ライフサイエンスコーパス: bioenergetic

1 pression of genes important in mitochondrial bioenergetics.

2 at ncOGT is a negative regulator of cellular bioenergetics.

3 nd enables reuse of organelle components for bioenergetics.

4 adaptive response to stimulate mitochondrial bioenergetics.

5 s by connecting ROS partitioning to cellular bioenergetics.

6 s, problems that are at the core of cellular bioenergetics.

7 increased mitochondrial biogenesis and tumor bioenergetics.

8 chondrial calcium transfer and mitochondrial bioenergetics.

9 ntial for functions apart from mitochondrial bioenergetics.

10 ll invasion without changes in mitochondrial bioenergetics.

11 microaerobic conditions to maintain membrane bioenergetics.

12 thermodynamic reference for calibrating PSII bioenergetics.

13 er doxorubicin, confirming impaired cellular bioenergetics.

14 es mitochondrial RNA (mtRNA) homeostasis and bioenergetics.

15 in many genes associated with mitochondrial bioenergetics.

16 tochondrial dysfunction and inhibiting tumor bioenergetics.

17 oxygen-deficient niches to maintain cellular bioenergetics.

18 ing to a general and important role in their bioenergetics.

19 bnormalities suggestive of impaired cellular bioenergetics.

20 d SOD2 expression and improved mitochondrial bioenergetics.

21 AMPK axis is critical to support cancer cell bioenergetics.

22 of mitochondrial DNA (mtDNA) alterations of bioenergetics.

23 ese signaling pathways as mediators of tumor bioenergetics.

24 central role in cellular energy sensing and bioenergetics.

25 ls plays a key role in shaping mitochondrial bioenergetics.

26 than widely used in discussions of bacterial bioenergetics.

27 ereas ncOGT predominantly regulates cellular bioenergetics.

28 luteotropin, and estrogen, on corneal stroma bioenergetics.

29 e regulation of mitochondrial biogenesis and bioenergetics.

30 lect intracellular ATP turnover and cellular bioenergetics.

31 the circadian clock governs skeletal muscle bioenergetics.

32 mportant role in mitochondrial processes and bioenergetics.

33 ndrial membrane potential, and mitochondrial bioenergetics.

34 se in FECD indicated deficient mitochondrial bioenergetics.

35 ty control, maintaining the functionality of bioenergetics.

36 Brain bioenergetic abnormalities have been observed frequently

37 Converging evidence suggests bioenergetic abnormalities in bipolar disorder (BD).

38 d endophenotypes of schizophrenia as well as bioenergetic abnormalities.

39 lly inhibits the mitochondrial complex I and bioenergetic activity in mammalian systems.

40 ndrial morphology may act as a mechanism for bioenergetic adaptation during cardiac pathological remo

41 Using transcriptomics and bioenergetic analysis, we discovered that DF induces gly

42 to enhance the propagation of intracellular bioenergetic and apoptotic waves through mitochondrial n

43 xited G0 but stalled in S phase, due to both bioenergetic and biosynthetic defects.

44 Beyond meeting the bioenergetic and biosynthetic demands of T-cell differen

45 To accommodate increased bioenergetic and biosynthetic demands, metabolic pathway

46 Tumour cells fulfil the bioenergetic and biosynthetic needs of proliferation usi

47 s and how they are utilized to satisfy their bioenergetic and biosynthetic needs.

48 switch between growth states with different bioenergetic and biosynthetic requirements.

49 By providing bioenergetic and biosynthetic substrates, autophagy supp

50 ogrammed glucose metabolism will disrupt the bioenergetic and biosynthetic supply for uncontrolled gr

51 In the young adult brain, differences in bioenergetic and immunoregulatory pathways were the majo

52 ssion of molecular chaperones, antioxidants, bioenergetic and protein synthesis biomarkers) to experi

53 in resistance causes alterations in cellular bioenergetics and activation of inflammatory signaling i

54 Our methodology combines optical bioenergetics and advanced signal processing and allows

55 chondrial biogenesis, improved mitochondrial bioenergetics and attenuated mitochondria-regulated apop

56 genation by maintaining better mitochondrial bioenergetics and by decreasing ROS.

57 ondrial Ca(2+) uptake, a process crucial for bioenergetics and Ca(2+) signaling, is catalyzed by the

58 vels, and deregulation of both mitochondrial bioenergetics and Ca(2+)homeostasis was rescued by Mcl-1

59 are fundamental mechanisms for mitochondrial bioenergetics and cell function.

60 cell cycle progression, repair/maintenance, bioenergetics and cell-cell signaling - whose disrupted

61 g AMPKalpha1 displayed reduced mitochondrial bioenergetics and cellular ATP in response to glucose li

62 e investigated reactivation of mitochondrial bioenergetics and dynamics using Arabidopsis thaliana as

63 Virtual fish were realistic both in terms of bioenergetics and feeding.

64 These changes impact T cell bioenergetics and function.

65 e Mfn2 overexpression enhances mitochondrial bioenergetics and functions, and promotes the differenti

66 of Bnip3 knockdown on adipose mitochondrial bioenergetics and glucose disposal.

67 of mitochondrial CypD results in a shift in bioenergetics and in activation of glucose-metabolism re

68 atic airway epithelium with consequences for bioenergetics and inflammation.

69 rely on multiple nutrients to meet cellular bioenergetics and macromolecular synthesis demands of ra

70 larly dependent on glucose and glutamine for bioenergetics and macromolecule biosynthesis.

71 oxidative phosphorylation complexes, altered bioenergetics and metabolic shift are often seen in canc

72 Bioenergetics and mitochondrial DNA (mtDNA) damage were

73 nteract HD-related deficits in mitochondrial bioenergetics and motor function.SIGNIFICANCE STATEMENT

74 Differences in mitochondrial bioenergetics and mtDNA damage associated with maternal

75 pt and whether SIRT5 regulates mitochondrial bioenergetics and neuroprotection against cerebral ische

76 of these methodologies can help tease apart bioenergetics and other biological complexities in C. el

77 nk TDP-43 toxicity directly to mitochondrial bioenergetics and propose the targeting of TDP-43 mitoch

78 rough TRPM2 is required to maintain cellular bioenergetics and protect against hypoxia-reoxygenation

79 fies HSF1 as a central regulator of cellular bioenergetics and protein homeostasis that benefits mali

80 ic approach in form of altered mitochondrial bioenergetics and redox status of cancer cells with unde

81 n lymphatic muscle cells (LMCs) affects cell bioenergetics and signaling pathways that consequently a

82 holipid with critical roles in mitochondrial bioenergetics and signaling.

83 ajor ion reservoir that can be mobilized for bioenergetics and signaling.

84 LPS-induced TLR4 activation alters cellular bioenergetics and triggers proteolytic cleavage of AMPKa

85 mitochondrial metabolism to maintain T cell bioenergetics and viability.

86 Bok controls neuronal Ca(2+)homeostasis and bioenergetics and, contrary to previous assumptions, exe

87 ual roles of mitochondria in ATP production (bioenergetics) and apoptosis (cell life/death decision)

88 ake, a process crucial for Ca(2+) signaling, bioenergetics, and cell death.

89 l functions, mitochondrial functions such as bioenergetics, and functions related to transcription su

90 omena that are also at play in photobiology, bioenergetics, and information processing.

91 is work resolves a long-standing question in bioenergetics, and renders a chemical-biological basis f

92 g the integrity of the genome and sustaining bioenergetics are both fundamental functions of the cell

93 Mitochondrial bioenergetics are critical for cellular homeostasis and

94 rgeting mitochondria protection and cellular bioenergetics are presented, with emphasis on those that

95 gaba mutants display a general disruption in bioenergetics as measured by altered levels of tricarbox

96 The enhancement of mitochondrial bioenergetics as well as the increase in mitochondrial p

97 rial biogenesis, coupled with aberrant tumor bioenergetics, as a potential therapy escape mechanism a

98 secting fields of mitochondrial dynamics and bioenergetics, as treatment of defective dynamics in mit

99 TMX1 reduce ER-mitochondria contacts, shift bioenergetics away from mitochondria, and accelerate tum

100 Mitochondria are bioenergetic, biosynthetic, and signaling organelles tha

101 by a prolonged deregulation of mitochondrial bioenergetics.bok deficiency led to a specific reduction

102 ected proteostasis to maintain mitochondrial bioenergetics, buffer oxidative stress, and enable metas

103 ative phosphorylation is central to cellular bioenergetics but cumbersome to measure.

104 e of BMI1 in the regulation of mitochondrial bioenergetics, but also provide new mechanistic insights

105 r the risk of proteotoxic stress to preserve bioenergetics, but the role of these mechanisms in disea

106 ed to occur independently of follicular bulb bioenergetics by a tractor mechanism involving the inner

107 pocytes were additionally examined for their bioenergetics by extracellular flux analysis as well as

108 Improving bioenergetics by overexpression of PGC-1alpha enhanced f

109 Real-time monitoring of changes to cellular bioenergetics can provide new insights into mechanisms o

110 onging to haplogroup L had decreased maximal bioenergetic capacities compared with haplogroup H.

111 velop BPD or die have impaired mitochondrial bioenergetic capacity and produce more oxidants at birth

112 esis and OXPHOS assembly events and thus the bioenergetic capacity of the mitochondria.

113 s overall flexibility of ATP supply; and the bioenergetic capacity quantifies the maximum rate of tot

114 Differences in bioenergetic capacity were also observed in that human u

115 drial trafficking and altering mitochondrial bioenergetic capacity.

116 y and increased ROS levels, culminating in a bioenergetic catastrophe.

117 ORP4L knockdown results in suboptimal bioenergetics, cell death and abrogation of T-ALL engraf

118 of all mammalian tissues, where it regulates bioenergetics, cell death, and Ca(2+) signal transductio

119 Therefore, T cell remodeling represents a bioenergetic challenge to mitochondria.

120 At the molecular level, bioenergetic challenges result in the activation of tran

121 Brain cells normally respond adaptively to bioenergetic challenges resulting from ongoing activity

122 st that lifestyles that include intermittent bioenergetic challenges, most notably exercise and dieta

123 Mitochondria respond to bioenergetic changes by continuous fission and fusion.

124 data indicate a mechanistic link between the bioenergetic characteristics of different muscle fibre t

125 The CP reflects the bioenergetic characteristics of highly oxidative type I

126 ings indicate a mechanistic link between the bioenergetic characteristics of muscle fibre types and t

127 broblasts displayed suppressed mitochondrial bioenergetics consistent with a lower substrate availabi

128 In pancreatic beta-cells, mitochondrial bioenergetics control glucose-stimulated insulin secreti

129 ke and mitochondrial pyruvate import prevent bioenergetic crises and allow LLPCs to persist.

130 xon-Schwann cell relationship and associated bioenergetic crosstalk, and the rapid expansion of our k

131 rial biogenesis and consequent mitochondrial bioenergetic defect could contribute to the neurodegener

132 The bioenergetics defect in AOA1-mutant fibroblasts and APTX

133 protein complexes, leading to rescue of the bioenergetic defects and cell death caused by mutations

134 omplexes, thereby likely contributing to the bioenergetic defects characteristic of AD.

135 zation-defective mutant BMI1 rescued several bioenergetic defects that we observed in BMI1-depleted c

136 d with inhibition of mitochondrial fusion or bioenergetic defects, supporting the possibility that MA

137 a, acutely lowered SNPH levels, resulting in bioenergetics defects and increased superoxide productio

138 an adaptive response to manassantin-induced bioenergetic deficiency, mammalian cells up-regulated ae

139 ) experience mitochondrial dysfunction and a bioenergetic deficit that occurs early and promotes the

140 oxicity also resulted in mitochondrial loss, bioenergetic deficits, and increased PARKIN mitochondria

141 tes ROS production and may contribute to the bioenergetic differences between neurons and astrocytes.

142 arian cancer cell lines revealed significant bioenergetics diversity.

143 of mitochondrial mass and abrogates cellular bioenergetics during degeneration of post-mitotic cells

144 Deficits in bioenergetics during early postnatal brain development c

145 mming of hepatocellular lipid metabolism and bioenergetics during HCV infection, which are predicted

146 econd-messenger production and mitochondrial bioenergetics during oxidative stress.

147 toration of N source preference and cellular bioenergetics during the early stage of recovery; (2) fl

148 Here, we report a neglected but important bioenergetic effect of mTOR inhibition in neurons.

149 Finally, we found differential bioenergetic effects of palmitate and glucose on resting

150 tling between normoxia and hypoxia, maintain bioenergetic efficiency and stably uphold antiapoptotic

151 onal energy requirements at the synapse, and bioenergetic failure at the synapse may impair neural tr

152 Live-cell bioenergetic flux analysis confirmed that mensacarcin di

153 dentify whether differences in mitochondrial bioenergetic function and oxidant generation in human um

154 unidentified mammalian NDH-2 enzymes, whose bioenergetic function could be supplemental NADH oxidati

155 pport a model that includes changes in brain bioenergetic function in subjects with major depression.

156 rns, muscle fibre contractile properties and bioenergetic function, can impact force-generating capac

157 detail the central subunits that execute the bioenergetic function.

158 altered mitochondrial dynamics; and reduced bioenergetic function.

159 whether polymeric NTs keep endosomolytic and bioenergetic functions of NTs in drug delivery and cell

160 through a pathway distinct from that of its bioenergetic functions.

161 he detection of analytes central to cellular bioenergetics: glucose, lactate, oxygen, and pH.

162 Mitochondrial bioenergetics has been implicated in a number of vital c

163 hondrial dysfunction and associated cellular bioenergetics has been recently identified as a promisin

164 l (Deltapsi), which is central to organismal bioenergetics, has been successfully measured via flow c

165 is, phototoxic cell death, and mitochondrial bioenergetic homeostasis.

166 o unsuspected functionality for 1,5-InsP8 to bioenergetic homeostasis.

167 nt for maintaining cardiac and mitochondrial bioenergetic homeostasis.

168 other proton-selective molecules engaged in bioenergetics, homeostasis, and signaling.

169 Body-wide changes in bioenergetics, i.e., energy metabolism, occur in normal

170 We evaluated mitochondrial bioenergetics in 10 sets of LCLs from children with ASD,

171 -RELB-SIRT3 adaptation link to mitochondrial bioenergetics in both TLR4-stimulated normal and sepsis-

172 HCFs revealing a novel role for hormones on bioenergetics in KC.

173 onfirmed that miR-29a inhibits mitochondrial bioenergetics in LCC9 cells.

174 kinase) activation and altered mitochondrial bioenergetics in MTC cells, as indicated by depolarized

175 PGC-1alpha and Tug1 modulates mitochondrial bioenergetics in podocytes in the diabetic milieu.

176 of evidence suggests abnormalities in brain bioenergetics in psychiatric disorders, including both b

177 Examination of mitochondrial bioenergetics in stable cell lines overexpressing GFP-ta

178 Assessments of mitochondrial bioenergetics in the cortex of wild type (WT) and SIRT5-

179 t obese women exhibit impaired mitochondrial bioenergetics in the form of decreased efficiency and im

180 haracterized the effects of CypD ablation on bioenergetics in the kidney.

181 ssociated with improvements in mitochondrial bioenergetics in the podocytes of diabetic mice.

182 haviors and motor function, as well as brain bioenergetics, in a mouse model (luc) carrying a spontan

183 al deregulation and changes in mitochondrial bioenergetics, including pyruvate dehydrogenase (PDH) dy

184 xpression, fragmented mitochondria, impaired bioenergetics, increased autophagy and mitophagy.

185 tion, dynamically modulated by mitochondrial bioenergetics, independent of known inter-mitochondrial

186 We report findings on the bioenergetic interplay of astrocytes and neurons and dis

187 Suppression of T cell bioenergetics involved restricted glucose uptake and use

188 transport activities without perturbation by bioenergetics ion fluxes encountered in vivo.

189 Reactivation of mitochondrial bioenergetics is followed by dramatic reorganization of

190 ssociation is reflected in the intramuscular bioenergetics is unknown.

191 ributions from oxidative and substrate-level bioenergetics is unknown.

192 sphate carrier (PiC), encoded by SLC25A3, in bioenergetics is well accepted.

193 t role for 14-3-3zeta in regulating platelet bioenergetics, leading to decreased platelet PS exposure

194 In total, this bioenergetic liquid exhibits increased energy output and

195 idem were recently shown to be protective of bioenergetic loss in cell models of optic neuropathy.

196 proteome, is of paramount importance for the bioenergetic machinery of oxidative phosphorylation that

197 ATP synthase is the most prominent bioenergetic macromolecular motor in all life forms, uti

198 abolism, occur in normal aging and disturbed bioenergetics may be an important contributing mechanism

199 These studies shed light on the unique bioenergetic mechanisms within astrocytes that may contr

200 In this study, we showed that this bioenergetics mechanistic modeling approach provided a p

201 irment in multiple interacting components of bioenergetic metabolism may be a key mechanism contribut

202 Mitochondria are responsible for bioenergetics, metabolism and apoptosis signals in healt

203 des are redox coenzymes that are critical in bioenergetics, metabolism, and neurodegeneration.

204 We used a spatio-temporal bioenergetics model of the Northeast Pacific Ocean to qu

205 ics data from the literature, to construct a bioenergetics model to quantify predation rates on key f

206 and abiotic parameters can be obtained, then bioenergetics modelling offers an alternative approach t

207 dent upon prey availability than traditional bioenergetic models suggest.

208 Bioenergetics models indicate that the sharks require ap

209 cy in the pass and feeding behavior and used bioenergetics models to understand energy flow.

210 y (31P MRS) allows for the quantification of bioenergetic molecules, containing high-energy phosphate

211 ired oxidative phosphorylation to meet their bioenergetic needs.

212 necessary to simulate the kinetics of muscle bioenergetics observed in humans.

213 (+) T cells were already unable to match the bioenergetics of effector T cells generated during acute

214 d human osteosarcoma clones and explored the bioenergetics of IF1 null cancer cells.

215 The bioenergetics of IF1 transiently silenced cancer cells h

216 whether bone marrow stromal cells impact the bioenergetics of primary CLL cells.

217 In this study, we defined the bioenergetics of Th17 effector cells generated in vivo.

218 organelles occupy a critical position in the bioenergetics of the cardiovascular system, mitophagy is

219 ought to have been needed to account for the bioenergetics of the first single-celled organisms.

220 rentiation has been extensively studied, the bioenergetics of Treg cell trafficking remains undefined

221 e-purposing of these fuels for biosynthetic, bioenergetic or signaling pathways.

222 hloroplasts and mitochondria are subcellular bioenergetic organelles with their own genomes and genet

223 preciated for their role as biosynthetic and bioenergetic organelles.

224 microscopy was used to study functional and bioenergetic parameters in cardiomyocytes isolated after

225 of H2S-producing enzymes suppresses critical bioenergetics parameters in lung adenocarcinoma cells.

226 tetrapyrrole(s) in a unique redox-regulated bioenergetic pathway governing terminal megakaryocytopoi

227 l epithelial cell line accelerated oxidative bioenergetic pathways and suppressed hypoxia-inducible f

228 ing appreciation that cellular metabolic and bioenergetic pathways do not play merely passive roles i

229 Bioenergetic pathways have emerged as important regulato

230 a novel mechanism via which MeCP2 regulates bioenergetic pathways in microglia and suggest a therape

231 Moreover, multiple bioenergetic pathways, including aerobic glycolysis, oxi

232 and phosphoproteome and reveal signaling and bioenergetics pathways that mediate lymphocyte exit from

233 The bioenergetics phenotype of ovarian cancer cell lines cor

234 We introduce novel indices to quantify bioenergetic phenotypes.

235 physiological role is important for cellular bioenergetic plasticity and may contribute to Oma1-assoc

236 istory, there is no reason to think membrane bioenergetics played a direct, causal role in the transi

237 in this study suggest that endosomolytic and bioenergetic pNTs serve as a non-toxic gene carrier comp

238 This alters the bioenergetic potential and mitochondrial activity of mel

239 data revealed that genomic regions encoding bioenergetic processes are under selection in PAH-adapte

240 to our knowledge, the first evidence of how bioenergetic processes determine flux through monoterpen

241 ed utilization of glutamine for anabolic and bioenergetic processes.

242 xysmal manifestations and a normalised brain bioenergetics profile in patients with GLUT1-DS.

243 We investigated the bioenergetic profiles of fibroblasts from LOAD patients

244 ndicate that GM-MO and M-MO display distinct bioenergetic profiles, and that hypoxia triggers a trans

245 Cellular bioenergetic profiling of 13 established and 12 patient

246 Through bioenergetic profiling, we found that human and mouse LL

247 sm was associated with increased NCM356 cell bioenergetics, proliferation, invasion through Matrigel,

248 lated this injury response to their distinct bioenergetic properties.

249 such, assessment of skeletal muscle cellular bioenergetics provides a powerful means to understand th

250 Bioenergetic reactivation, visualized by presence of a m

251 t surprising that mitochondrial dynamics and bioenergetics reciprocally influence each other.

252 , and to support structural, functional, and bioenergetic recovery of the recipient hearts.

253 is an important process regulating cellular bioenergetics, redox responses, and apoptosis.

254 To better understand muscle bioenergetic regulation, a previously-developed model of

255 Lignin biosynthetic genes and bioenergetics-related genes were up-regulated in the hig

256 t MYC-overexpressing TNBC shows an increased bioenergetic reliance on FAO and identify the inhibition

257 eptions of physical layout do indeed reflect bioenergetic resources.

258 prion infection have been reported, yet the bioenergetic respiratory status of mitochondria from pri

259 Abeta levels and compromise in mitochondrial bioenergetics result in dysfunctional synaptic plasticit

260 Analysis of bioenergetics revealed thatNrf2(-/-)white adipose tissue

261 r comprehensive analysis of pancreatic islet bioenergetics reveals that Drp1 does not control insulin

262 Mitochondria are renowned for their central bioenergetic role in eukaryotic cells, where they act as

263 s a caspase-independent cell death effector, bioenergetic roles of AIF, particularly relating to comp

264 Lower bioenergetics segregated with increased incidence of low

265 remodeling, mitochondrial regression, and a bioenergetic shift from oxidative phosphorylation to ana

266 We examined bioenergetic shifts and associated consequences in PAH-r

267 stant subpopulations showed organismal level bioenergetic shifts in ER fish that are associated with

268 ting a D-lactate- and mannitol/sucrose-based bioenergetic shunt that greatly minimizes false-positive

269 induced by CXCL12 reflected a biased agonist bioenergetic signaling that might be exploited to interf

270 hat the interleukin 33/ST2 axis and changing bioenergetic sources are potential therapeutic targets t

271 tral regulator of the metabolic function and bioenergetic state of macrophages that is under evolutio

272 mics of synthasome assembly depending on the bioenergetic state of the mitochondria.

273 chondrial biogenesis to control the cellular bioenergetic state.

274 l of Arabidopsis mitochondria under specific bioenergetic states.

275 ised link between retinal pigment epithelium bioenergetic status and tissue remodelling of choroidal

276 changes in mitochondrial calcium uptake, and bioenergetic status in the heart during sepsis.

277 and provided direct evidence of the elevated bioenergetic status of muscle mitochondria relative to t

278 Mitochondria communicate their bioenergetic status to the cell via mitochondrial retrog

279 al viability and for responses to changes in bioenergetic status.

280 esent fundamental compensatory adaptation to bioenergetic stress providing protection against mitopha

281 lucose, and had greater glycolytic flux in a bioenergetics stress test.

282 iple aspects of mitochondrial biology beyond bioenergetics support transformation, including mitochon

283 ve stress and maintains complex II-dependent bioenergetics, sustaining local tumor growth while restr

284 -developed model of the skeletal muscle cell bioenergetic system was used to simulate the influence o

285 ly, accumulating evidence has suggested that bioenergetic systems, important in both synaptic functio

286 chrome bc1 is one of the key enzymes of many bioenergetic systems.

287 tively greater fluctuations in intramuscular bioenergetics than in VO2 compared to longer intervals.

288 ata identify Arg1 as a key regulator of ILC2 bioenergetics that controls proliferative capacity and p

289 consumption rate and impairment of cellular bioenergetics that was related to the redox state of the

290 n demonstrated by comparison of mitochondria bioenergetics through extracellular flux analyses.

291 zed physiological regulator of mitochondrial bioenergetics through its ability to interact with ATP s

292 We used simulations of skeletal muscle bioenergetics to identify key system features that contr

293 We examined mitochondrial bioenergetics, transcript and protein levels of oxidativ

294 as a therapeutic approach to reduce cellular bioenergetics, tumor growth, and enhance susceptibility

295 re was no marked alteration in mitochondrial bioenergetics under basal conditions, culture of patient

296 argeting mitochondrial function and cellular bioenergetics upstream of cellular damage may offer adva

297 Improved bioenergetics were confirmed in vivo after dosing with A

298 To test this hypothesis, mitochondrial bioenergetics were determined in endothelial cells from

299 ly activates genes involved in mitochondrial bioenergetics, whereas it normally down-regulates genes

300 ytes, Akt activation disrupted mitochondrial bioenergetics, which could be partially reversed by main