ライフサイエンスコーパス: metabolic stress

1 osphorylation.AMPK is involved in sensing of metabolic stress.

2 wn of TFII-I alters the cellular response to metabolic stress.

3 umor cell survival upon serum deprivation or metabolic stress.

4 ling, reduced oxygen supply to the brain and metabolic stress.

5 r metastases must overcome hypoxia and other metabolic stress.

6 ting to beta-cell failure in the presence of metabolic stress.

7 mulation represented an adaptive response to metabolic stress.

8 s HSC lineage commitment under conditions of metabolic stress.

9 g the role of p73 to help cancer cells under metabolic stress.

10 adipose tissue expansion even under extreme metabolic stress.

11 eath often involves arrhythmias triggered by metabolic stress.

12 pH homeostasis of hippocampal neurons during metabolic stress.

13 pact the adaptation of beta cell function to metabolic stress.

14 e modes of metabolism enable cells to resist metabolic stress.

15 taining metabolic homeostasis in response to metabolic stress.

16 rmful stimuli such as pathogens, injury, and metabolic stress.

17 l effect of hepatic ABCA1 is decreased under metabolic stress.

18 o protect cells from the damaging effects of metabolic stress.

19 tream targets leading to cell survival under metabolic stress.

20 mal fetal growth and postnatal adaptation to metabolic stress.

21 as been shown to activate p53 in response to metabolic stress.

22 or protecting haematopoietic stem cells from metabolic stress.

23 glucose deprivation that protects cells from metabolic stress.

24 ilitate fat storage in WAT, despite on-going metabolic stress.

25 NA damage as a survival program to cope with metabolic stress.

26 eficient cells unable to appropriately sense metabolic stress.

27 tions by promoting cancer cell adaptation to metabolic stress.

28 n regulating responses to starvation-induced metabolic stress.

29 is hypothesis, Bax activation was induced by metabolic stress.

30 r layer of complexity to UPR activation upon metabolic stress.

31 licating c-MYC in the biological response to metabolic stress.

32 eostasis across the circadian cycle or under metabolic stress.

33 an essential mechanism protecting HSCs from metabolic stress.

34 erplay of apoptosis, autophagy, and cellular/metabolic stress.

35 cardiac sarcolemma turnover in dependence on metabolic stress.

36 nd proliferation to favour adaptation during metabolic stress.

37 indicated as mediators of resistance against metabolic stress.

38 ucose, glycogen, and lipid metabolism during metabolic stress.

39 pogenesis, FA oxidation, and lipolysis under metabolic stress.

40 oxidative cellular injury in the absence of metabolic stress.

41 of jak2 deletion in response to diet-induced metabolic stress.

42 buting to cellular resilience in the face of metabolic stress.

43 tty acid (FA) oxidation, and lipolysis under metabolic stress.

44 ellular homeostasis and cellular response to metabolic stress.

45 nase C (PKC) is involved in this response to metabolic stress.

46 pathways involved in neuronal adaptations to metabolic stress.

47 igm for maintaining tissue homeostasis under metabolic stress.

48 stresses, including calorie restriction and metabolic stress.

49 ic factor (BDNF) and increased oxidative and metabolic stress.

50 r total protein levels are affected by acute metabolic stress.

51 ivated Bax and decreased cell survival after metabolic stress.

52 ability of neurons to adapt to oxidative and metabolic stress.

53 for robust activation of LKB1 in response to metabolic stress.

54 targets for a number of conditions involving metabolic stress.

55 to developing steatohepatitis in the face of metabolic stress.

56 s conditions such as nutrient starvation and metabolic stress.

57 d apoptosis and improved cell survival after metabolic stress.

58 ne and recovery of cellular metabolism after metabolic stress.

59 ments increase under conditions of sustained metabolic stress.

60 rtant for myotube maintenance in response to metabolic stress.

61 P1 inhibits cell death induced by unresolved metabolic stress.

62 inflammation in VAT and liver in response to metabolic stress.

63 sing CaO2, thereby relieving cerebral oxygen metabolic stress.

64 ciated with the level of fetal hypoxemia and metabolic stress.

65 ntial against ccRCC development by relieving metabolic stress.

66 sensor in the liver under lipid overload and metabolic stress.

67 cell survival under conditions of sustained metabolic stress.

68 assemblies, and link this modification to a metabolic stress.

69 utes to calcium homeostasis in situations of metabolic stress.

70 to maintain early hyperproliferation during metabolic stress.

71 d chemokines in response to inflammatory and metabolic stress.

72 decreased cell survival under conditions of metabolic stress.

73 mitochondrial biogenesis and as a sensor of metabolic stress.

74 regulation of energy balance in response to metabolic stress.

75 ing pathway is implicated in the response to metabolic stress.

76 h governs cell-autonomous adaptations during metabolic stress.

77 d their contributions to the pathogenesis of metabolic stress.

78 s play a role in the activation of PKR under metabolic stress.

79 ing targets to protect cells or tissues from metabolic stress.

80 ity glucose transporter, GLUT3, to withstand metabolic stress.

81 observed in cells subjected to oxidative or metabolic stress.

82 f cellular energy homeostasis in response to metabolic stresses.

83 ver, their degradation can result in certain metabolic stresses.

84 toxic, oncogenic, thermal, inflammatory, and metabolic stresses.

85 pacity to increase glycolysis in response to metabolic stresses.

86 these conditions represent or reflect minor metabolic stresses.

87 ions with 14-3-3 increase during hypoxic and metabolic stress; 2) neuroglobin binding to 14-3-3 stabi

88 stress, p53 can promote cell survival during metabolic stress, a function that may contribute not onl

89 a potential mechanism by which exercise and metabolic stress activate the sodium pump in skeletal mu

90 her, the results unveil a mechanism by which metabolic stresses activate AMPK, which, in turn, phosph

91 Exposure of renal epithelial cells to metabolic stress activated GSK3beta, Bax, and caspase 3

92 ase in embryogenesis, reveal a mitochondrial metabolic stress-activated checkpoint in the control of

93 Under metabolic stress, activation of the AMP dependent Protei

94 tion METHODS: Survival of retinal neurons to metabolic stress after overexpression and knock-down of

95 iggered in RPE, we show that hypoxia-induced metabolic stress alone leads to photoreceptor atrophy.

96 In response to metabolic stress, AMPK maintains energy homeostasis by p

97 Upon metabolic stress, AMPK suppresses anabolic and promotes

98 agy, a highly conserved cellular response to metabolic stress and a catabolic process of self-digesti

99 locytomatosis oncogene (c-Myc), which led to metabolic stress and a defect in cell growth.

100 Metabolic stress and a physiological rise in glucagon lo

101 ion in glioma may be a response mechanism to metabolic stress and anticancer agents.

102 azolid suggested that its ability to trigger metabolic stress and apoptosis associated with tumor gro

103 ppress the PI3K-PDK1-Akt pathway and trigger metabolic stress and apoptosis.

104 cardiomyopathy.The mechanistic link between metabolic stress and associated cardiomyopathy is unknow

105 sma levels of glucagon are characteristic of metabolic stress and because this hormone stimulates ene

106 The data point to cross talk between metabolic stress and candidate genes at the beta-cell le

107 ldh1l1, similar to folate deficiency, evokes metabolic stress and causes apoptosis in cancer cells.

108 Metabolic stress and changes in nutrient levels modulate

109 against excessive ROS production induced by metabolic stress and could be a therapeutic target in tr

110 tion, providing a potential new link between metabolic stress and development of B and T lymphocytes.

111 Although SIRT1 activity is regulated by metabolic stress and DNA damage, its function in these s

112 (AMPK) family is required for adaptation to metabolic stress and energy homeostasis.

113 r processes critical for cell survival under metabolic stress and energy starvation is autophagy, a c

114 types of neuroinflammatory insults, namely, metabolic stress and exposure to amyloid beta fibrils, a

115 ogical events, encompassing viral infection, metabolic stress and genotoxic compounds.

116 gesting a potential mechanistic link between metabolic stress and HRG/TGZ-induced cell death.

117 Here we show that beta-cell metabolic stress and hyperglycemia enhance the prolifera

118 persisters to ampicillin form from the same metabolic stress and identify the shared and unique elem

119 skeletal muscles from young mice exposed to metabolic stress and in muscles from healthy older human

120 utrient deficiency, and hypoxia resulting in metabolic stress and increased DNA damage.

121 , these results identify a critical role for metabolic stress and invasive bacterial pathogens in U b

122 hway is activated under common conditions of metabolic stress and may have a role in the pathogenesis

123 y contribute to pubertal disorders linked to metabolic stress and negative energy balance.

124 d by its own family of enzymes responding to metabolic stress and participating in metabolic signalin

125 ECM detachment induces metabolic stress and programmed cell death via anoikis.

126 HSP90 chaperones, including TRAP-1, overcome metabolic stress and promote tumor cell metastasis by li

127 vior observed in cardiomyocytes subjected to metabolic stress and provides a new tool for examining h

128 important regulator of cancer survival under metabolic stress and resistance to apoptosis, which may

129 This allows cells to survive metabolic stress and seek out favorable growth condition

130 esults indicate that AMPK protects LICs from metabolic stress and that combining AMPK inhibition with

131 t pathways regulate p53 after DNA damage and metabolic stress and that inhibiting glucose metabolism

132 1 in modulating the cellular adaptability to metabolic stress and uncover a pivotal function of BAP1

133 rdiopulmonary reserve required to respond to metabolic stress and, therefore, are ideal to predict op

134 echanism for understanding how patients with metabolic stress and/or diabetes are predisposed to deve

135 perioperative immuno-nutrition, minimizing 'metabolic stress' and insulin resistance by preoperative

136 esis, increased synaptic aberrations, higher metabolic stress, and augmented inflammation.

137 te ROS in response to nutrient starvation or metabolic stress, and functions to inhibit autophagy.

138 dative stress, endoplasmic reticulum stress, metabolic stress, and genotoxic stress, as well as pathw

139 y MAGP1 is protective against the effects of metabolic stress, and its absence predisposes individual

140 ng glycolysis, sensing low-glutamine-induced metabolic stress, and promoting cellular adaptation to n

141 hagy in vitro and in vivo, at rest and after metabolic stress, and that TAT-p27 inhibits apoptosis by

142 etween genetic risk factors for AD, cellular metabolic stress, and transcription/translation regulati

143 mechanisms of cell death and survival under metabolic stress are not well understood.

144 are critical for OGT-mediated regulation of metabolic stress, as overexpression of stable HIF-1 or G

145 Metabolic stress, as well as several antidiabetic agents

146 pendent on AMPK beta-subunit myristoylation, metabolic stress associated with elevated AMP/ATP ratio,

147 association may be related to the effects of metabolic stress associated with mild hypoxia in individ

148 risk in pediatric SCA by relieving cerebral metabolic stress at patient- and tissue-specific levels.

149 ile tumor cells utilize autophagy to survive metabolic stress, autophagy also mitigates the resulting

150 bolism, which restores energy balance during metabolic stress both at the cellular and physiological

151 Myeloma cells counteracted the metabolic stress by activating autophagy.

152 A that interacts with PKR after induction of metabolic stress by palmitic acid (PA) treatment.

153 PRC also orchestrates a robust response to metabolic stress by promoting the expression of multiple

154 Thereby, during metabolic stress, cAMP and ppGpp control group II intron

155 may be an important adaptive response to the metabolic stress caused by alcohol intake and could pote

156 on stress via Rev1-deficiency contributes to metabolic stress caused by compromized mitochondrial fun

157 f ERBB2 that protects cells from anoikis and metabolic stress caused by decreased matrix adhesion.

158 MPK inhibition synergized with physiological metabolic stress caused by dietary restriction and profo

159 F21 is highly expressed in hepatocytes under metabolic stress caused by starvation, hepatosteatosis,

160 The resulting metabolic stress caused by these mutations or caused by

161 In preclinical trials toward metabolic stress, certain KL ADC can develop drug resist

162 brain-derived oligodendrocytes challenged by metabolic stress conditions (low nutrient/glucose).

163 ts of hyperglycemic and/or insulin-resistant metabolic stress conditions on human and mouse islets, w

164 derived OLs cultured under either optimal or metabolic stress conditions, deprivation of growth facto

165 ERK2 activation during metabolic stress contributes to changes in TCA cycle and

166 In particular, we show that during metabolic stress, cortical but not hippocampal astrocyte

167 At this point, the nitro oxidative metabolic stress develops and its action in vivo over ti

168 x signaling, whereby oxidants resulting from metabolic stress directly alter protein palmitoylation b

169 ulated insulin secretion and the response to metabolic stress, e.g., glucolipotoxicity, in beta-cells

170 ive effect of DDT required activation of the metabolic stress enzyme AMP-activated protein kinase (AM

171 Metabolic stress evokes significant penetration of comme

172 Here, we report a novel mechanism by which metabolic stress facilitates proteasomal degradation of

173 e, TBC1D5 shuttling to autophagosomes during metabolic stress facilitates retromer-dependent GLUT1 tr

174 Chronic metabolic stress factors found in CKD promote vascular K

175 by which other stimuli such as cytokines or metabolic stress function to stimulate NF-kappaB activat

176 The prevalence of cardiomyopathy from metabolic stress has increased dramatically; however, it

177 s (nitrosocysteine and hydrogen peroxide) or metabolic stress (high palmitate and high glucose) inact

178 rrier is stimulated during acute and chronic metabolic stress; however, the mechanism of acute transp

179 opment in vivo but its overactivation during metabolic stress impairs neuronal polarization in a mTOR

180 amine how leukemia-initiating cells react to metabolic stress imposed by different tissue environment

181 ugh repression of DPYD expression, following metabolic stress imposed by nucleotide imbalance.

182 milation and biosynthesis in accord with the metabolic stress imposed by oxidative and nitrosative st

183 osamine-induced or genome instability-driven metabolic stress in a murine model of hepatocarcinoma.

184 es in mediating the inflammatory response to metabolic stress in different tissues and highlight the

185 It was hypothesized that maternal calcium metabolic stress in early pregnancy, rather than subopti

186 in this study highlights a potential role of metabolic stress in genomic instability and therapeutic

187 th-receptor activation or starvation-induced metabolic stress in human and murine macrophages increas

188 tion, Gatm(c/c) colonocytes showed increased metabolic stress in response to DSS with higher levels o

189 ose found in vertebrates, including inducing metabolic stress in sensory cells.

190 However, in mice PKR is also activated by metabolic stress in the absence of viral infection, and

191 he impact of RNS60 on the response of OLs to metabolic stress in vitro (glucose-nutrient deprivation,

192 r-osmotic conditions tested did not impose a metabolic stress, in as much as the metabolic network is

193 tes survival of renal epithelial cells after metabolic stress, in part by inhibiting Bax in a phospha

194 of p53 Ser18 (murine Ser15) led to increased metabolic stress, including severe defects in glucose ho

195 ive response to maintain cell survival under metabolic stresses, including androgen deprivation.

196 ocks apoptosis induced by multiple cytotoxic metabolic stresses, including deprivation of glucose or

197 rotects the heart against different types of metabolic stresses, including ischaemia/reperfusion and

198 olve in response to certain environmental or metabolic stresses, including the presence of oxygen?

199 Here we show that metabolic stresses induce AMPK-mediated phosphorylation

200 nd NF-kappaB in protecting cancer cells from metabolic stress induced by inhibiting FAS.

201 did reduce the sensitivity of U2OS cells to metabolic stress induced by metformin, PML loss did not

202 Diverse metabolic stresses induced Ser473 phosphorylation of KAP

203 entify an indispensable function of ROCK1 in metabolic stress-induced autophagy.

204 grity has therapeutic potential for treating metabolic stress-induced cardiomyopathy.The mechanistic

205 a critical step in monocyte priming and the metabolic stress-induced conversion of blood monocytes i

206 ession of MKP-1 protects macrophages against metabolic stress-induced dysfunction.

207 mitochondrial sirtuin activity, and prevents metabolic stress-induced non-alcoholic fatty liver disea

208 Mechanically, we show that BAP1 represses metabolic stress-induced UPR and cell death through acti

209 nd correlates with its ability to dampen the metabolic stress-induced UPR transcriptional network.

210 OR complex 1 (mTORC1) and sensitivity to the metabolic stress inducer phenformin.

211 ing those representing pathways in oxidative/metabolic stress, inflammation, DNA damage-repair, and a

212 Overcoming metabolic stress is a critical step for solid tumour gro

213 Overcoming metabolic stress is a critical step in tumor growth.

214 The ability to sense metabolic stress is critical for successful cellular ada

215 t potentially leads to PKR activation during metabolic stress is unknown.

216 mitter in the brain, but under conditions of metabolic stress it can accumulate to excitotoxic levels

217 During metabolic stress, LC3(+) autophagic compartments bind an

218 In normal cells, such metabolic stress leads to inhibition of signaling throug

219 notype and function and its dysregulation by metabolic stress may be a major contributor to atherogen

220 tive defense mechanism" and "insulin-induced metabolic stress" may provide explanation for some of th

221 rtantly, LMO4 palmitoylation is sensitive to metabolic stress; mice challenged with a brief high-fat

222 Metabolic stress modeled by anisomycin, thapsigargin, or

223 ic subunit of AMPK (dnAMPK), suggesting that metabolic stress modulates TREK channels by an AMPK mech

224 ditional areas of metabolism impacted by the metabolic stress of 2AA in Salmonella enterica.

225 sponse (UPR) and angiogenesis to survive the metabolic stress of hypoxia.

226 l is elevated in retina by oxidative stress, metabolic stress of insulin-deficient diabetes, or light

227 in" primary immune mediated and "inside-out" metabolic stress of oligodendrocyte (OL) related mechani

228 ogical changes that impose both cellular and metabolic stress on the liver.

229 prevents spurious activation in response to metabolic stress or low doses of TNF.

230 trains disruption of luxS caused significant metabolic stress or no stress at all.

231 asis and protects the cell during periods of metabolic stress or nutrient deprivation.

232 ant survival mechanism in cancer cells under metabolic stress or subjected to chemotherapy.

233 epatic induction of FGF21 is limited to only metabolic stress, or to a more general hepatic stress re

234 Thus, death by metabolic stress parallels cellular attempts to survive.

235 combining AMPK inhibition with physiological metabolic stress potently suppresses AML by inducing oxi

236 nced sensitivity to apoptosis in response to metabolic stress (pre-B cell receptor crosslinking, onco

237 g and to adapt beta-cell mass in response to metabolic stress, pregnancy hormones, and acute inductio

238 rived hormones to prepare the mother for the metabolic stress presented by fetal development and to e

239 Here we show that internal metabolic stress produced by reactive intermediates resu

240 Metabolic stress promoted the S-glutathionylation of MKP

241 These results suggest that metabolic stress rapidly stimulates blood-brain barrier

242 Maternal calcium metabolic stress, rather than low calcium intake or insu

243 ated JNK activation plays a critical role in metabolic stress regulation of the JNK signaling pathway

244 by which AMPK mediates cellular responses to metabolic stress remain unclear.

245 function, mechanisms of action, and roles in metabolic stress remain unknown.

246 The cross-talk between UPR activation and metabolic stress remains largely unclear.

247 e role of mutant p53 (mutp53) in response to metabolic stress remains unclear.

248 When confronted with metabolic stress, replicative Legionella pneumophila bac

249 Through AMPK activation, metabolic stress represses HSF1, rendering cells vulnera

250 promotes glucose-independent cell growth and metabolic stress resistance in human tumors.

251 MPK), a metabolic checkpoint kinase, confers metabolic stress resistance to leukemia-initiating cells

252 Thus, a metabolic stress response is established and propagated

253 As in general and as an upstream mediator of metabolic stress response pathways through the regulatio

254 e Escherichia coli small RNA SgrS controls a metabolic stress response that occurs upon accumulation

255 ics, we speculate that metformin may block a metabolic stress response that stimulates the inflammato

256 tivates AMPK and thereby interferes with the metabolic stress response.

257 (JNK) signaling pathway is a key mediator of metabolic stress responses caused by consuming a high-fa

258 Yet, accumulating metabolic stress resulting from as few as four rounds of

259 We propose that metabolic stress resulting from recurring SDs facilitate

260 gramming during prostate carcinogenesis, the metabolic stress role in tumor survival, and the diagnos

261 The metabolic-stress sensing protein kinase GCN2 is a primar

262 ted protein kinase (AMPK) is a nutrient- and metabolic stress-sensing enzyme activated by the tumor s

263 AMP-activated protein kinase (AMPK) is a metabolic stress-sensing enzyme responsible for maintain

264 They find that inhibition of the metabolic stress sensor AMP-activated protein kinase (AM

265 ndings uncover a novel interplay between the metabolic stress sensor AMPK and the proteotoxic stress

266 tream, DRP1 activity regulated the essential metabolic stress sensor, AMP-activated protein kinase (A

267 The study shows that K-Ras is a target of a metabolic stress-signaling pathway that can be leveraged

268 tic evidence for p53-mediated integration of metabolic stress signals, which modulate the activity of

269 godendrogliopathy has been linked with local metabolic stress, similar to the penumbra of ischemic/hy

270 no acid catabolism is especially relevant in metabolic stress situations (e.g. limited carbohydrate a

271 ogical interventions such as ARVs can induce metabolic stress, skewing the cell's immune response and

272 AMPK, a key sensor of metabolic stress stabilizes cell-cell junctions and main

273 insulin resistance that occur in response to metabolic stresses such as obesity and cytokine stimulat

274 P concentrations increase significantly upon metabolic stress, such as glucose deprivation in yeast.

275 lls and was associated with the induction of metabolic stresses, such as AAS or endoplasmic reticulum

276 Surprisingly, we discovered that metabolic stress suppresses the PSR.

277 drocyte progenitor cells under conditions of metabolic stress that model the initial relapsing and su

278 ch signifies a decrease in energy) caused by metabolic stresses that interfere with ATP production (e

279 With prolonged metabolic stress, the absence of Atg7 resulted in augmen

280 ogical and pathological consequences of this metabolic stress, the adaptive responses that cells util

281 t intervals, as a consequence of physical or metabolic stress, the virus is activated and transported

282 c membrane structure and function even under metabolic stress, thereby identifying cardiolipin syntha

283 f a growth state that provides resistance to metabolic stress through excess redox and energy product

284 y circuit that functions under conditions of metabolic stress to control systemic energy homeostasis

285 can trigger the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and p

286 truistic mechanism to eliminate cells during metabolic stress to the advantage of a multicellular org

287 t link the sensing of microbial products and metabolic stress to the proteolytic activation of the pr

288 er homeostatic conditions and in response to metabolic stress using mice with hepatocyte-specific del

289 Intriguingly, exposing neurons to extreme metabolic stress using oxygen/glucose deprivation (OGD)

290 Acute cellular metabolic stress was induced by glucose depletion, by po

291 The PRC response to metabolic stress was investigated by subjecting cells to

292 The essential role of HRas in metabolic stress was made evident by the similar effects

293 d OL spare respiratory capacity (SRC) when a metabolic stress was present.

294 (36%, 38%, and 40%), as a metric of regional metabolic stress, were compared pre- and posttransfusion

295 early universal cell death in the absence of metabolic stress, whereas expression of active Bax or NP

296 own of MKP-1 mimicked the priming effects of metabolic stress, whereas MKP-1 overexpression blunted b

297 tegrated response to insulin stimulation and metabolic stress, which associates with reduced Tyr(P)(I

298 es Bax-mediated apoptosis after induction of metabolic stress, which occurs during renal ischemia, we

299 ral for promoting cellular adaptation during metabolic stress while also functioning as a cellular ho

300 a core component of beta-cell adaptation to metabolic stress, with failure of this response from imp