ライフサイエンスコーパス: AMPK

1 AMPK has emerged as a pertinent stress-activated kinase

2 AMPK induces actin depolymerization, which reduces vascu

3 AMPK is a conserved serine/threonine kinase whose activi

4 AMPK is a highly conserved master regulator of metabolis

5 AMPK, mTOR and PI3K/Akt pathways were verified after gem

6 AMPK-related protein kinases (ARKs) coordinate cell grow

7 AMPK/sirtuin-1 inhibit the activity of STAT3 (signal tra

8 AMPK/SNF1 also promotes longevity in several model organ

9 e extracted a core circuit containing HIF-1, AMPK, and ROS.

10 ts phosphorylation at threonine residue 172 (AMPK-Thr(P)(172)).

11 Other environmental stresses also activate AMPK, but it is unclear whether cellular energy status a

12 ted from Chloranthus japonicus, can activate AMPK and modulate glucose metabolism both in vitro and i

13 hed light both into how nucleotides activate AMPK and, importantly, also into the sites bound by smal

14 kinase upstream of AMPK, failed to activate AMPK and sustain energy homeostasis and resulted in apop

15 inhibited the ability of leptin to activate AMPK, induce KATP and Kv2.1 channel trafficking, and pro

16 till mobilized sufficient Ca(2+) to activate AMPK.

17 M-CSF-activated AMPK is via M-CSF receptor-dependent reactive oxygen spe

18 The reduced ATP hydrolysis activated AMPK activity in IF1 KO hearts, which together facilitat

19 activation despite the presence of activated AMPK.

20 During acute glucose restriction, activated AMPK was stabilized from degradation and interacted with

21 lated factor (M-CSF) significantly activated AMPK and promoted monocyte-to-macrophage differentiation

22 Our findings that activated AMPK and Atg14p are required to orchestrate micro-lipoph

23 Knockdown of aldolases activates AMPK even in cells with abundant glucose, whereas the ca

24 ochondrial depolarization but also activates AMPK signaling and increases autophagy.

25 nduced matrix protein increase by activating AMPK in renal cells, we examined whether H2S inhibits hi

26 iral overexpression of constitutively active AMPK downregulated mitochondrial superoxide, lowered lev

27 ddition, it regulates cell-to-cell adhesion, AMPK signaling, autophagy and apoptosis in different cel

28 stress, but blocking fission did not affect AMPK activation.

29 clear whether cellular energy status affects AMPK activation under these conditions.

30 These included activation of Akt, AMPK (only in males) and p70S6K kinases.

31 ivation of glucose-metabolism regulating Akt/AMPK/p70S6 kinase pathways that is expected to affect th

32 knockout (mKO) of Rac1, a kinase-dead alpha2 AMPK (alpha2KD), and double knockout (KO) of beta1 and b

33 transport, whereas only Rac1, but not alpha2 AMPK, regulates muscle glucose uptake during submaximal

34 K function and downstream effects of altered AMPK activity on neuronal metabolism have been investiga

35 AICAR, an AMPK activator, led to a strong reduction of myotonia, w

36 Compound C, an AMPK inhibitor, prevented NaHS inhibition of high glucos

37 ion elevates SIRT1 levels and activity in an AMPK (AMP-activated protein kinase alpha)-dependent mann

38 eases glucose uptake, and overcomes IR in an AMPK-dependent manner in cardiomyocytes.

39 pan of animals fed a high glucose diet in an AMPK-dependent manner.

40 ha-induced CFB expression in RPE cells in an AMPK-independent mechanism, and could be used as a thera

41 n of an intracellular calcium chelator or an AMPK inhibitor to either mouse macrophages or mouse embr

42 glucocorticoids, identifying TXNIP, CNR2 and AMPK as potential therapeutic targets.

43 ently decreased intracellular ATP levels and AMPK activity, as evaluated by its phosphorylation at th

44 ragulator, axin, liver kinase B1 (LKB1) and AMPK, which has previously been shown to be required for

45 METHODS AND AMPK induced a slowly developing dilation at unchanged c

46 ange the phosphorylation of ULK1 by mTOR and AMPK.

47 ion abrogated, while LKB1-overexpression and AMPK-activation potentiated HNK's effects.

48 It is concluded that Rac1 and AMPK together account for almost the entire ex vivo cont

49 identified the interaction between Sesn2 and AMPK in the ischemic heart.

50 rest, the binding affinity between Sesn2 and AMPK upstream LKB1 is impaired in aged hearts during isc

51 luripotency factors since LKB1-silencing and AMPK-inhibition abrogated, while LKB1-overexpression and

52 stress induces transient energy stress, and AMPK activation allows cells to manage this energy stres

53 s, and atherosclerosis in diabetic ApoE(-/-)/AMPK-alpha2(-/-) mice, indicating that metformin exerts

54 lates and requires AMPK signaling as well as AMPK-independent suppression of mTORC1 activity for prov

55 Augmenting AMPK activity by intra-NAc core infusions of the AMPK ac

56 and double knockout (KO) of beta1 and beta2 AMPK subunits (beta1beta2 KO) each partially decreased c

57 oma, we confirmed an anticorrelation between AMPK and HIF-1 activities and the association of metabol

58 inally, we demonstrate that Rheb-WT can bind AMPK to facilitate AMPK activation, whereas Rheb-Y35N co

59 ation, whereas Rheb-Y35N competitively binds AMPK, impairing AMPK phosphorylation.

60 dolase mutant, which still binds FBP, blocks AMPK activation.

61 However, both AMPK activation and glucose release from the liver are i

62 abolic processes (FAO) that are activated by AMPK.

63 d oxidation (FAO) is specifically induced by AMPK complexes containing the alpha2 subunit.

64 ng osmotic stress requires energy sensing by AMPK heterotrimer, and osmotic stress leads to decreased

65 apacities of cancer cells through the CamKKB/AMPK pathway.

66 We further demonstrate cellular AMPK signaling independent of activation loop Thr172 pho

67 y modulation of the TORC1 pathway components AMPK, RAGA-1 and RSKS-1/S6 kinase.

68 In contrast, AMPK-alpha2 deficiency abolished the effects of metformi

69 n Treg cells was independent of conventional AMPK signalling or the mTORC1-HIF-1alpha axis, but contr

70 a key determinant of cardiac energy demand, AMPK functions in an organ-specific manner to maintain c

71 are required to coordinate an IL6-dependent AMPK nuclear signaling pathway converging on FoxO3 trans

72 e inhibition of the CamKKB or the downstream AMPK pathway partly abolished the resveratrol-induced in

73 lutaryl-CoA/tryptophan degradations and EIF2/AMPK/mTOR signaling.

74 cal Rac1 inhibition was combined with either AMPK beta1beta2 KO or alpha2KD, contraction-stimulated g

75 The Nisch mutations enhanced AMPK activation and inhibited mechanistic target of rapa

76 Eukaryotic AMPK exists as alphabetagamma complexes, whose regulator

77 ate that Rheb-WT can bind AMPK to facilitate AMPK activation, whereas Rheb-Y35N competitively binds A

78 human cells, using fluorescent reporters for AMPK activity, Akt activity, and cytosolic NADH/NAD(+) r

79 has previously been shown to be required for AMPK activation.

80 P-binding sites on AMPK are not required for AMPK activation.

81 cKO hearts because of upregulation of gamma1-AMPK, the lack of gamma2-AMPK sensitizes the heart to my

82 Here, we show that gamma2 AMPK activation downregulates fundamental sinoatrial cel

83 Deleting gamma2-AMPK led to increases in pre-rRNA level, ER stress marke

84 Increased gamma2-AMPK activity is required to protect against ischemia/re

85 del with cardiac-specific deletion of gamma2-AMPK (cardiac knockout [cKO]).

86 We sought to determine the role of gamma2-AMPK in cardiac stress response using bioengineered cell

87 veals an isoform-specific function of gamma2-AMPK in modulating ribosome biosynthesis, cell survival,

88 To study the function of gamma2-AMPK in the heart, we generated a mouse model with cardi

89 egulation of gamma1-AMPK, the lack of gamma2-AMPK sensitizes the heart to myocardial ischemia/reperfu

90 The gamma2-AMPK translocates into the nucleus to suppress pre-rRNA

91 Here, we sought to test the role of hepatic AMPK in the regulation of in vivo glucose-producing and

92 In summary, activation of hepatic AMPK/sirtuin-1 and FGF21/beta-klotho signaling pathways

93 numerous AMPK targets has helped explain how AMPK restores energy homeostasis.

94 Our findings suggest how AMPK activation by cyclin D1 may couple cell proliferati

95 id metabolism that were associated with IL6, AMPK and PPAR signal pathways.

96 Several studies have linked impaired AMPK function to peripheral metabolic diseases such as d

97 heb-Y35N competitively binds AMPK, impairing AMPK phosphorylation.

98 results indicate that Nisch is an important AMPK inhibitor and a critical regulator of energy homeos

99 Fluctuations in AMPK activity, Akt activity, and cytosolic NADH/NAD(+) r

100 ncluding the molecular basis of mutations in AMPK that alter cardiac physiology and the proposed mech

101 e observed a cyclin D1-mediated reduction in AMPK activation.

102 Accordingly, tensin silencing in AMPK-depleted fibroblasts impedes enhanced cell spreadin

103 tated cocaine-seeking behavior and increased AMPK and p70s6k phosphorylation in the NAc core but not

104 not detectably prevent energy stress-induced AMPK activation, it enforced mTORC1 activation despite t

105 r demonstration that GOF mutant p53s inhibit AMPK, our current study, establishes and demonstrates a

106 that depends on energy but not on the intact AMPK heterotrimer.

107 2 levels in aging lead to a blunted ischemic AMPK activation, alterations in substrate metabolism, an

108 ld-type aged hearts (i.e., impaired ischemic AMPK activation and higher sensitivity to ischemia- and

109 Of interest, ischemic AMPK activation was blunted in aged hearts compared with

110 To determine whether ischemic AMPK activation-modulated by the Sesn2-AMPK complex in t

111 The heterotrimeric kinase AMPK acts as an energy sensor to coordinate cell metabol

112 Activation of the master metabolic kinase AMPK enhances autophagy.

113 AMP-activated kinase (AMPK) is a key player in energy sensing and metabolic re

114 5' adenosine-monophosphate activated kinase (AMPK), and that the silencing or pharmacological inhibit

115 kinase beta, activates AMP-activated kinase (AMPK), leading to increased glucose uptake.

116 valuate the role of an AMP-dependent kinase (AMPK) activator, 5-aminoimidazole-4-carboxamide riboside

117 AMP-activated protein kinase (AMPK) activation triggered this pathway, which required

118 of aspirin to AMP-activated protein kinase (AMPK) activation, mTORC1 inhibition, and autophagy induc

119 In contrast AMP-activated protein kinase (AMPK) activation, which can be induced with metformin an

120 CR mediators, AMP-activated protein kinase (AMPK) and sirtuin-1 are activated.

121 The AMP-activated protein kinase (AMPK) and the Gsk3 kinase inhibit TOR during stress.

122 AMP-activated protein kinase (AMPK) and the homologous yeast SNF1 complex are key regu

123 its substrate, AMP-dependent protein kinase (AMPK) are important for HNK-mediated inhibition of pluri

124 tabolic sensor AMP-activated protein kinase (AMPK) as a beta1-integrin inhibitor in fibroblasts.

125 Activation of AMP-activated protein kinase (AMPK) by metformin, inhibition of mTORC by torin 1, or C

126 Hepatic AMP-activated protein kinase (AMPK) has been proposed to inhibit anabolic processes su

127 he activity of AMP-activated protein kinase (AMPK) in aged and Ang II-induced hypertrophic hearts in

128 by inhibiting AMP-activated protein kinase (AMPK) in renal cells.

129 ss mediated by AMP-activated protein kinase (AMPK) independently of HIF-1alpha.

130 The AMP-activated protein kinase (AMPK) is a key regulator of cellular and whole-body ener

131 AMP-activated protein kinase (AMPK) is a key sensor and regulator of glucose metabolis

132 sine monophosphate-activated protein kinase (AMPK) is a master regulator of energy homeostasis in euk

133 AMP-activated protein kinase (AMPK) is a metabolic stress-sensing enzyme responsible f

134 meostasis, and AMP-activated protein kinase (AMPK) is regulated, in part, by intracellular calcium, w

135 RATIONALE: The AMP-activated protein kinase (AMPK) is stimulated by hypoxia, and although the AMPKalp

136 onstrated that AMP-activated protein kinase (AMPK) modulates PXR transcriptional activity and that ph

137 olic regulator AMP-activated protein kinase (AMPK) plays a critical role in blocking modifications to

138 AMP-activated protein kinase (AMPK) plays an essential role as a cellular energy senso

139 onstrated that AMP-activated protein kinase (AMPK) regulates neuronal morphology and membrane excitab

140 ells activated AMP-activated protein kinase (AMPK) signaling and stimulated mitochondrial biogenesis

141 ivators of the AMP-activated protein kinase (AMPK) signaling pathway and this fact might explain the

142 se A (PKA) and AMP-activated protein kinase (AMPK) signaling pathways are activated, resulting in "br

143 gulate PKA and AMP-activated protein kinase (AMPK) to protect against DXR in part by activating the m

144 ting VEGFR2 or AMP-activated protein kinase (AMPK), a major decorin-activated energy sensor kinase, p

145 amycin (mTOR), AMP-activated protein kinase (AMPK), and autophagy pathways-processes implicated in lo

146 sine monophosphate-activated protein kinase (AMPK), and facilitated elongation of mitochondria along

147 activation of AMP-activated protein kinase (AMPK), because both inhibition of AMPK and IL-1R8 defici

148 tion activates AMP-activated protein kinase (AMPK), but it is unclear whether this activation occurs

149 we showed that AMP-activated protein kinase (AMPK), the master metabolic regulator of the cell, contr

150 anges activate AMP activated protein kinase (AMPK), which in turn directly suppresses sterol regulato

151 y by promoting AMP-activated protein kinase (AMPK)-dependent trafficking of KATP and Kv2.1 channels t

152 ion results in AMP-activated protein kinase (AMPK)-mediated acetyl-CoA synthetase 2 (ACSS2) phosphory

153 decreases the AMP-activated protein kinase (AMPK)-mediated phosphorylation of FOXO3a, a tumor suppre

154 sine monophosphate-activated protein kinase (AMPK)-play important roles in regulating physiological d

155 trate that the AMP-activated protein kinase (AMPK)-related protein Snf1-related kinase (SNRK) decreas

156 and activates AMP-activated protein kinase (AMPK).

157 expression via AMP-activated protein kinase (AMPK).

158 targeting the AMP-activated protein kinase (AMPK).

159 AMP-related kinase (AMPK) is an important cellular energy sensor in VSM.

160 re corroborated by showing that MEFs lacking AMPK activity also failed to up-regulate IFN-beta and TN

161 f LKB1 and the subsequent activation of LKB1-AMPK signaling.

162 lly, TGF-beta1 signaling suppressed the LKB1-AMPK axis, thereby facilitating the nuclear translocatio

163 rylation, which largely compromises the LKB1/AMPK signaling axis, in turn leading to the elevation of

164 ct, allosteric activator of all 12 mammalian AMPK complexes.

165 ivity and that pharmacologically manipulated AMPK activation exhibits an inverse relation to PXR acti

166 rodents and rhesus monkeys, MK-8722-mediated AMPK activation in skeletal muscle induced robust, durab

167 that AbetaO-induced, NMDA receptor-mediated AMPK inhibition may play a key role in early brain metab

168 e, Sesn2 is a scaffold protein that mediates AMPK activation in the ischemic myocardium via an intera

169 TXNIP and CNR2 agonists and a small-molecule AMPK inhibitor strongly synergized with glucocorticoids,

170 Moreover, AMPK-directed SIRT1 phosphorylation is required for ener

171 tabolic changes with higher levels of muscle AMPK, greater rates of oxygen consumption, and increased

172 g specific activation of the skeletal muscle AMPK pathway.

173 Notably, AMPK activation alone is sufficient to induce PTEN S-nit

174 The identification of numerous AMPK targets has helped explain how AMPK restores energy

175 Moreover, in the absence of AMPK, cells generate more mechanical stress and increase

176 Nuclear accumulation of AMPK complexes containing gamma2-subunit phosphorylated

177 Activation of AMPK by salicylate and the thienopyridone A-769662 is cr

178 we aimed to determine whether activation of AMPK is also a prerequisite for the ability of muscle co

179 While pharmacological activation of AMPK is anticipated to improve these parameters, the dis

180 cently demonstrated that prior activation of AMPK is sufficient to increase insulin sensitivity in mo

181 se model for DM1 (HSALR mice), activation of AMPK signaling in muscle was impaired under starved cond

182 Activation of AMPK was shown to downregulate PXR activity and, consist

183 Pharmacological or genetic activation of AMPK, similar to PON2 inhibition, blocks PDAC tumor grow

184 nversion of AICAR to the direct activator of AMPK, ZMP, did not reverse the effects on TNF-alpha-indu

185 rtant fibrosis target and that activators of AMPK, may be an important therapeutic approach for treat

186 s in AMP or ADP, the classical activators of AMPK.

187 gest that this lack of success is because of AMPK-mediated energy metabolism rewiring, protecting can

188 and the intrinsic energy sensing capacity of AMPK; features consistent with an AMP-induced myristoyl

189 l, we developed two signatures consisting of AMPK and HIF-1 downstream genes, respectively, to quanti

190 iggers the ubiquitination and degradation of AMPK-alpha2.

191 of 15d-PGJ2 partially rescued the effects of AMPK activation, suggesting the importance of Cox-1 in m

192 heart, but the isoform-specific function of AMPK remains unclear.

193 aling, mTORC1 inactivation is independent of AMPK activation during DENV infection.

194 To assess the influence of AMPK on the actin cytoskeleton in VSM of resistance arte

195 In contrast, inhibition of AMPK activity by intra-NAc core infusions of the AMPK in

196 e silencing or pharmacological inhibition of AMPK activity decreases DENV replication and the inducti

197 in kinase (AMPK), because both inhibition of AMPK and IL-1R8 deficiency abrogated the positive effect

198 AMPKalpha1 or pharmacological inhibition of AMPK blunted monocyte-to-macrophage differentiation and

199 n prevented the AbetaO-induced inhibition of AMPK.

200 n HepG2 cells, confirming the involvement of AMPK in the beneficial effects exerted by strawberry aga

201 nase B1 (LKB1), the major upstream kinase of AMPK, as the direct target of SIRT2.

202 Indeed, knockout of AMPK in RPE cells using Clustered Regularly Interspaced

203 Loss of AMPK also led to dephosphorylation at Ser-555 of the kno

204 Loss of AMPK promotes beta1-integrin activity, the formation of

205 advancements illustrate novel mechanisms of AMPK regulation, including changes in subcellular locali

206 liferation, we observed distinct patterns of AMPK activity, including both stable adaptation and high

207 Notably, the therapeutic potential of AMPK is widely recognized and heavily pursued for treatm

208 airment could be overcome by pretreatment of AMPK-deficient MEFs with type I IFN, illustrating that d

209 The regulation of AMPK activity in the NAc shell had no effect on cue-indu

210 ansient and leads to transient regulation of AMPK targets, unlike sustained activation by low glucose

211 y, the loss of SIRT2 blunted the response of AMPK to metformin treatment in mice infused with Ang II

212 Here, we investigated the role of AMPK activity in the nucleus accumbens (NAc) in relapse

213 e has been controversy regarding the role of AMPK in cancer, some of which may be due to functional d

214 portant and physiologically relevant role of AMPK in skeletal muscle.

215 In this review, we discuss the role of AMPK in the cardiovascular system, including the molecul

216 Our findings demonstrate a new role of AMPK in the control of actin cytoskeletal dynamics, pote

217 The potential role of AMPK in this setting is widely unknown.

218 es of investigation, the biological roles of AMPK and its potential as a drug target remain incomplet

219 er, the recently solved crystal structure of AMPK has shed light both into how nucleotides activate A

220 he latter encoding the regulatory subunit of AMPK.

221 expressing constitutively active subunits of AMPK decreased cue-induced reinstatement of cocaine seek

222 rus expressing dominant-negative subunits of AMPK increased cue-induced reinstatement of cocaine seek

223 serine/threonine protein kinase upstream of AMPK, failed to activate AMPK and sustain energy homeost

224 isorders, such as Alzheimer disease (AD), on AMPK function and downstream effects of altered AMPK act

225 rcise in mice, and show this is dependent on AMPK and ULK1 signaling.

226 108 phosphorylation by ULK1 was dependent on AMPK beta-subunit myristoylation, metabolic stress assoc

227 And this activation is not dependent on AMPK.

228 The effect of GDH1 on AMPK is evident in LKB1-deficient lung cancer, where AMP

229 gamma3 subunit translocated into nucleus on AMPK activation.

230 starvation, and intact AMP-binding sites on AMPK are not required for AMPK activation.

231 ar parameters including plasma lactate and p-AMPK/AMPK, as well as Ach-mediated vascular relaxation.

232 nstrate an increase in fatty acid content, p-AMPK, mitochondrial content, mitochondrial respiratory r

233 vel transcription-independent GOF mutant p53-AMPK-FOXO3a-FOXM1 signaling cascade that plays an import

234 esponse to DSS with higher levels of phospho-AMPK and lower levels of phosphorylation of mammalian ta

235 asis independently of Thr172 phosphorylation.AMPK is involved in sensing of metabolic stress.

236 ignaling pathway of VEGF/VEGFR2/calpain/PI3K/AMPK/Akt/eNOS.

237 le of calpain in mediating VEGF-induced PI3K/AMPK/Akt/eNOS activation through Ezrin.

238 d activation of Ulk proteins by potentiating AMPK-dependent phosphorylation.

239 While Us3 does not prevent AMPK activation by low energy, it enforces mTORC1 activa

240 ivated kinases Sty1 and Pmk1 did not promote AMPK activation but contributed to subsequent inactivati

241 SIRT2 promotes AMPK activation by deacetylating the kinase LKB1.

242 RATIONALE: AMPK (AMP-activated protein kinase) is a heterotrimeric

243 ensor of glucose availability that regulates AMPK.

244 and requires the central metabolic regulator AMPK for its replication and the induction of lipophagy.

245 Thus, DENV stimulates and requires AMPK signaling as well as AMPK-independent suppression o

246 As a result, AMPK-deficient MEFs exhibit impaired control of vesicula

247 on the regulatory beta1-subunit, sensitizing AMPK to allosteric drugs, and activates signaling pathwa

248 om secretory neurons via the nutrient sensor AMPK.

249 utive activation of the energy-stress sensor AMPK.

250 hemic AMPK activation-modulated by the Sesn2-AMPK complex in the heart-is impaired in aging that sens

251 Additionally, liver-specific AMPK alpha1 and alpha2 subunit KO and WT mice were utili

252 keletal muscle, suggesting a tissue-specific AMPK-dependent increase in TBC1D1-driven glucose uptake.

253 In the absence of applied low-energy stress, AMPK activity in infected cells was restricted in a Us3-

254 activates CamKK2 by enhancing its substrate AMPK binding, which contributes to energy production tha

255 TNF-alpha-induced CFB expression, suggesting AMPK-independent effects.

256 Pharmacological approaches targeting AMPK/mTORC1 signaling greatly ameliorated muscle functio

257 last 2 decades, it has become apparent that AMPK regulates several other cellular functions and has

258 ation and confocal microscopy, we found that AMPK induced depolymerization of F-actin (filamentous ac

259 Altogether, these results indicate that AMPK activity in the NAc core is critical for the cue-in

260 munoprecipitation experiments indicated that AMPK leads to the liberation of cofilin from 14-3-3 prot

261 responded normally to DMXAA, indicating that AMPK promotes STING-dependent signaling independent of U

262 by intracellular calcium, we postulated that AMPK participates in STING activation; however, its role

263 Further we show that AMPK activation by metformin reduced collagen III levels

264 Our findings suggest that AMPK regulates the activity of the chromatin modifying C

265 s compared with young hearts (P < 0.05); the AMPK downstream glucose uptake and the rate of glucose o

266 city and fatty acid oxidation, activated the AMPK-acetyl-CoA carboxylase pathway, and promoted ineffi

267 s cellular energy metabolism, activating the AMPK pathway in liver and muscle.

268 By applying the AMPK and HIF-1 signatures to The Cancer Genome Atlas pat

269 activity by intra-NAc core infusions of the AMPK activator 5-amino-1-beta-D-ribofuranosyl-imidazole-

270 t (P<0.05) increase in the expression of the AMPK cascade genes, involved in mitochondrial biogenesis

271 activity by intra-NAc core infusions of the AMPK inhibitor compound C or adenovirus expressing domin

272 of rapamycin pathways and activation of the AMPK pathway.

273 eceptor, reverses the abnormal levels of the AMPK-mTOR-S6K pathway and of active translation at synap

274 NUAK1 is a member of the AMPK-related family of kinases.

275 tivation of NUAK1 supports engagement of the AMPK-TORC1 metabolic checkpoint, thereby protecting tumo

276 es are associated with the activation of the AMPK/PGC1-alpha pathway.

277 Collectively, our data suggest that the AMPK-TBC1D4 signaling axis is likely mediating the impro

278 ogramme and fatty acid oxidation through the AMPK/PGC1-alpha pathway.

279 n antiatherosclerotic action in vivo via the AMPK-mediated blockage of Drp1-mediated mitochondrial fi

280 Here, we tested whether the AMPK activator metformin could affect the P23H rhodopsin

281 ated with elevated phosphorylation of Thr172-AMPK and Ser237-TBC1 domain family member 1 (TBC1D1) in

282 acts by upregulating microRNA let-7 through AMPK activation, leading to degradation of H19 long nonc

283 Low intracellular ATP leads to AMPK activation through phosphorylation of the activatio

284 Although the total AMPK activity was unaltered in cKO hearts because of upr

285 AMP/ADP-independent mechanism that triggers AMPK activation by sensing the absence of fructose-1,6-b

286 In turn, AMPK activates FOXO3A and its transcriptional target, PU

287 rial complex I subunit ND1, and the upstream AMPK/PGC1alpha signals.

288 ent regulation of mitochondrial function via AMPK.

289 ormal mice, but not when skeletal muscle was AMPK deficient.

290 evident in LKB1-deficient lung cancer, where AMPK activation predominantly depends on CamKK2.

291 ese findings uncover new mechanisms by which AMPK could potentially maintain cellular energy homeosta

292 siology and the proposed mechanisms by which AMPK regulates vascular function under physiological and

293 While AMPK normally stimulates TSC2-dependent inactivation of

294 encing either of the PKM isoforms along with AMPK in tumors.

295 aled that cardiac Sesn2 forms a complex with AMPK and upstream liver kinase B1 (LKB1) during ischemia

296 9 phosphorylation positively correlates with AMPK activity in glioma specimens and grades of glioma m

297 nce of fructose-1,6-bisphosphate (FBP), with AMPK being progressively activated as extracellular gluc

298 ischemic myocardium via an interaction with AMPK upstream LKB1.

299 e glucose transport in isolated muscles with AMPK loss of function combined with either pharmacologic

300 Fission yeast AMPK catalytic subunit Ssp2 is phosphorylated at Thr-189