ライフサイエンスコーパス: AICAR

1 AICAR (50 mg/kg, intraperitoneally) was given 6 hours pr

2 AICAR also heavily promoted EGFR ubiquitination in cell-

3 AICAR also reduced NF-kappaB translocation and CD14 expr

4 AICAR and 17-AAG, especially when combined, also show ef

5 AICAR and metformin, both of which are AMPK agonists cur

6 AICAR attenuates EAU by preventing generation of Ag-spec

7 AICAR did not affect the initiation of the ER stress res

8 AICAR did significantly inhibit BMDC maturation by reduc

9 AICAR increased GLUT4-EGFP translocation to both sarcole

10 AICAR induces p53-mediated apoptosis in primary mouse em

11 AICAR inhibited Rb cell growth, induced apoptosis and S-

12 AICAR inhibited tumor necrosis factor (TNF)-alpha- or in

13 AICAR reduced hepatic energy charge by approximately 20%

14 AICAR reduces systemic LPS susceptibility and attenuates

15 AICAR reduction of SOGA was blocked by adiponectin; howe

16 AICAR significantly increased phosphorylation of extrace

17 AICAR stimulation leads to methylation and dephosphoryla

18 AICAR thus prevents Ca(2+)-dependent increases in the am

19 AICAR treatment also induced a transition from epithelio

20 AICAR treatment induced superoxide production and was li

21 AICAR treatment significantly reduced clinical and histo

22 AICAR treatment significantly reduced EIU clinical sever

23 AICAR, an AMPK activator, led to a strong reduction of m

24 AICAR, metformin, or transduction of constitutively acti

25 AICAR-activated AMPK inhibited mTORC1 both directly by p

26 AICAR-induced depletion of EGFR protein can be abrogated

27 AICAR-induced meiotic resumption and AMPK activation wer

28 AICAR-induced stellation correlated with F-actin disasse

29 AICAR-stimulated AS160 phosphorylation was fully inhibit

30 Strains lacking PurH accumulate AICAR and have a defect in the synthesis of the 4-amino-

31 In contrast, the AMPK activator AICAR decreased IL-6-EGFP vesicles, an effect that was i

32 MP-activated protein kinase (AMPK) activator AICAR all increased AS160 phosphorylation in mouse skele

33 MP-activated protein kinase (AMPK) activator AICAR increased TBC1D1 PAS phosphorylation.

34 The AMP kinase (AMPK)-activator AICAR (5-aminoimidazole-4-carboxamide-1-beta-D-ribofuran

35 jected to contractions or the AMPK-activator AICAR.

36 Coincubation with the AMPK activators AICAR and alpha-lipoic acid substantially prevented all

37 In addition, AICAR treatment was associated with inhibition of the ma

38 tions, 1 min rest between sets) or 1 h after AICAR injection (1 mg (g body weight)(-1) subcutaneously

39 identified the energy stress-inducing agent AICAR, the protein folding inhibitor 17-AAG, and the aut

40 ested whether the orally active AMPK agonist AICAR might be sufficient to overcome the exercise requi

41 Treatment with the AMPK agonist AICAR or the antioxidant agent acetyl-l-carnitine (ALCAR

42 The AMPK-agonist AICAR, and activated AMPK adenovirus, inhibited mTOR sig

43 or 4 weeks with an established AMPK agonist, AICAR (5-aminoimidazole-4-carboxamide-1-beta-d-ribofuran

44 tment with the AMP-activated kinase agonist, AICAR, increases V(max) for net 3-O-methylglucose uptake

45 MPK activation by two indirect AMPK agonists AICAR and metformin (now in over 50 clinical trials on c

46 In agreement, AICAR-induced activation of AMPK was abolished by preinc

47 n G6P-insensitive GS knock-in mice, although AICAR-stimulated AMPK activation, glucose transport, and

48 Together, our results suggest that although AICAR and metformin are potent AMPK-independent antiprol

49 Two hours of the AMP analogue AICAR (1.0 g kg(-1)) or systemic hypoxia (6% O(2)) incre

50 onvergence linking insulin, contraction, and AICAR signaling.

51 ochemical analysis revealed that glucose and AICAR had opposing influences on the activation of the T

52 mpound C reversed the effects of hypoxia and AICAR on type I cell and carotid body activation.

53 ial for AS160 phosphorylation by insulin and AICAR, respectively, neither kinase is indispensable for

54 itoneally administered glucose, insulin, and AICAR.

55 for normal 5-h fasting glucose kinetics and AICAR-mediated inhibition of glucose production.

56 various stimulations including metformin and AICAR (5-amino-1-beta-D-ribofuranosyl-imidazole-4-carbox

57 ion, which can be induced with metformin and AICAR inhibited proliferation, TGF-beta expression, and

58 Of note, AMPK activators metformin and AICAR significantly attenuated PMA-induced monocyte-to-m

59 reasing STAT3 phosphorylation, metformin and AICAR through increased AMPK activation caused inhibitio

60 ric AMPK activator, as well as metformin and AICAR, was sufficient to reverse their mesenchymal pheno

61 macologic (nicotine, ONOO(-), metformin, and AICAR) or genetic (overexpression of constitutively acti

62 Although both PTX and AICAR stabilized p53, only AICAR activated Chk2 phosphor

63 d AMPK as a potential therapeutic target and AICAR and metformin as potential therapeutic agents for

64 eeding during the first 2 h of the test, and AICAR alone increased food intake only during the first

65 anide p-trifluoromethoxyphenylhydrazone, and AICAR also increase AMP-dependent kinase phosphorylation

66 y to the glucose-lowering effects of TZD and AICAR.

67 st and human cells for both AICAr uptake and AICAR accumulation.

68 hat blocks cellular glucose utilization, and AICAR which activates AMPK, both blocked GLP-1-induced r

69 -4-carboxamide ribonucleotide, also known as AICAR) brings about any metabolic changes remain unexpla

70 In purine biosynthesis, AICAR is the substrate of the bifunctional protein phosp

71 horylation, indicating that it did not block AICAR action by preventing its metabolism to the AMP ana

72 The p38 MAPK inhibitor SB203580 blocked AICAR-induced increase in VEGF mRNA and protein levels,

73 ent of cells with dipyridamole, which blocks AICAR cellular uptake abolished these effects.

74 Both AICAR and metformin reduced F-actin and significantly re

75 ykinase (Pepck) to an extent similar to both AICAR and constitutively active AMPK.

76 a drug that specifically activates AMPK, but AICAR treatment failed to improve muscle regeneration in

77 rget genes, including TSC2, was activated by AICAR but not by PTX.

78 AMPK activation by AICAR or metformin inhibits HSC proliferation via suppre

79 aB (p50 and p65), whereas AMPK activation by AICAR or overexpression of constitutively active AMPK ha

80 Inhibition of FBP activity by AICAR occurs at physiologically relevant concentrations

81 lso resulted in the overactivation of Akt by AICAR treatment; however, preventing Akt overactivation

82 ectively abolished AMPK activation caused by AICAR, did not reverse the anti-inflammatory effect of A

83 ocytes and protein leakage were decreased by AICAR treatment.

84 However, the increase in GU elicited by AICAR was significantly lower than that induced by eithe

85 ion activator complex, which was enhanced by AICAR treatment.

86 ogates the inhibition of Pepck expression by AICAR, but also importantly affects glucose production b

87 ack of growth is due to inhibition of FBP by AICAR.

88 l encode proteins resistant to inhibition by AICAR and the allosteric regulator AMP.

89 Inhibition of RPE cell phagocytosis by AICAR was fully reversed by blockade of AICAR translocat

90 The protection by AICAR is independent of AMP-activated protein kinase (AM

91 cle regeneration in obese mice is rescued by AICAR, a drug that specifically activates AMPK, but AICA

92 ivation of a p53 transcriptional response by AICAR was due to an activation of Chk2 that was not elic

93 sine kinase, folate transport stimulation by AICAR was absent.

94 other inositol phosphates were unaffected by AICAR.

95 eta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR) or adenovirus expressing constitutively active su

96 eta-d-ribofuranosyl-imidazole-4-carboxamide (AICAR).

97 ctively support the pharmacological compound AICAR as a novel inhibitor of EGFR protein abundance and

98 we found that the AMPK-activating compound, AICAR, induced NO release from L6 myotubes, and that AIC

99 At high concentration, AICAR is toxic for yeast and mammalian cells, but the mo

100 In contrast, AICAR-stimulated glucose uptake was ~1.5-fold greater fo

101 ation, or re-internalization, but diminished AICAR-induced translocation.

102 Long-term administration of low-dose AICAR significantly suppressed adipose inflammation in e

103 creased independently of hepatic AMPK during AICAR administration.

104 cose disposal was compared before and during AICAR with the euglycemic-hyperinsulinemic clamp.

105 gainst a more precipitous fall in ATP during AICAR administration.

106 Exposure of HUVECs to either AICAR or metformin caused AMPK-dependent upregulation of

107 Maximal insulin, together with either AICAR or contraction, increased AS160 phosphorylation in

108 Finally, AICAR markedly increased UCP-2 expression and reduced bo

109 The molecular bases for AICAR toxicity at the cellular level are poorly understo

110 AMPK was not required for AICAR-mediated suppression of glucose production and inc

111 used transcriptional profiling to search for AICAR-regulated genes in hepatocyte cell lines.

112 found MTX markedly reduced the threshold for AICAR-induced AMPK activation and potentiated glucose up

113 precursor of the active monophosphate form (AICAR), a small molecule with potent anti-proliferative

114 o-LC/MS/MS confirmed that eNOS purified from AICAR-treated ECs was phosphorylated at both Ser633 and

115 Furthermore, AICAR inhibited autophosphorylation of the ER stress sen

116 Furthermore, AICAR inhibited macrophage ER stress responses triggered

117 Furthermore, AICAR or overexpression of AMPK inhibited the high-gluco

118 Furthermore, AICAR pretreatment blocked PAR-1-induced increase in the

119 denine phosphoribosyl transferase under high AICAR conditions.

120 Recent studies identified AICAR (5-aminoimidazole-4-carboxamide-1-beta-D-ribofuran

121 Most importantly, AICAR treatment in mice significantly inhibited the grow

122 In AICAR-treated mdx mice, the exaggerated sensitivity of m

123 ereas overexpression of Ad-DN-AMPK inhibited AICAR-induced phosphorylation of p38 kinase at Thr180/Ty

124 e that is phosphorylated in vivo by insulin, AICAR, and contraction.

125 chronically treating the cells with insulin, AICAR specifically induced AMPK(Ser-485), but not AMPK(T

126 charide (1.5 mg/kg), Temsirolimus (5 mg/kg), AICAR (100 mg/kg).

127 pectrum of EGFR-activated cancer cell lines, AICAR was more effective than rapamycin at blocking tumo

128 AMPK activation by the AMP mimetic AICAR (5-aminoimidazole-4-carboxamide riboside) has been

129 cells, activation of AMPK by the AMP mimetic AICAR or by antimycin A, which blocks aerobic respiratio

130 sor digitorum longus (EDL) muscles with 2 mM AICAR for 20 min or electrical stimulation (10 Hz, 13 V)

131 amide-1-beta-D-ribofuranoside monophosphate (AICAR) is a natural metabolite with potent anti-prolifer

132 Moreover, AICAR-triggered dephosphorylation of the Na(+),K(+)-ATPa

133 re AKI than WT animals and died, and neither AICAR nor ALCAR treatment prevented death in Sirt3-/- AK

134 Regardless of the ability of AICAR to activate AMPK, the inhibitory effects of AICAR

135 esults show that the in vivo accumulation of AICAR decreased total CoA pools and, further, that AICAR

136 bacteria, yeast, and humans, accumulation of AICAR has been shown to affect an array of cellular proc

137 ned whether the antiproliferative actions of AICAR and metformin are AMPK independent.

138 active AMPK (Ad-CA-AMPK) or the addition of AICAR reduced both O(2).(-) and prostacyclin synthase ni

139 The administration of AICAR, an AMPK activator, or adenoviral overexpression o

140 s by AICAR was fully reversed by blockade of AICAR translocation into cells by dipyridamole or inhibi

141 diets, suggesting that the full capacity of AICAR to antagonize obesity-induced inflammation and ins

142 ubericidin, which inhibits the conversion of AICAR to the direct activator of AMPK, ZMP, did not reve

143 iodotubericidin to inhibit the conversion of AICAR to ZMP (the direct activator of AMPK) reversed mos

144 phate (ZMP), the monophosphate derivative of AICAR, within cells as established by liquid chromatogra

145 Compound C prevented the effect of AICAR on myocyte function.

146 The effect of AICAR on Na(+),K(+)-ATPase in L6 myotubes was attenuated

147 by siRNA abolished the inhibitory effect of AICAR on oxidant-induced phosphorylation of both caveoli

148 c-Abl and abolished the inhibitory effect of AICAR on the caveolin-1 phosphorylation.

149 osure and abolished the inhibitory effect of AICAR on the caveolin-1 phosphorylation.

150 esis rescued the growth inhibitory effect of AICAR, whereas inhibition of these lipogenic enzymes mim

151 not reverse the anti-inflammatory effect of AICAR.

152 determine whether the therapeutic effects of AICAR against insulin resistance involve its anti-inflam

153 The effects of AICAR and exercise on muscle AMPK activity/phosphorylati

154 hat some of the antiproliferative effects of AICAR are mediated through AMPK activation.

155 Interestingly, the beneficial effects of AICAR on adipose inflammation and insulin sensitivity we

156 to activate AMPK, the inhibitory effects of AICAR on cytokine production and ICAM-1 expression were

157 tutively active AMPK mimicked the effects of AICAR on GU, whereas a dominant interfering AMPK or shRN

158 The effects of AICAR on Na(+),K(+)-ATPase were completely abolished in

159 s9 did not abolish the inhibitory effects of AICAR on RPE CFB expression.

160 We studied the effects of AICAR on the growth of retinoblastoma cell lines (Y79, W

161 dded, suggesting other inhibitory effects of AICAR or activated AMPK.

162 These effects of AICAR required the catalytic activity of AMPK.

163 In comparison, anti-inflammatory effects of AICAR were mimicked by adenosine but not inosine, the me

164 Although the glucoregulatory effects of AICAR were shown to be independent of AMPK, these studie

165 sed most of the growth-inhibiting effects of AICAR, indicating that some of the antiproliferative eff

166 lammatory and insulin-sensitizing effects of AICAR.

167 ti-inflammatory and anti-diabetic effects of AICAR.

168 wed that it did not mediate these effects of AICAR.

169 damole, an inhibitor that blocks entrance of AICAR into cells.

170 l the AICAR/NTP balance as a major factor of AICAR antiproliferative effects.

171 ylation was unchanged after 20 min or 3 h of AICAR, but AMPK phosphorylation significantly increased

172 into cells by dipyridamole or inhibition of AICAR conversion to ZMP by adenosine kinase inhibitor 5-

173 by treatment with two specific inhibitors of AICAR, dipyridamole, and 5-iodotubericidin.

174 of the sciatic nerve (HFES) or injection of AICAR, an activator of AMPK.

175 isorders and overcome current limitations of AICAR monotherapy.

176 These results demonstrated a mechanism of AICAR action and provide new insights into the metabolic

177 The mechanism of AICAR inhibition may be attributed to the interference o

178 denosine but not inosine, the metabolites of AICAR.

179 A study of AICAR accumulation in human cells revealed substantial d

180 pectedly, even in sedentary mice, 4 weeks of AICAR treatment alone induced metabolic genes and enhanc

181 kinase with SB239063, which had no effect on AICAR-induced AMPK-Thr172 phosphorylation, dose dependen

182 ough both PTX and AICAR stabilized p53, only AICAR activated Chk2 phosphorylation, stimulating p53-de

183 ective in reducing this cycle in vitro, only AICAR prevents heat-induced death in vivo.

184 risingly, AICAR acted independent of AMPK or AICAR conversion to 5-aminoimidazole-4-carboxamide-1-bet

185 -deoxy-d-glucose, with or without insulin or AICAR, before isolation of ~10-30 single fibers from eac

186 and were then exposed to 5-iodotubercidin or AICAR-free buffer, the ZMP level markedly decreased and

187 Treatment with either metformin or AICAR also led to enhanced fatty acid beta-oxidation in

188 r, we found that application of metformin or AICAR, potent AMPK activators, inhibit axogenesis and ax

189 ) via activation of phospholipase C (PLC) or AICAR activation of AMP-activated protein kinase (AMPK)

190 aling downstream of AMPK activated by PTX or AICAR differed.

191 In healthy people, AICAR acutely stimulates muscle 2DG uptake with a minor

192 es cultured in dbcAMP-containing medium plus AICAR possessed elevated levels of active AMPK, and this

193 syl-5'-monophosphate (ZMP) and its precursor AICAR, which is a pharmacological AMPK activator.

194 ng AMPK or shRNA silencing of AMPK prevented AICAR-stimulated GU and Met-induced AMPK signaling but o

195 armacological inhibitor compound C prevented AICAR-induced stellation demonstrating necessity of AMPK

196 ion of an activated RhoA construct prevented AICAR-induced stellation, indicating a mechanism upstrea

197 Furthermore, prior AICAR stimulation enhanced insulin-stimulated phosphoryl

198 We found that prior AICAR stimulation of wild-type mouse muscle increases in

199 We asked whether prolonged AICAR treatment is beneficial in a mouse model of slowly

200 azole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), an analog of AMP, is widely used as an activator

201 oimidazole-4-carboxamide-1-4-ribofuranoside (AICAR), metformin, or high molecular weight (HMW) adipon

202 oimidazole-4-carboxamide-1-d-ribofuranoside (AICAR) attenuated LPS-induced endothelial hyperpermeabil

203 midazole-4-carboxamide-1-b-D-ribofuranoside (AICAR) has been shown to improve muscle mitochondrial fu

204 zole-4-carbox-amide-1-beta-D-ribofuranoside (AICAR) is intracellularly converted to the AMP analog ZM

205 azole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) or with FSH or AR, and this staining was eliminat

206 azole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) potently suppressed upregulation of ER stress mar

207 azole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) promoted robust neurite outgrowth in Neuro2a cell

208 azole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) resulted in STIM1 phosphorylation on serine resid

209 azole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), activates AMPK and promotes translocation of the

210 azole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), an activator of AMP-activated protein kinase (AM

211 azole-4-carboxamide 1-beta-d-ribofuranoside (AICAR), and adiponectin increases glucose uptake.

212 azole-4-carboxamide 1-beta-D-ribofuranoside (AICAR), induced AMPK phosphorylation at both Thr-172 and

213 azole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), which has been shown to reduce insulin resistanc

214 azole-4-carboxamide-1-beta-D-ribofuranoside (AICAR).

215 azole-4-carboxamide 1-beta-D-ribofuranoside (AICAR; 8 mg.kg(-1).min(-1))-euglycemic clamps were perfo

216 dazole-4-carboxamide-1beta-4-ribonucleoside (AICAR; an activator of AMP kinase), or glucose plus rapa

217 om aminoimidazolecarboxamide ribonucleoside (AICAR) or from inhibition of purine synthesis by the ant

218 aminoimidazole-4-carboxamide ribonucleoside (AICAR) ex vivo.

219 aminoimidazole-4-carboxamide ribonucleoside (AICAR) prevents this heat-induced sudden death in this m

220 aminoimidazole-4-carboxamide ribonucleoside (AICAR), a pharmacological activator of AMPK, increases t

221 aminoimidazole-4-carboxamide ribonucleoside (AICAR), so as to simulate elevated AMP levels, reduced t

222 minoimidazole-4-carboxyamide ribonucleoside (AICAR), an inhibitor and activator of AMPK, to identify

223 minoimidazole-4-carboxyamide ribonucleoside (AICAR)-induced downstream signaling.

224 oimidazole-4-carboxamide 1-D-ribonucleoside (AICAR), a prototypical AMPK activator, caused opposite c

225 aminoimidazole-4-carboxamide ribonucleotide (AICAR) at 2.0 and 2.6 A resolution, respectively.

226 aminoimidazole-4-carboxamide ribonucleotide (AICAR) resulted in increased myocyte contractility witho

227 aminoimidazole-4-carboxamide ribonucleotide (AICAR) significantly reduced ROS levels induced by palmi

228 (aminoimidazole carboxamide ribonucleotide (AICAR)) or genetic means (overexpression of constitutive

229 f aminoimidazole carboxamide ribonucleotide (AICAR), an analog of adenosine monophosphate (AMP), in e

230 aminoimidazole-4-carboxamide ribonucleotide (AICAR), leading to attenuated phosphorylation of BRAF-S7

231 aminoimidazole-4-carboxamide ribonucleotide (AICAR), suppressed both.

232 drug 5-amino-4-imidazolecarboxamide ribose (AICAR), we showed that, by 12 h post-HCMV infection, inh

233 armacological AMPK activator, AICA-riboside (AICAR) resulted in a time- and concentration-dependent i

234 th 5-amino-4-imidazole carboxamide riboside (AICAR) for the detection of AMPK phosphorylation and the

235 ing 5-aminoimidazole-4-carboxamide riboside (AICAR) inhibited O2-sensitive K+ currents (carried by la

236 ss, 5-aminoimidazole-4-carboxamide riboside (AICAR), a pharmacological activator of AMPK, inhibited R

237 5-Aminoimidazole-4-carboxamide riboside (AICAR), an agent with diverse pharmacological properties

238 in, 5-aminoimidazole-4-carboxamide riboside (AICAR), and ischemia, well established triggers of AMPK

239 K, 5-amino-4-imidazole carboxamide riboside (AICAR), inhibited oxidative stress-induced phosphorylati

240 or, 5-aminoimidazole-4-carboxamide riboside (AICAR), on tumor necrosis factor alpha (TNF-alpha) induc

241 tor 5-aminoimidazole-4-carboxamide riboside (AICAR).

242 ing 5-aminoimidazole-4-carboxamide riboside [AICAR]) induces raptor phosphorylation and inhibits mTOR

243 te 5-amino-4-imidazole carboxamide ribotide (AICAR) and are unable to utilize glycerol as sole carbon

244 Aminoimidazole carboxamide ribotide (AICAR) is a purine biosynthetic intermediate and a by-pr

245 ii) 5-amino-4-imidazolecarboxamide ribotide (AICAR) has accumulated.

246 Strikingly, AICAR-induced glycogen synthesis was completely abolishe

247 In summary, AICAR negatively regulates HF diet-induced inflammation,

248 phosphorylation, dose dependently suppressed AICAR-induced upregulation of UCP-2, suggesting that AMP

249 Surprisingly, AICAR acted independent of AMPK or AICAR conversion to 5

250 nduced NO release from L6 myotubes, and that AICAR-induced upregulation of PGC-1alpha mRNA was preven

251 We found that AICAR increased skeletal muscle regeneration thereby dec

252 We found that AICAR inhibited TNF-alpha-induced CFB expression in ARPE

253 Indeed, we found that AICAR toxicity in yeast and human cells is alleviated wh

254 decreased total CoA pools and, further, that AICAR inhibited the activity of pantoate beta-alanine li

255 Our results indicate that AICAR-induced activation of AMPK inhibits retinoblastoma

256 EGF mRNA and protein levels, indicating that AICAR-mediated VEGF induction is dependent on p38 MAPK s

257 Here, we report that AICAR induces profound cytostatic and metabolic effects

258 We further showed that AICAR injection increased the expression of Trx and decr

259 o-immunoprecipitation experiment showed that AICAR suppressed the oxidant-induced dissociation betwee

260 Collectively, our results suggest that AICAR can suppress TNF-alpha-induced CFB expression in R

261 Our findings suggest that AICAR is probably effective in prophylactic treatment of

262 ntitative analysis of spectra suggested that AICAR caused greater overall phosphorylation of TBC1D1 s

263 hus, these data show for the first time that AICAR activation of AMPK inhibits Na(+) transport via a

264 the nucleotide inhibitor 3 also binds to the AICAR Tfase domain of ATIC, which now provides a lead co

265 addition, metabolite profiling points to the AICAR/NTP balance as crucial for optimal utilization of

266 Together, our metabolic analyses unveil the AICAR/NTP balance as a major factor of AICAR antiprolife

267 Even though AICAR caused a modest inactivation of GS, it stimulated

268 Exposure of HeLa cells to AICAR resulted in augmentation of methotrexate, 5-formyl

269 +/- 0.8- and 4.7 +/- 1.7-fold in response to AICAR or bicycle exercise, respectively.

270 ss fibers and focal adhesions in response to AICAR was assessed.

271 SOGA decreased in response to AICAR, an activator of AMPK, and LY294002, an inhibitor

272 PK alpha2 activity was equally responsive to AICAR treatment in both age groups.

273 lls are fourfold preferentially sensitive to AICAR compared to diploid cells.

274 4-carboxamide ribonucleotide transformylase (AICAR Tfase, residues 200-593)/IMPCH (ATIC) catalyzes th

275 Using AICAR, we recently demonstrated that prior activation of

276 progeny virion production is inhibited when AICAR is added, suggesting other inhibitory effects of A

277 dies indicate that glucose enhances, whereas AICAR and rapamycin both impair, long-term spatial memor

278 AMPK(Thr-172), hyperphosphorylation whereas AICAR-induced Tau dephosphorylation was inhibited.

279 ng PRAS40's association with RAPTOR, whereas AICAR blocked the cell cycle through proteasomal degrada

280 e aim of this study was to determine whether AICAR stimulates muscle glucose uptake in humans.

281 may contribute, the main mechanism by which AICAR improves the myopathy phenotype is by promoting mu

282 These results suggest a mechanism by which AICAR inhibits the proliferation of EGFRvIII expressing

283 e-body glucose disposal increased by 7% with AICAR from 9.3 +/- 0.6 to 10 +/- 0.6 mg x kg(-1) x min(-

284 AMPK activation with AICAR attenuated LPS-induced endothelial hyperpermeabili

285 Activation of AMPK with AICAR or, where used, expression of a constitutively act

286 Unexpectedly, treatment of 1CT+7 cells with AICAR led to a reversible 3.5-fold reduction (P=0.0025)

287 Cotherapy with AICAR and MTX could represent a novel strategy to treat

288 C57BL/6 mice were injected daily with AICAR (200 mg/kg, intraperitoneally [IP]) from day 0, th

289 Culturing of MSCs and fibroblasts with AICAR (5-aminoimidazole-4-carboxamide-1-beta-d-ribofuran

290 y mutants that are synthetically lethal with AICAR accumulation.

291 e and Treg population were not observed with AICAR treatment.

292 this anti-inflammatory effect observed with AICAR.

293 Pretreatment with AICAR reduced these lung injury indicators in LPS-treate

294 reased albuminuria that was not reduced with AICAR treatment.

295 agmentation, while restoration of SIRT3 with AICAR and ALCAR improved cisplatin-induced mitochondrial

296 ICAM-1 levels in retina were suppressed with AICAR treatment.

297 derived dendritic cells (BMDCs) treated with AICAR was measured.

298 Moreover, treatment with AICAR reduced EGFR protein levels in a panel of human co

299 Treatment with AICAR, another AMPK activator, also showed a selective a

300 es DUSP4 expression following treatment with AICAR, further supporting a direct link between EGR1 and