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 acts as an exercise mimetic in settings of fatty l

3 AICAR also heavily promoted EGFR ubiquitination in cell-

4 AICAR also reduced NF-kappaB translocation and CD14 expr

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

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

7 AICAR attenuates EAU by preventing generation of Ag-spec

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

9 AICAR did significantly inhibit BMDC maturation by reduc

10 AICAR increased GLUT4-EGFP translocation to both sarcole

11 AICAR induces p53-mediated apoptosis in primary mouse em

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

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

14 AICAR proved to have promising anti-proliferative proper

15 AICAR reduced hepatic energy charge by approximately 20%

16 AICAR reduces systemic LPS susceptibility and attenuates

17 AICAR reduction of SOGA was blocked by adiponectin; howe

18 AICAR stimulation leads to methylation and dephosphoryla

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

20 AICAR treatment also induced a transition from epithelio

21 AICAR treatment induced superoxide production and was li

22 AICAR treatment significantly reduced clinical and histo

23 AICAR treatment significantly reduced EIU clinical sever

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

25 AICAR, metformin, or transduction of constitutively acti

26 AICAR-activated AMPK inhibited mTORC1 both directly by p

27 AICAR-induced depletion of EGFR protein can be abrogated

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

29 llets containing vehicle, the AMPK activator AICAR (200 mg kg(-1) day(-1) ), or the AMPK inhibitor Co

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

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

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

33 jected to contractions or the AMPK-activator AICAR.

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

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

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

37 contrast, 3 h after contraction or 6 h after AICAR stimulation, enhanced insulin-stimulated glucose u

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

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

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

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

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

43 lls and was augmented with the AMPK agonist, AICAR.

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 found that immediately after contraction and AICAR stimulation, phosphorylation of AMPKalpha-Thr172 a

51 Both exercise and AICAR improved survival after extended hepatectomy in mi

52 itoneally administered glucose, insulin, and AICAR.

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

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

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

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

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

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

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

60 tion in the uterine artery and placenta, and AICAR increased AMPK activation in these tissues compare

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

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

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

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

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

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

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

68 -4-carboxamide ribonucleotide, also known as AICAR) brings about any metabolic changes remain unexpla

69 ing 41 that were found neither as AMP nor as AICAR or succinyl-ZMP binders.

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

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

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

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

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

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

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

77 Pharmacological AMPK activation by AICAR partially prevented hypoxia-induced fetal growth r

78 rotein trafficking as a function affected by AICAR.

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

80 , HK2, TPI, and MCT4); activation of AMPK by AICAR treatment reduced this response.

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

82 ocytes and protein leakage were decreased by AICAR treatment.

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

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

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

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

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

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

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

90 other inositol phosphates were unaffected by AICAR.

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

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

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

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

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

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

97 To exert cytotoxicity, AICAR needs to be metabolized, but the AICAR-derived tox

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

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

100 armacological activation of AMPK by the drug AICAR improved fetal growth and elevated uterine artery

101 creased independently of hepatic AMPK during AICAR administration.

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

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

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

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

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

107 ntly demonstrated that AMPK is necessary for AICAR, contraction, and exercise to enhance muscle and w

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

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

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

111 s abundant on nuclei-enriched fractions from AICAR-fed cells, this effect being compensated by overex

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

113 Furthermore, AICAR inhibited autophosphorylation of the ER stress sen

114 Furthermore, AICAR inhibited macrophage ER stress responses triggered

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

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

117 ivities during stress, in unstressed hearts, AICAR induced a mild activation of Akt signaling, and, i

118 denine phosphoribosyl transferase under high AICAR conditions.

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

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

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

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

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

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

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

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

127 ntracellular concentration of the metabolite AICAR, resulting in AMPK activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 ow that ZMP is the major toxic derivative of AICAR in yeast and establish that its metabolization to

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

145 or ZTP (di- and triphosphate derivatives of AICAR) strongly reduced its toxicity.

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

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

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

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

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

151 ), suggesting that the vasodilator effect of AICAR was selective for the uterine circulation.

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

153 not reverse the anti-inflammatory effect of AICAR.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 lammatory and insulin-sensitizing effects of AICAR.

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

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

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

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

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

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

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

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

177 isorders and overcome current limitations of AICAR monotherapy.

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

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

180 denosine but not inosine, the metabolites of AICAR.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 the ZMP-specific binders, partially rescued AICAR toxicity.

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

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

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

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

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

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

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

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), and adiponectin increases glucose uptake.

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

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

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

214 azole-4-carboxamide 1-beta-d-ribofuranoside (AICAR, or acadesine) is a precursor of the monophosphate

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

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

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

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

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

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

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

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

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

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

225 aminoimidazole-4-carboxamide ribonucleotide (AICAR) or metformin during sepsis improved the survival,

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-4-carboxamide ribonucleotide (AICAR) to activate AMPK transiently before transverse ao

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

230 Aminoimidazole-4-carboxamide ribonucleotide (AICAR), an AMPK activator, elicits a similar effect.

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

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

233 aminoimidazole-4-carboxamide ribonucleotide (AICAR), metformin, and a specific AMPKalpha activator (G

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

235 aminoimidazole-4-carboxamide ribonucleotide (AICAR).

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

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

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

239 5-Aminoimidazole-4-carboxamide riboside (AICAR), an agent with diverse pharmacological properties

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

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

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

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

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

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

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

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

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

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

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

263 city, AICAR needs to be metabolized, but the AICAR-derived toxic metabolite was not identified.

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

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

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

267 Exercising, or its substitution through AICAR, may provide a feasible strategy to negate the hep

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

269 ng muscle insulin sensitivity in response to AICAR and contraction.

270 +/- 0.8- and 4.7 +/- 1.7-fold in response to AICAR or bicycle exercise, respectively.

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

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

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

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

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

282 AMPK activation with AICAR attenuated LPS-induced endothelial hyperpermeabili

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

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

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

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

287 Replacing exercise with AICAR was sufficient to replicate the above benefits.

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

289 hrough the uterine artery was increased with AICAR in hypoxic mice (P < 0.001), suggesting that the v

290 ithelial keratinocytes after incubation with AICAR, the agonist for AMPK signaling which activates PP

291 y mutants that are synthetically lethal with AICAR accumulation.

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

293 this anti-inflammatory effect observed with AICAR.

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

295 reased albuminuria that was not reduced with AICAR treatment.

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

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

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

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

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