ライフサイエンスコーパス: anisomycin

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

2 as prevented by protein synthesis inhibitor (anisomycin).

3 tion that was induced by hyperosmolarity and anisomycin.

4 irolimus and the protein synthesis inhibitor anisomycin.

5 e blocked by the protein synthesis inhibitor anisomycin.

6 the protein synthesis inhibitors emetine and anisomycin.

7 T yet fail to antagonize SERT stimulation by anisomycin.

8 infusion of the protein synthesis inhibitor anisomycin.

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

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

11 t sensitive to disruption by intra-accumbens anisomycin.

12 othiourea abolished the protective effect of 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 voked in the presence of either rapamycin or anisomycin.

22 t shock, and the protein synthesis inhibitor anisomycin.

23 inhibited by the protein synthesis inhibitor anisomycin.

24 ypersensitive to the translational inhibitor anisomycin.

25 eled by the selective activation of p38 with anisomycin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 Anisomycin activated the p38 pathway in fetal hepatocyte

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

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

47 In contrast, anisomycin administered after context memory retrieval d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 ion attenuated by the translation inhibitors anisomycin and emetine.

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

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

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

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

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

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

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

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

76 blocked by the protein synthesis inhibitors anisomycin and rapamycin and by the inhibitor of gene ex

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 In addition, the EMs cinobufagin, anisomycin, and narciclasine induced more lethality in h

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 Anisomycin (Aniso) increased p38 MAPK phosphorylation an

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

104 Anisomycin application to the MeA prevented the formatio

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

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

107 8 immunoreactivity being upregulated and (2) anisomycin attenuates the increase in phosphorylated p38

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

109 Intraamygdala injections of anisomycin before inhibitory avoidance training impaired

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

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

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

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

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

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

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

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

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

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

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

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

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

123 Anisomycin, cycloheximide, emetine, puromycin, and purom

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

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

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

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

128 infusion of the protein synthesis inhibitor anisomycin disrupts both the updated information and the

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

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

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

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

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

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

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

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

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

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

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

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

141 Anisomycin, however, eliminated long-term memory lasting

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

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

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

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

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

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

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

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

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

151 Injection of anisomycin in M1 had a marked effect on the performance

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

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

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

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

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

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

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

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

160 293 cells expressing dominant-negative Akt, anisomycin-increased JNK activity was not suppressed by

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

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

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

164 In contrast, JNK activator (anisomycin)-induced autophagy was blocked by Beclin1 kno

165 This anisomycin-induced amnesia was abolished after cotreatme

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

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

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

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

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

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

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

173 The anisomycin-induced phosphorylation of Ser359 was unaffec

174 vCA1-BA synapses, which was prevented under anisomycin-induced retrograde amnesia.

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

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

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

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

179 In contrast, the anisomycin injection did not have a significant effect o

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

181 When anisomycin injections followed acquisition, freezing was

182 When anisomycin injections followed normal retrieval of conte

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

184 For instance, anisomycin interferes with protein synthesis by inhibiti

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

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

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

188 Injecting anisomycin into the VH prior to contextual fear conditio

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

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

191 injected an inhibitor of protein synthesis, anisomycin, into M1 to disrupt information storage in th

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

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

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

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

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

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

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

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

200 Since anisomycin may alter MAP kinase activity and affect neur

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

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

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

204 Neither anisomycin nor actinomycin D altered p73-mediated transc

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

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

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

208 However, anisomycin only minimally effected PB induction, ascerta

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

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

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

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

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

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

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

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

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

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

219 lication of the protein synthesis inhibitors anisomycin or rapamycin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 Anisomycin (protein synthesis inhibitor) or KT5720 (prot

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

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

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

241 isomycin, suggesting a competitive model for anisomycin resistance.

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

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

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

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

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

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

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

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

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

251 Because anisomycin specifically inhibits peptidyl transfer, poss

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

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

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

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

256 o significant impact on ROS generation under anisomycin stress.

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

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

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

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

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

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

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

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

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

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

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

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

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

270 Anisomycin treatment of human SMA fibroblasts and sciati

271 Anisomycin treatment of NIH 3T3 cells increased phosphor

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

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

274 During anisomycin treatment, the phosphorylation of HMGN1 prece

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

276 Anisomycin treatments that stimulate SERT activity do no

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

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

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

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

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

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

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

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

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

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

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

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

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

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

294 38-activating stresses, such as H(2)O(2) and anisomycin, were able to activate TORC1.

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

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

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

298 Cycloheximide and anisomycin, which inhibit only eukaryotic protein synthe

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

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