ライフサイエンスコーパス: AMPK

1 AMPK activation or caspase-6 inhibition, even after the

2 AMPK activation targets Kruppel-like factor 4 (KLF4), kn

3 AMPK activity is increased by nutrient deprivation and i

4 AMPK and insulin signaling intersect at mammalian target

5 AMPK consists of three subunits: alpha, beta, and gamma.

6 AMPK inhibitors prevented Ghr-induced FOXO1 nuclear tran

7 AMPK inhibits mTOR, and the mTOR inhibitor rapamycin als

8 AMPK is a central regulator of metabolism and autophagy.

9 AMPK is a key regulator at the molecular level for maint

10 AMPK maintains energy homeostasis in the cell by promoti

11 AMPK phosphorylated proapoptotic caspase-6 protein to in

12 AMPK-driven protection was associated with increased Sir

13 ha2-double knockout cells and discovered 160 AMPK-dependent phosphorylation sites.

14 glucose supplementation profoundly abrogated AMPK activation and rescued bladder cancer cells from Vi

15 In all, the AC6-AMPK pathway, which is tunable to cellular cues, could p

16 n and ubiquitin systems converge to activate AMPK and autophagy during endomembrane homeostasis.

17 lular free Ca(2+) concentrations to activate AMPK is reduced in cells lacking IQGAP1.

18 on male diabetic placental explant activated AMPK and stimulated PGC-1alpha expression, concomitant w

19 ed on its ability to inhibit virus-activated AMPK.

20 Here we show how lysosomal damage activates AMPK.

21 rointestinal cancer cells, glucose activates AMPK to selectively induce EP300, but not CREB-binding p

22 hat glucose starvation transiently activates AMPK, whereas changes in glucagon and insulin levels had

23 s intracellular AMP content, which activates AMPK, leading to inhibition of mTORC1.

24 s K63 ubiquitination of TAK1 thus activating AMPK on damaged lysosomes.

25 Granule trafficking was driven by active AMPK enriched on adjacent lysosomes, revealing previousl

26 studies, absence of GI neuron activity after AMPK suppression in the VMN had no impact on the counter

27 whereas neither glucagon nor insulin altered AMPK activation.

28 uman macrophages in vitro, heme activates an AMPK (AMP-activated protein kinase)/ATF1 (activating tra

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

30 This activity was reversed by an AMPK inhibitor (compound C).

31 anslocation of NFATc1 in keratinocytes in an AMPK-dependent manner.

32 rbed signaling network with PI3K, MEK1/2 and AMPK inhibitors.

33 active oxygen species (ROS) accumulation and AMPK activation in response to glucose in previously non

34 s were associated with activation of Akt and AMPK in these tissues.

35 d KDM5C associate with high angiogenesis and AMPK/fatty acid oxidation gene expression, while CDKN2A/

36 Our results indicate that various CaMKK and AMPK isoforms contribute to infection in unique ways.

37 Both CaMKK2 and AMPK associate with IQGAP1 in cells.

38 d strengthen the rationale to choose CD2 and AMPK as therapeutic targets to enhance CTL activity.

39 In DM and AMPK-DN mice, the inhibitory effect of SF-PreCon upon p3

40 ion of ERK1/2, a pro-survival MAPK in DM and AMPK-DN mice.

41 activation are resistant to ferroptosis and AMPK inactivation sensitizes these cells to ferroptosis.

42 unexpected coupling between ferroptosis and AMPK-mediated energy-stress signalling.

43 lucidated that the inhibition of insulin and AMPK signaling pathways by CSE deficiency resulted in nu

44 ed functional interaction between IQGAP1 and AMPK and suggest that IQGAP1 modulates AMPK signaling.

45 ntributions that specific CaMKK isoforms and AMPK subunit isoforms make toward HCMV infection.

46 ay, or in upstream signalling via mTORC1 and AMPK.

47 -mediated gene editing revealed that PKA and AMPK are not required for the starvation-dependent incre

48 he mechanisms of cellular energy sensing and AMPK-mediated mTORC1 inhibition are not fully delineated

49 SIRT1 and AMPK also act on sodium transport mechanisms to reduce i

50 acterized by marked suppression of SIRT1 and AMPK, leading to a diminution in autophagic flux in glom

51 WT) and that the combination of EGFR TKI and AMPK activator may be a potentially effective therapeuti

52 pro-respiratory effects of methotrexate are AMPK-dependent, as cells with reduced AMPK activity are

53 ucose, an inhibitor of glycolysis, augmented AMPK activity and attenuated ZIKV replication.

54 Cancer cells with high basal AMPK activation are resistant to ferroptosis and AMPK in

55 nvolved in mediating the interaction between AMPK and TSC2 and facilitate TSC2 phosphorylation at Ser

56 ed mice with liver-specific knockout of both AMPK catalytic alpha1 and alpha2 subunits exhibited sign

57 n-induced metabolic stress strengthened both AMPK activation and cellular energy depletion under limi

58 n together, these data demonstrate that both AMPK and ATF1 are required for normal hematoma resolutio

59 reated with metformin was largely ablated by AMPK deficiency under the conditions examined, indicatin

60 exacerbated under fasting conditions and by AMPK deficiency in hepatocytes, revealing metabolic infl

61 e native and neo-phosphorylations of BRD4 by AMPK or PKC.

62 in the absence of PINK1 and is regulated by AMPK-dependent signaling.

63 colysis, and metabolic pathways regulated by AMPK.

64 interactions with TBC1D1 were unaffected by AMPK activation, distinguishing them from the AMPK regul

65 TORC1 pathway) or of energy supply in cells (AMPK pathway).

66 t of beclin 1 or UVRAG inhibits the cellular AMPK activation induced by glucose starvation.

67 Collectively, AMPK and CK2 signaling converge on histone kinase Tda1 t

68 n, with increased Tor activity and decreased AMPK activity reported.

69 stigations elucidating the role of dedicated AMPK subunits in the modulation of gene expression.

70 Here we investigated the role of direct AMPK-mediated serine phosphorylation of RAPTOR in a new

71 ivated FPR2/ALX receptors and the downstream AMPK signaling cascade, leading to macrophage skewing, d

72 Consistent with its antiviral effect, AMPK activation potentiated the expression of genes with

73 present at day 9 in mice deficient in either AMPK (Prkab1(-/-)) or ATF1 (Atf1(-/-); n=6 each).

74 Mechanistically, we observed elevated AMPK activity and the AMPKbeta1 abundance in the liver o

75 Ornithine enhances AMPK mediated autophagy whereas imidazole directly kills

76 Metformin is an established AMPK agonist that can promote autophagy, but its effects

77 ion from healthy to tumor tissue may explain AMPK switching from tumor suppressor to activator during

78 levels and produced more glucose than floxed AMPK catalytic alpha1 and alpha2 mice after long-term me

79 plicity of infection, but is dispensable for AMPK activation at the earliest times of infection, whic

80 autophagy protein, beclin 1, is required for AMPK activation in skeletal muscle(3).

81 We also identify a separate role for AMPK regulating myometrial contractions that may influen

82 We show that impaired SIRT1, FoxO3a, AMPK, and PPAR-alpha signaling are responsible for autop

83 s defective autophagy, restores SIRT1/FoxO3a/AMPK/PPAR-alpha signaling and rectifies metabolic abnorm

84 s mediated by downregulation of SIRT1/FoxO3a/AMPK/PPAR-alpha signaling.

85 tively, these data identified the AnxA1/FPR2/AMPK axis as an important pathway in skeletal muscle inj

86 ormin, which also occurs in hepatocytes from AMPK knockout mice, is best explained by allosteric regu

87 min promotes the formation of the functional AMPK alphabetagamma heterotrimeric complex.

88 The repression of hepatic AMPK activity permits the transition from simple steatos

89 Thus, our data identify AMPK and autophagy as targetable components of ADOA path

90 abolic and catabolic processes and implicate AMPK activation as a metabolic determinant of methotrexa

91 regulates liver damage in NASH, implicating AMPK and caspase-6 as therapeutic targets.

92 ns in rodents are associated with changes in AMPK activation and the cellular energy state in the liv

93 w-derived macrophages from mice deficient in AMPK (Prkab1(-/)(-)) or ATF1 (Atf1(-/-)).

94 SF-PreCon decreased MI/R injury in AMPK-DN mice.

95 rial oxygen consumption, which may result in AMPK activation and the consequent mitochondrial fission

96 ration of the metabolite AICAR, resulting in AMPK activation.

97 metformin and many natural products increase AMPK activity and exert a multitude of health benefits,

98 ine artery and placenta, and AICAR increased AMPK activation in these tissues compared to vehicle.

99 omous fashion in ex vivo contraction-induced AMPK activation, glucose uptake and beclin 1-UVRAG compl

100 sis significantly blocked Vitamin K2-induced AMPK activation and subsequently prevented autophagic ce

101 Methotrexate-induced AMPK activation leads to decreased one-carbon metabolism

102 enes included axonal guidance, inflammation (AMPK, NFKB, APK/JNK signaling), and antioxidant signalin

103 fied viral restriction factor TDRD7 inhibits AMPK and thereby blocks HSV-1 replication independently

104 Insulin, AMPK, and mTOR signalling activity was similar in contro

105 The AMP-activated kinase AMPK was investigated as a potential mediator of pMLC do

106 xamples include AMP-activated protein kinase AMPK, nutrient/energy sensor mTOR, NAD(+)-dependent deac

107 es adenosine monophosphate-activated kinase (AMPK) and mitigates steatosis; however, its impact on is

108 itro that AC6 inhibits AMP-activated kinase (AMPK), an important modulator of cellular energy-conserv

109 , we show that the energy sensor AMP kinase (AMPK) governs gastric epithelial progenitor differentiat

110 metformin-mediated activation of AMP kinase (AMPK).

111 hat PF induces AMP-activated protein kinase (AMPK) activation before inhibiting S6K1.

112 sine monophosphate activated protein kinase (AMPK) activation by 991 promote mitochondrial fission vi

113 AMP-activated protein kinase (AMPK) activation vasodilates arteries and may increase u

114 pa1, active 5' AMP-activated protein kinase (AMPK) and its autophagy effector ULK1 accumulate at axon

115 tivation of 5'-AMP-activated protein kinase (AMPK) and neuroprotective induction of autophagy, implic

116 Yeast AMP-activated protein kinase (AMPK) directly phosphorylates Tda1 to govern Tda1 activi

117 belong to the AMP-activated protein kinase (AMPK) family, whose members control central and protein

118 e 5'-monophosphate-activated protein kinase (AMPK) in HSPC, dramatically increasing mitochondria tran

119 sine monophosphate-activated protein kinase (AMPK) in skeletal muscle coordinates systemic metabolic

120 The AMP-activated protein kinase (AMPK) inhibitor dorsomorphin decreased lysosomal V-ATPas

121 AMP-activated protein kinase (AMPK) is a fundamental component of a protein kinase cas

122 AMP-activated protein kinase (AMPK) is a key energy sensor, activated by glucose limit

123 AMP-activated protein kinase (AMPK) is a key regulator of energy metabolism that phosp

124 energy sensor AMP-activated protein kinase (AMPK) is a metabolic regulator that mediates adaptation

125 The AMP-activated protein kinase (AMPK) is a molecular sensor to maintain energy homeostas

126 sine monophosphate-activated protein kinase (AMPK) is an evolutionary conserved serine/threonine kina

127 onophosphate (AMP)-activated protein kinase (AMPK) is repressed in NASH.

128 hich activated AMP-activated protein kinase (AMPK) negatively regulates autophagy remains nearly unex

129 ated through a AMP-activated protein kinase (AMPK) pathway and a novel downstream transcriptional tar

130 se (CaMKK) and AMP-activated protein kinase (AMPK) regulate metabolic activation and have been found

131 Activation of AMP-activated protein kinase (AMPK) results in vasodilatation and is therefore a poten

132 AMP-activated protein kinase (AMPK) senses energy status and regulates metabolic proce

133 ue to impaired AMP-activated protein kinase (AMPK) signaling.

134 olic regulator AMP-activated protein kinase (AMPK) was a critical node in the CD2 network, which prom

135 AMP-activated protein kinase (AMPK), a key energy stress sensor, responds to increases

136 ed the role of AMP-activated protein kinase (AMPK), a master regulator of energy metabolism, in respo

137 nactivation of AMP-activated protein kinase (AMPK), a sensor of cellular energy status, largely aboli

138 ways involving AMP-activated protein kinase (AMPK), Akt and eNOS, and inhibits iNOS and NADPH oxidase

139 ling involving AMP-activated protein kinase (AMPK), Akt, endothelial nitric oxide synthase (eNOS), nu

140 uin-1 (SIRT1), AMP-activated protein kinase (AMPK), and hypoxia inducible factors (HIFs; especially H

141 uin-1 (SIRT1), AMP-activated protein kinase (AMPK), and hypoxia-inducible factors (HIF-1alpha and HIF

142 t activator of AMP-activated protein kinase (AMPK), can reduce beta-catenin expression and downstream

143 substrate for AMP-activated protein kinase (AMPK), constitutively suppresses this central metabolic

144 nsing protein, AMP-activated protein kinase (AMPK), in the autophagic degradation of intracellular va

145 ion of hepatic AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor alpha

146 box O (FoxO), AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor-alpha

147 irus-activated AMP-activated protein kinase (AMPK), which was essential for HSV-1 replication.

148 and attenuates AMP-activated protein kinase (AMPK)-dependent inhibition of mTOR; this in turn reduces

149 muscles in an AMP-activated protein kinase (AMPK)-dependent manner, and with increased intracellular

150 odulated in an AMP-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR)-S6 kinase-dep

151 stimulation of AMP-activated protein kinase (AMPK).

152 he activity of AMP-activated protein kinase (AMPK).

153 or mediated by AMP-activated protein kinase (AMPK).

154 es (PHICS), which enable two example kinases-AMPK and PKC-to phosphorylate target proteins that are n

155 nctional and lipidomic analyses further link AMPK regulation of ferroptosis to AMPK-mediated phosphor

156 The LKB1/AMPK pathway plays a major role in cellular homeostasis

157 ndrial transport was less sensitive to local AMPK stimulus, with the imbalance of bidirectional mitoc

158 uctures and to investigate whether localized AMPK signaling influenced axonal mitochondrial transport

159 GC-1alpha acetylation (inactive form), lower AMPK activity, and overactive mTOR pathway in AMD RPE as

160 Mammalian AMPK is a heterotrimeric complex, and its catalytic alph

161 Mechanistically, AMPK localizes in the mitochondrial matrix and phosphory

162 microdomain signaling impairs MYH7-mediated, AMPK-dependent sarcomere-cytoskeleton filament interacti

163 r response to low energy levels and mediates AMPK-mTORC1 signaling.

164 MPKalpha2 dominant negative expressing mice (AMPK-DN).

165 ce, we investigated whether IQGAP1 modulates AMPK signaling.

166 1 and AMPK and suggest that IQGAP1 modulates AMPK signaling.

167 for a Toll-like receptor in skeletal-muscle AMPK activation and glucose metabolism during exercise,

168 oxia, and that protection relied on neuronal AMPK.

169 was strongly downregulated in the absence of AMPK activity and that reexpression of Txn2 in Sf1 neuro

170 eased intracellular Ca(2+) and activation of AMPK and FOXO1, maintaining a low rate of cholangiocyte

171 cient in both exercise-induced activation of AMPK and plasma membrane localization of the GLUT4 gluco

172 to the effects of CO-EtOAc on activation of AMPK and promotion of mitochondrial fission.

173 Pharmacological activation of AMPK at the distal axon (0.1 mm 5-aminoimidazole-4-carbo

174 s (GLUT1, HK2, TPI, and MCT4); activation of AMPK by AICAR treatment reduced this response.

175 In this study, pharmacological activation of AMPK by the drug AICAR improved fetal growth and elevate

176 Small molecule-based activation of AMPK can restore TnT microdomain interactions, and parti

177 Metformin-dependent activation of AMPK classically inhibits mTORC1 via TSC/RHEB, but sever

178 9a levels upon pharmacological activation of AMPK in airway epithelial cells correlated with elongate

179 beclin 1, in exercise-induced activation of AMPK in skeletal muscle.

180 Because the activation of AMPK is crucial for the initiation of autophagy, we hypo

181 of NRF2 resulted in a constant activation of AMPK leading to hyperactivation of autophagy during oxid

182 In the absence of AC6, activation of AMPK mobilizes Kif19a into autophagosomes for degradatio

183 Instead, activation of AMPK pathway mainly and activation of both HIF-1/REDD1 a

184 Activation of AMPK requires phosphorylation by the liver kinase B1 or

185 Pharmacological activation of AMPK using 5-aminoimidazole-4-carboxamide ribonucleotide

186 Pharmacologic activation of AMPK with 5-aminoimidazole-4-carboxamide ribonucleotide

187 DPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabo

188 drastically reduced metformin activation of AMPK.

189 In contrast, direct allosteric activators of AMPK (A-769662, 991, and C-13) had opposite effects from

190 th benefits, developing direct activators of AMPK to elicit beneficial effects has been challenging.

191 The activity of AMPK is regulated by the availability of nutrients, such

192 In C. elegans, deletion of AMPK or of key autophagy and mitophagy genes normalizes

193 rylation of AS160 and p38 MAPK downstream of AMPK and AKT, and the resultant GLUT4 translocation.

194 The transcription factor downstream of AMPK that is relevant to cAMP signaling is CREB; decreas

195 dy demonstrates that the anti-ZIKV effect of AMPK signaling in endothelial cells is mediated by reduc

196 lly rescues viral replication in the face of AMPK inhibition.

197 at expression of a dominant negative form of AMPK or inactivation of AMPK alpha1 and alpha2 subunit g

198 the pathogenesis of NAFLD and the impact of AMPK activity state on hepatic steatosis, inflammation,

199 lexibility and emphasizing the importance of AMPK for maintaining hepatic energy charge.

200 ant negative form of AMPK or inactivation of AMPK alpha1 and alpha2 subunit genes in Sf1 neurons of t

201 e of general autophagy and is independent of AMPK.

202 tion of beta-catenin occurs independently of AMPK activation and does not involve transcriptional or

203 regulated by AMP/ATP levels independently of AMPK, and point to hypoxia/energy depletion as potential

204 Genetic ablation or chemical inhibition of AMPK activity suppressed HSV-1 replication in multiple h

205 nt that is restored by genetic inhibition of AMPK and autophagy.

206 uted to activation of mTOR and inhibition of AMPK signaling.

207 Further, pharmacological inhibition of AMPK with Compound C reduced uterine artery diameter and

208 Inhibition of AMPK-mediated autophagy led to reduced lung branching in

209 seline levels, confirming the involvement of AMPK.

210 ring starvation, Lkb1, an upstream kinase of AMPK, represses mTOR, which induces a reversible glycoly

211 Lentivirus-mediated knockdown of AMPK and the use of AMPKalpha(-/-) mouse embryonic fibro

212 viding evidence that physiological levels of AMPK activation are necessary for vasodilatation in heal

213 hosphorylation and lysosomal localization of AMPK.

214 2) protein expression and phosphorylation of AMPK, upregulating the expression of a key regulatory gl

215 The purpose was to determine the role of AMPK activation in the renal metabolic response to sepsi

216 This study highlights a role of AMPK signaling in the depression of axonal mitochondrial

217 To determine the relevant role of AMPK, the effect of SF-PreCon was determined in cardiac-

218 uction in the active phosphorylated state of AMPK and of its downstream target acetyl-CoA carboxylase

219 In primary myoblast cells, stimulation of AMPK and AKT was observed in response to CHI3L1, undersc

220 GAP1 binds directly to the alpha1 subunit of AMPK.

221 Suppression of AMPK activity relieved this inhibition, rendering caspas

222 Suppression of AMPK/aak-2 by NRF2/SKN-1 down-regulates autophagy during

223 RE11A and inefficient lysosomal tethering of AMPK due to deficiency of N-myristoyltransferase 1 (NMT1

224 -1 replication after viral entry depended on AMPK but not on its function in autophagy.

225 ised mice into sedentary mice and depends on AMPK-mediated signaling in both muscle and adipocytes.

226 roles of glucose and pancreatic hormones on AMPK activation in mouse primary hepatocytes.

227 glucagon and insulin levels had no impact on AMPK.

228 e glycolytic flux via pharmacological Akt or AMPK activation, thus providing a molecular platform for

229 Pharmacological AMPK activation by AICAR partially prevented hypoxia-ind

230 Pharmacological AMPK activators that generate AMP, unlike allosteric act

231 tigation into the utility of pharmacological AMPK activation for treatment of fetal growth restrictio

232 NOVA analyses indicated that hypoxia reduced AMPK activation in the uterine artery and placenta, and

233 te are AMPK-dependent, as cells with reduced AMPK activity are less affected by methotrexate treatmen

234 Renal AMPK activation in response to sepsis/IM is an adaptive

235 ed in AKI, increased mortality, and in renal AMPK activation 6-24 hours after CLP/IM.

236 hepatocytes and intact murine liver requires AMPK regulation of both RAPTOR and TSC2 to fully inhibit

237 ly, glycogen content and activity of the ROS/AMPK/EP300/beta-catenin axis are opposite in healthy ver

238 esponse that reactivates the redox-sensitive AMPK and activates the redox-sensitive stress kinase JNK

239 (i.e. the glucagon/insulin ratio), sensitize AMPK activation to the energetic stress induced by the d

240 the activation of the cellular energy sensor AMPK (AMP-activated protein kinase), and decreases EC pr

241 The hypothesis that the energy sensor AMPK is necessary to offset the metabolic burden of over

242 h-promoting Tor kinase and the energy sensor AMPK, appear to show reciprocal changes in activity duri

243 tations showed activation of energy shortage AMPK-dependent sensing, leading to mTORC1 inhibition.

244 The cells respond by downregulating SIRT1, AMPK, and HIF-2alpha, thus leading to an impairment of a

245 The activation of SIRT1, AMPK, and HIF-2alpha enhances autophagy, a lysosome-depe

246 mimicry, which includes activation of SIRT1, AMPK, and HIF-2alpha, enhanced autophagic flux, reduced

247 ts show a surprising reciprocity between SkM AMPK signaling and insulin action that manifests with di

248 Liver-specific AMPK knockout aggravated liver damage in mouse NASH mode

249 Importantly, Ca(2+)-stimulated AMPK phosphorylation was rescued by re-expression of IQG

250 ciated dementia can be improved by targeting AMPK remains unclear, and roles of AMPKalpha isoforms in

251 Finally, we demonstrate that AMPK affects cellular physiology by engaging in the regu

252 c fibroblasts provided further evidence that AMPK has an antiviral effect on ZIKV replication.

253 Further, we find that AMPK-mediated glycolytic activation is important for inf

254 Results did not support the hypothesis that AMPK is protective during overnutrition.

255 Our study reveals that AMPK-mediated PDHA phosphorylation drives PDHc activatio

256 Here, we show that AMPK (AMP-activated protein kinase), activated in mouse

257 These results suggest that AMPK activation is a potential strategy for improving fe

258 These findings suggest that AMPK inhibition represents a potential strategy to manag

259 Administering the AMPK activator metformin decreases epithelial progenitor

260 he detailed molecular interplays between the AMPK and the mTORC1 pathway in the hepatic benefits of m

261 To elucidate the AMPK-dependent signaling pathways, we performed global q

262 MPK activation, distinguishing them from the AMPK regulated interaction between TBC1D1 and AMPKalpha1

263 The two isoforms of the AMPK catalytic subunit (AMPKalpha1 and alpha2) are both

264 ositive regulators and key components of the AMPK pathway, autophagy, proteasome function, and the un

265 ver kinase B1 (LKB1), a master kinase of the AMPK subfamily, via CpG island methylation.

266 rentiation programs via misregulation of the AMPK-mTOR-ULK axis.

267 pressin activates one or more members of the AMPK/SNF1-subfamily of basophilic protein kinases.

268 vator AICAR (200 mg kg(-1) day(-1) ), or the AMPK inhibitor Compound C (20 mg kg(-1) day(-1) ) beginn

269 dence supporting that E4BP4 may suppress the AMPK activity via promoting the AMPKbeta1 ubiquitination

270 rocyte and organotypic cultures, through the AMPK signaling pathway and neuropeptidergic circuitry go

271 Thus, the AMPK-caspase-6 axis regulates liver damage in NASH, impl

272 subcutaneous pellets containing vehicle, the AMPK activator AICAR (200 mg kg(-1) day(-1) ), or the AM

273 e evaluated after treatment of mice with the AMPK activator 5-aminoimidazole-4-carboxamide ribonucleo

274 ly, the combination of methotrexate with the AMPK activator, phenformin, potentiates its anti-prolife

275 This AMPK activation triggers localized hillock autophagosome

276 This AMPK-PDHc axis is activated in advanced breast cancer an

277 y stress inhibits ferroptosis partly through AMPK and reveals an unexpected coupling between ferropto

278 sion of invasion associated proteins through AMPK activation; and potential rescue of amyloid-beta (A

279 Thus, AMPK activates KLF4 in progenitors to reduce self-renewa

280 Thus, AMPK activation promotes mitophagy by enhancing mitochon

281 Thus, AMPK is required for GI neuron activity by controlling t

282 rther link AMPK regulation of ferroptosis to AMPK-mediated phosphorylation of acetyl-CoA carboxylase

283 ced cell surface GLUT4 levels in response to AMPK activation.

284 Transcriptionally, AMPK and mTORC1 were both important for regulation of an

285 K2 could induce metabolic stress and trigger AMPK-dependent autophagic cell death in bladder cancer c

286 ay suppression, which subsequently triggered AMPK-dependent autophagic cell death.

287 We posit that the VEGFR2/AMPK/PEG3 axis integrates the anti-angiogenic and pro-au

288 SF-PreCon exerts cardioprotective action via AMPK-independent activation of a pro-survival MAPK membe

289 ipoRs) decrease myometrial contractility via AMPK to promote uterine quiescence in pregnancy.

290 strate that SF-PreCon protects the heart via AMPK-dependent inhibition of pro-death MAPK in ND mice.

291 but not DG, decreased cell proliferation via AMPK activation in cholangiocytes in vitro.

292 al and osteogenic regeneration while in vivo AMPK inhibition increased stromal recovery.

293 ce self-renewal and promote PC fate, whereas AMPK-PGC1alpha activation within the PC lineage promotes

294 R in a new Raptor (AA) mouse model, in which AMPK phospho-serine sites Ser722 and Ser792 of RAPTOR we

295 n in diabetes or clinical scenarios in which AMPK signaling is impaired.

296 n during sepsis improved the survival, while AMPK inhibition with Compound C increased mortality, imp

297 arkedly induced metabolic stress, along with AMPK activation and mTORC1 pathway suppression, which su

298 ves ketogenesis, and working in concert with AMPK, it can directly inhibit inflammasome activation an

299 riments recapitulated these properties, with AMPK-null macrophages lacking AnxA1-mediated polarizatio

300 oreover, combined treatment of EGFR TKI with AMPK activators synergistically increases EGFR TKI sensi