induced signaling to SAPK/JNK1.

171 active oxygen species (ROS) generated during anisomycin-induced stress in HeLa cells.

172 (DA), and serotonin, measured at the site of anisomycin infusions, increased quickly by approximately

173 confirmed that intrahippocampal infusions of anisomycin inhibited protein synthesis locally and that

174 Anisomycin inhibited X-box-binding protein 1 (XBP1) mRNA

175 These results suggest that anisomycin injections after retrieval do not retroactive

176 When anisomycin injections followed acquisition, freezing was

177 When anisomycin injections followed normal retrieval of conte

178 ct temporal properties for amnesia following anisomycin injections into the hippocampus or amygdala m

179 For instance, anisomycin interferes with protein synthesis by inhibiti

180 hibiting protein synthesis by microinjecting anisomycin into mPFC blocked the therapeutic effect of e

181 Infusion of the protein synthesis inhibitor anisomycin into the LBA shortly after training prevents

182 ol prior to context preexposure or injecting anisomycin into the VH after preexposure significantly i

183 Injecting anisomycin into the VH prior to contextual fear conditio

184 ppocampus and that stereotactic injection of anisomycin into this region impairs memory consolidation

185 reated with the protein synthesis inhibitor, anisomycin, into either the CA1 or BLA were unable to re

186 , similar to the effects on memory seen with anisomycin, intraamygdala injections of a high dose of N

187 for the drug indicates that its response to anisomycin is determined primarily by the binding of the

188 A is ERK-dependent, whereas that elicited by anisomycin is p38 MAPK-dependent.

189 tration of the protein translation inhibitor anisomycin it is reflected by changes in the peripheral

190 a), tumor necrosis factor alpha(TNFalpha, or anisomycin, kinase function was determined by in vitro k

191 ransduction pathways, whereas the effects of anisomycin largely involved p38 and phosphatidyl inosito

192 ddress the issue of whether postreactivation anisomycin leads to an inability to retrieve the consoli

193 eatment with the protein synthesis inhibitor anisomycin, LTS was disrupted.

194 Since anisomycin may alter MAP kinase activity and affect neur

195 nd shown to block p53-mediated apoptosis and anisomycin-mediated WOX1 phosphorylation but could not i

196 In separate hearts, anisomycin mimicked the anti-infarct effect of PC, and t

197 application of the protein synthesis blocker anisomycin (n = 11).

198 Neither anisomycin nor actinomycin D altered p73-mediated transc

199 le (VEH), of the protein synthesis inhibitor anisomycin, of the D1/D5 dopaminergic antagonist SCH2339

200 ds were applied to prove that the effects of anisomycin on programmed -1 frameshifting are statistica

201 The inhibitory effect of anisomycin on protein synthesis was determined by measur

202 However, anisomycin only minimally effected PB induction, ascerta

203 d if protein synthesis was blocked by either anisomycin or cycloheximide after the representation of

204 inomycin D) or protein synthesis inhibitors (anisomycin or cycloheximide) attenuated the ability of N

205 were pretreated with translation inhibitor (anisomycin or cycloheximide), group I mGluRs elicited a

206 that were induced to undergo apoptosis using anisomycin or etoposide.

207 kinase kinase MEKK1, and (ii) treatment with anisomycin or heat shock.

208 NFalpha, UV irradiation, and PKC, but not by anisomycin or MEKK1.

209 he activation was similar to treatments with anisomycin or okadaic acid and correlated with the hypox

210 is in other cell types, e.g. incubation with anisomycin or overexpression constitutively active MEKK-

211 orylation can be modulated by treatment with anisomycin or phorbol 12-myristate 13-acetate (PMA/12-O-

212 the responses to 4 h exposure to 300 microM anisomycin or puromycin were refractory to SB203580.

213 ina, but these increases were not blocked by anisomycin or rapamycin.

214 lication of the protein synthesis inhibitors anisomycin or rapamycin.

215 or ultraviolet radiation, or co-culture with anisomycin or staurosporine) but not proliferative (CD3

216 cted JNK activity was strongly stimulated by anisomycin or tumor necrosis factor-alpha, and 10 nM IGF

217 By stimulating cells with anisomycin or UV light, JNK1 became activated, and WOX1

218 ther peptide growth factors, phorbol esters, anisomycin or UV.

219 ibit the >50-fold JNK activation effected by anisomycin or UV.

220 the previous training under the influence of anisomycin or vehicle resulted in the acquisition of con

221 cells that were treated with actinomycin D, anisomycin or with the radiomimetic drug neocarzinostati

222 the translation inhibitors cycloheximide and anisomycin, or local presynaptic injection of mRNA cap a

223 protein synthesis inhibitors cycloheximide, anisomycin, or puromycin as well as prolonged exposure t

224 tiple apoptotic stimuli (e.g., Fas ligation, anisomycin, or ultraviolet irradiation), an effect that

225 hesis inhibitor and protein kinase activator anisomycin, or with the combination of cycloheximide and

226 ardiac myocytes, protected cells from either anisomycin- or MEKK-1COOH-induced apoptosis.

227 pid activation of NF-kappaB DNA binding with anisomycin, peaking at 30 minutes.

228 o blocked signaling induced by carbachol and anisomycin, pharmacological MAP kinase agonists.

229 nfusions of the protein synthesis inhibitor, anisomycin, prior to defeat training, however, failed to

230 Doses of 0.04, 10, or 40 nmol of anisomycin produced 21, 82, or 83% inhibition of [(35)S]

231 K1, we found that UV, gamma irradiation, and anisomycin prolonged JNK activation in parallel with Fas

232 r of p38 MAPK and c-Jun NH2-terminal kinase, anisomycin, protected cardiac myocytes from ischemic inj

233 Anisomycin (protein synthesis inhibitor) or KT5720 (prot

234 uced by protein synthesis inhibitors such as anisomycin provides major support for the prevalent view

235 vidence that in order to activate SAPK/JNK1, anisomycin requires ribosomes that are translationally a

236 vation of JNK and SEK1 by palytoxin, but not anisomycin, requires extracellular sodium.

237 the Tetrahymena thermophila LSU rRNA confers anisomycin resistance (an-r) as well as extremely slow g

238 ffinity for aminoacyl-tRNA and the extent of anisomycin resistance and a decreased peptidyltransferas

239 isomycin, suggesting a competitive model for anisomycin resistance.

240 nd 3.3-fold in hearts pretreated with PIA or anisomycin, respectively.

241 ation of the JNK/SAPK signaling pathway with anisomycin resulted in enhanced phosphorylation of eIF4E

242 , and activation of p38 and JNK signaling by anisomycin resulted in increased cell death independent

243 Exposure to anisomycin resulted in rapid activation of p38(MAPK).

244 As in the case of anisomycin, ribosomes that were active at the time of ex

245 lective inhibitor sp600125 without affecting anisomycin's ability to effectively inhibit protein synt

246 s in a growth defect phenotype and increased anisomycin sensitivity.

247 Saturation kinetic analyses of anisomycin-SERT activity reveal a selective reduction in

248 eturn to a labile state in which infusion of anisomycin shortly after memory reactivation produces am

249 and of nonsense-mediated mRNA decay (NMD) by anisomycin shows that even wild-type CHRNE produces an e

250 Because anisomycin specifically inhibits peptidyl transfer, poss

251 Our data show that anisomycin stimulates phosphorylation of Ser(1210) of TS

252 K phosphorylation, as well as suppression of anisomycin stimulation by p38 MAPK siRNA treatments.

253 rs (fostriecin and calyculin A) to attenuate anisomycin stimulation of 5-HT transport suggests that p

254 rbol myristate acid (PMA), H(2)O(2), UV, and anisomycin stimulation.

255 o significant impact on ROS generation under anisomycin stress.

256 the A site-specific translational inhibitor anisomycin, suggesting a competitive model for anisomyci

257 etics after induction of ribotoxic stress by anisomycin, suggesting relatively rapid signal propagati

258 ancement was resistant to rapamycin, but not anisomycin, suggesting that altered translation control

259 This rescuing effect was blocked by anisomycin, suggesting that WM-tagged synapses were not

260 protein synthesis inhibitors (cycloheximide, anisomycin) suggests a mechanism of gene regulation that

261 Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many

262 The potency of anisomycin to stimulate transport acutely (30 min of exp

263 On the other hand, incubation with anisomycin, to prevent the upregulation of TrkB.T, prote

264 n the basis of live-cell studies, that 75 nM anisomycin transiently (1 hr) activates p38 which, in tu

265 nitric oxide (NO) synthesis were enhanced in anisomycin-treated mice.

266 rmined by comparing [(35)S] incorporation of anisomycin-treated samples with vehicle controls.

267 However, while anisomycin treatment of cells leads to M3/6 protein degr

268 gen peroxide, UVC irradiation, sorbitol, and anisomycin treatment of gadd45(+/+) and gadd45(-/-) fibr

269 Anisomycin treatment of NIH 3T3 cells increased phosphor

270 nd that JNK activation by UV irradiation and anisomycin treatment precedes the induction of gadd45 mR

271 hosphorylation was observed 15 minutes after anisomycin treatment which subsided by 30 minutes.

272 During anisomycin treatment, the phosphorylation of HMGN1 prece

273 ion of p50 and p65 in nuclear extracts after anisomycin treatment.

274 Anisomycin treatments that stimulate SERT activity do no

275 y, the protein synthesis inhibitors Stx1 and anisomycin triggered limited apoptosis and prolonged JNK

276 li and activators, including EGF, TNF-alpha, anisomycin, UV irradiation, MEKK1, and small GTP binding

277 ecanoylphorbol-13-acetate, fetal calf serum, anisomycin, UV irradiation, tumor necrosis factor-alpha,

278 rious agonists including PMA plus ionomycin, anisomycin, UV-C, gamma radiation, TNF-alpha, and sodium

279 osphorylation of IRS-1 serine 307 induced by anisomycin was abolished, leading to a sensitization of

280 ore, postischemic cardioprotective effect of anisomycin was absent in mice with targeted ablation of

281 g a 30-min reexposure to the context or when anisomycin was administered 25 min after a 5-min reexpos

282 The protein synthesis inhibitor anisomycin was administered at different doses (0.04, 10

283 This effect was not seen when anisomycin was administered following a 30-min reexposur

284 A low dose of anisomycin was also remarkably effective in treating est

285 on during ischemia in hearts pretreated with anisomycin was blocked by genistein.

286 on of both p38(MAPK) and GLUT1 by 0.3 microM anisomycin was cancelled by puromycin.

287 by ultraviolet light, hydrogen peroxide, and anisomycin was completely normal in T cells lacking Lck.

288 In the present experiments, anisomycin was infused into either the hippocampus or th

289 Sensitivity to intrahippocampal anisomycin was observed only in the protocol involving n

290 This effect of anisomycin was partly inhibited in the presence of the p

291 ute activation of MAPKAP kinase-2 induced by anisomycin was unaffected by rapamycin.

292 The effect of anisomycin was verified using a single dose of the prote

293 revented when a protein synthesis inhibitor, anisomycin, was administered to the MEA.

294 teady-state responses of JNK to sorbitol and anisomycin were found to be highly ultrasensitive in HeL

295 38-activating stresses, such as H(2)O(2) and anisomycin, were able to activate TORC1.

296 esults show that intra-amygdala infusions of anisomycin, whether given after the initial devaluation

297 Treatment of cells with anisomycin, which activates MK2, also results in phospho

298 hypersensitive to the translation inhibitor anisomycin, which affects the peptidyl transferase react

299 Cycloheximide and anisomycin, which inhibit only eukaryotic protein synthe

300 F2(50-100) to apoptosis after treatment with anisomycin, which is used as a model drug.

301 he RQT mutants correlate with sensitivity to anisomycin, which stalls ribosome at the rotated form.