ライフサイエンスコーパス: bioenergetics

1 ntial for functions apart from mitochondrial bioenergetics.

2 chondrial calcium transfer and mitochondrial bioenergetics.

3 ll invasion without changes in mitochondrial bioenergetics.

4 microaerobic conditions to maintain membrane bioenergetics.

5 thermodynamic reference for calibrating PSII bioenergetics.

6 er doxorubicin, confirming impaired cellular bioenergetics.

7 es mitochondrial RNA (mtRNA) homeostasis and bioenergetics.

8 in many genes associated with mitochondrial bioenergetics.

9 tochondrial dysfunction and inhibiting tumor bioenergetics.

10 oxygen-deficient niches to maintain cellular bioenergetics.

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

12 bnormalities suggestive of impaired cellular bioenergetics.

13 d SOD2 expression and improved mitochondrial bioenergetics.

14 AMPK axis is critical to support cancer cell bioenergetics.

15 of mitochondrial DNA (mtDNA) alterations of bioenergetics.

16 ese signaling pathways as mediators of tumor bioenergetics.

17 central role in cellular energy sensing and bioenergetics.

18 ls plays a key role in shaping mitochondrial bioenergetics.

19 than widely used in discussions of bacterial bioenergetics.

20 vivo reversed the sepsis-induced changes in bioenergetics.

21 fusion by macrophages, resulting in enhanced bioenergetics.

22 time, the HMGB1-RAGE pathway with changes in bioenergetics.

23 itochondrial Ca(2+) flux in shaping cellular bioenergetics.

24 ereas ncOGT predominantly regulates cellular bioenergetics.

25 n rescued mitochondrial Ca(2+) transport and bioenergetics.

26 hown that mitochondrial activities go beyond bioenergetics.

27 aerobic glycolysis, which enhances cellular bioenergetics.

28 higher concentrations, it inhibited cellular bioenergetics.

29 stimulating effect of 3-MP on mitochondrial bioenergetics.

30 colon cancer) did not affect tumor growth or bioenergetics.

31 to explore the effects of XN on muscle cell bioenergetics.

32 o-ATP ratio, a cornerstone parameter of cell bioenergetics.

33 mitochondrial electron transport or cellular bioenergetics.

34 some adult tissues by reprogramming cellular bioenergetics.

35 eals its role in regulation of mitochondrial bioenergetics.

36 itochondrial electron transport and cellular bioenergetics.

37 in the long range, could compromise cellular bioenergetics.

38 luteotropin, and estrogen, on corneal stroma bioenergetics.

39 diverse as electrochemistry, catalysis, and bioenergetics.

40 l regimens for extended analyses of cellular bioenergetics.

41 19S mutant LRRK2 expression on mitochondrial bioenergetics.

42 e regulation of mitochondrial biogenesis and bioenergetics.

43 lect intracellular ATP turnover and cellular bioenergetics.

44 the circadian clock governs skeletal muscle bioenergetics.

45 mportant role in mitochondrial processes and bioenergetics.

46 ndrial membrane potential, and mitochondrial bioenergetics.

47 se in FECD indicated deficient mitochondrial bioenergetics.

48 ty control, maintaining the functionality of bioenergetics.

49 pression of genes important in mitochondrial bioenergetics.

50 at ncOGT is a negative regulator of cellular bioenergetics.

51 nd enables reuse of organelle components for bioenergetics.

52 adaptive response to stimulate mitochondrial bioenergetics.

53 s by connecting ROS partitioning to cellular bioenergetics.

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

55 increased mitochondrial biogenesis and tumor bioenergetics.

56 sion is an important determinant of cellular bioenergetics, (99m)Tc-pertechnetate uptake, and BLI sig

57 healthy controls suggest that the underlying bioenergetics abnormality is not associated with change

58 tional repercussions on muscle perfusion and bioenergetics after a hypoxic stress vary depending on s

59 Consistent with the recovery of cellular bioenergetics, ALKBH7-depleted cells maintain their mito

60 Cellular bioenergetics analysis, metabolomics, and radiotracer st

61 chondrial calcium loading in turn stimulated bioenergetics and a persistent elevation in NADH.

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

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

64 Mitochondria have a crucial role in cellular bioenergetics and apoptosis, and thus are important to s

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

66 , we investigated the roles of mitochondrial bioenergetics and autophagy during cell polarization of

67 cells consume more glucose to cope with the bioenergetics and biosynthetic demands of rapidly dividi

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

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

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

71 dria using a computer model of mitochondrial bioenergetics and cation handling.

72 Mitochondria control bioenergetics and cell fate decisions, but how they infl

73 are fundamental mechanisms for mitochondrial bioenergetics and cell function.

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

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

76 This reprogramming stimulated cellular bioenergetics and conferred a HIF-dependent tumorigenic

77 nd promethazine, exert no effect on cellular bioenergetics and do not inhibit GBM cell proliferation.

78 Mitochondrial calcium uptake stimulates bioenergetics and drives energy production in metabolic

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

80 ochondria and its prolonged loss jeopardizes bioenergetics and excitation-contraction coupling, provi

81 mtDNA can mediate cellular bioenergetics and expression levels of nuclear genes rel

82 l mechanisms underlying the altered cellular bioenergetics and failure of epithelial and endothelial

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

84 LPS-mediated AKT activation in mitochondrial bioenergetics and function in cultured murine macrophage

85 These changes impact T cell bioenergetics and function.

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

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

88 pment, a time of dramatic transitions in the bioenergetics and growth of the heart.

89 the Cox7a1 isoform results in reduced muscle bioenergetics and hindlimb capillarity, helping to expla

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

91 urn makes this enzyme an important player in bioenergetics and in the regulation of NAD-using enzymes

92 T1 and may provide important clues about how bioenergetics and inflammation are linked.

93 atic airway epithelium with consequences for bioenergetics and inflammation.

94 strate the integrated roles of mitochondrial bioenergetics and lipidomic flux in modulating mPTP open

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

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

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

98 Bioenergetics and mitochondrial DNA (mtDNA) damage were

99 plogroups, to investigate their effects upon bioenergetics and molecular pathways.

100 ckdown of OMA1 in zebrafish leads to impeded bioenergetics and morphological defects of the heart and

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

102 To explore the link between bioenergetics and motor neuron degeneration, we used a c

103 Differences in mitochondrial bioenergetics and mtDNA damage associated with maternal

104 d reveal a fundamental link between cellular bioenergetics and mucosal barrier.

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

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

107 lic alterations on mouse brain mitochondrial bioenergetics and oxidative status.

108 ia affect mitochondrial functions, including bioenergetics and oxygen-sensing processes.

109 in the regulation of mitochondrial shape and bioenergetics and play a role in oxidative stress.

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

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

112 n the effects of added molecules on cellular bioenergetics and protection against IR injury were also

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

114 eveals a unique regulatory mechanism in cell bioenergetics and provokes a substantial reconsideration

115 Taken together, our findings depict how bioenergetics and redox characteristics could be therape

116 hondria, allowing for study of mitochondrial bioenergetics and redox function under defined substrate

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

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

119 at impacts multiple aspects of mitochondrial bioenergetics and signaling.

120 holipid with critical roles in mitochondrial bioenergetics and signaling.

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

122 of cell dissociation/suspension on cellular bioenergetics and the signal obtained by firefly lucifer

123 protein 90s are adaptive regulators of tumor bioenergetics and tractable targets for cancer therapy.

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

125 gies might also be directed at mitochondrial bioenergetics and turnover, the prevention of protein dy

126 mitochondrial metabolism to maintain T cell bioenergetics and viability.

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

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

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

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

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

132 lude vasorelaxation, stimulation of cellular bioenergetics, and promotion of angiogenesis.

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

134 Subsequent declines in liver bioenergetics appear to be a result of necrosis and acti

135 Here we take a bioenergetics approach to address this gap in our knowle

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

137 Mitochondrial bioenergetics are critical for cellular homeostasis and

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

139 tatively robust explanation for why membrane bioenergetics are universal, yet ion pumps and phospholi

140 Membrane bioenergetics are universal, yet the phospholipid membra

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

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

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

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

145 itochondrial electron transport and cellular bioenergetics at low concentrations (10-100 nM), while a

146 ssential for the regulation of mitochondrial bioenergetics, autophagy and cell death, even in the blo

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

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

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

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

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

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

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

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

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

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

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

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

159 f carbon metabolism that plays a key role in bioenergetics, cell proliferation, and the regulation of

160 cts on proton movements involving endogenous bioenergetics components could not be excluded.

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

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

163 The bioenergetics defect in AOA1-mutant fibroblasts and APTX

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

165 arian cancer cell lines revealed significant bioenergetics diversity.

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

167 Deficits in bioenergetics during early postnatal brain development c

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

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

170 and adenylate kinase as key determinants of bioenergetics during PARP-1 hyperactivation and unequivo

171 eases mitochondrial biogenesis, which alters bioenergetics during sepsis adaptation.

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

173 Hence, we here characterized bioenergetics during transient excitotoxicity in rat and

174 ments as evidenced by enhanced mitochondrial bioenergetics efficiency and decreased mtH2O2 production

175 f neurons to stress led to neurotoxicity and bioenergetics failure after cerebrospinal fluid exposure

176 polymerase (Parp) hyperactivation, cellular bioenergetics failure, and necrosis; indeed, steady-stat

177 e that RCAN1-1L induction can shift cellular bioenergetics from aerobic respiration to glycolysis, ye

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

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

180 regulation of mitochondrial Ca(2+)-dependent bioenergetics has been implicated in various pathophysio

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

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

183 id droplets, but the accompanying changes in bioenergetics have been little studied so far.

184 bnormalities in neural activity and cerebral bioenergetics have been observed in schizophrenia (SZ).

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

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

187 red mitochondrial oxidative phosphorylation, bioenergetics imbalance, deficit of Fe-S cluster enzymes

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

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

190 rovides quantitative insights into metabolic bioenergetics in cyanobacteria.

191 everely abnormal heterogeneity of myocardial bioenergetics in hearts with postinfarction LV remodelin

192 h this technique is commonly used to measure bioenergetics in intact cells, we outline here a detaile

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

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

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

196 -mediated mitochondrial Ca(2+) transport and bioenergetics in multiple cell types, including fibrobla

197 lity to cell death and altered mitochondrial bioenergetics in neural stem cells.

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

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

200 cessible source of mitochondria, the role of bioenergetics in regulating platelet function remains un

201 Analysis of bioenergetics in skeletal muscle mitochondria revealed t

202 estigate whether HDL modulates mitochondrial bioenergetics in skeletal muscle.

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

204 Stemming from the pioneering studies of bioenergetics in the 1950s, 1960s, and 1970s, mitochondr

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

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

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

208 the physiologic importance of mitochondrial bioenergetics in the metabolic regulation of sirtuins an

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

210 This study aimed to investigate hepatocyte bioenergetics in this well-studied hepatitis model.

211 ng may be useful for in vivo optimization of bioenergetics in transplanted cells.

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

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

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

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

216 termediate, oxaloacetate (OAA) affects brain bioenergetics, insulin signaling, inflammation and neuro

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

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

219 Impaired bioenergetics is a prominent feature of the failing hear

220 Reactivation of mitochondrial bioenergetics is followed by dramatic reorganization of

221 Based on these results, liver tissue bioenergetics is increased 3 hr after ConA exposure.

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

223 ssociation is reflected in the intramuscular bioenergetics is unknown.

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

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

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

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

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

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

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

231 Predictions from a bioenergetics model that excludes water as a source unde

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

233 y combining surveys of reef communities with bioenergetics modeling, we showed that fish excretion su

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

235 Bioenergetics models indicate that the sharks require ap

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

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

238 ulate the major alterations of mitochondrial bioenergetics observed in infectious cell systems, we sh

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

240 hese pharmacological approaches also improve bioenergetics of human cells harboring mitochondrial def

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

242 The bioenergetics of IF1 transiently silenced cancer cells h

243 stringent association between morphology and bioenergetics of mitochondria.

244 Efavirenz affects the bioenergetics of neurons through a mechanism involving a

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

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

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

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

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

250 ) handling were not due to enhanced cellular bioenergetics or increased Ca(2+) uptake into mitochondr

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

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

253 The bioenergetics phenotype of ovarian cancer cell lines cor

254 ng evidence has revealed that metabolism and bioenergetics play important roles in determining stem c

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

256 about cell differentiation, replication, and bioenergetics, possibly linking mitochondrial functions

257 Bioenergetics profile analysis of proliferating alloreac

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

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

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

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

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

263 ) via IP(3)Rs, BI-1 influences mitochondrial bioenergetics, reducing oxygen consumption, impacting ce

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

265 wth regulation by the mTOR pathways, and the bioenergetics requirements of cancer cells were also dis

266 deprivation, we identified a similarly rapid bioenergetics response, yet with incomplete ATP recovery

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

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

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

270 Lower bioenergetics segregated with increased incidence of low

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

272 itochondria in these cells and mitochondrial bioenergetics studies in the resistance cells further su

273 f disorders with compromised skeletal muscle bioenergetics, such as mitochondrial myopathies and age-

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

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

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

277 se, a major sensor and regulator of cellular bioenergetics that also is implicated in inhibiting infl

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

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

280 serves to (i) maintain colon cancer cellular bioenergetics, thereby supporting tumor growth and proli

281 protect against ALI by restituting alveolar bioenergetics through Cx43-dependent alveolar attachment

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

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

284 phate receptors (IP(3)Rs) maintains cellular bioenergetics, thus suppressing autophagy.

285 ine kinase and tumor suppressor that couples bioenergetics to cell-growth control through regulation

286 relays through glycolysis and mitochondrial bioenergetics to control root meristem activation, which

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

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

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

290 arburg effect by rapidly fueling cancer cell bioenergetics, ultimately resulting in metabolic exhaust

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

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

293 simulated I/R model, aberrant mitochondrial bioenergetics was exacerbated in KO myocytes.

294 s did not show major differences in cellular bioenergetics, we find extensive metabolic aberrations i

295 Improved bioenergetics were confirmed in vivo after dosing with A

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

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

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

299 aling and support the concept of integrating bioenergetics with cellular differentiation.

300 ow a calcium-mediated acceleration in matrix bioenergetics would influence cellular metabolism in gly