ライフサイエンスコーパス: oxidative phosphorylation

1 e differentiation, which primarily relies on oxidative phosphorylation.

2 itically depend on enhancement of macrophage oxidative phosphorylation.

3 level associated with deleterious effects on oxidative phosphorylation.

4 f energy generation to one more dependent on oxidative phosphorylation.

5 iogenesis through enhancement of endothelial oxidative phosphorylation.

6 enome (mtDNA) encoding 37 genes required for oxidative phosphorylation.

7 d glucose uptake and glycolysis and promotes oxidative phosphorylation.

8 drial ATP synthase catalyzes the coupling of oxidative phosphorylation.

9 Mitochondrial tracking confirmed enhanced oxidative phosphorylation.

10 olipids and to inhibit insulin signaling and oxidative phosphorylation.

11 riched in cell maintenance processes such as oxidative phosphorylation.

12 on the rate constants for beta-oxidation and oxidative phosphorylation.

13 escent T cells by controlling glycolysis and oxidative phosphorylation.

14 ssion of genes involved in the TCA cycle and oxidative phosphorylation.

15 lates in stimulated T cells in proportion to oxidative phosphorylation.

16 ced endoplasmic reticulum Ca(2+) release and oxidative phosphorylation.

17 regulated the expression of genes that favor oxidative phosphorylation.

18 mediated by the inhibition of mitochondrial oxidative phosphorylation.

19 lar proliferation and were less dependent on oxidative phosphorylation.

20 n of the electron transport chain (ETC) with oxidative phosphorylation.

21 thiamine metabolism, and tight regulation of oxidative phosphorylation.

22 in neural progenitor cells (NPC) to neuronal oxidative phosphorylation.

23 and was insensitive to various inhibitors of oxidative phosphorylation.

24 ator of healthy mitochondria and physiologic oxidative phosphorylation.

25 e pathways as well as abnormal mitochondrial oxidative phosphorylation.

26 ide m-chlorophenylhydrazone, an inhibitor of oxidative phosphorylation.

27 cipating in the tricarboxylic acid cycle and oxidative phosphorylation.

28 hondrial network and increased mitochondrial oxidative phosphorylation.

29 Mitochondria provide energy for cells via oxidative phosphorylation.

30 iated with tubular mitochondria and enhanced oxidative phosphorylation.

31 a efficiently allows the formation of ATP by oxidative phosphorylation.

32 s solely affect substrate supply upstream of oxidative phosphorylation.

33 ng of calcium to the mitochondria to promote oxidative phosphorylation.

34 via modulation of genes that are involved in oxidative phosphorylation.

35 toxic effect on nematodes as a modulator of oxidative phosphorylation.

36 oved to sustain metabolism in the absence of oxidative phosphorylation.

37 kalinizing effect and supplies substrate for oxidative phosphorylation.

38 on flows in TCA cycle, leading to attenuated oxidative phosphorylation.

39 ion in the mitochondria through FAO, fueling oxidative phosphorylation.

40 nct metabolic phenotype characterized by low oxidative phosphorylation.

41 r rates of oxygen consumption, and increased oxidative phosphorylation.

42 ty acids to sustain fatty acid oxidation and oxidative phosphorylation.

43 g larger aldehydes produced as byproducts of oxidative phosphorylation [12].

44 date targets of miR-106a-5p were involved in oxidative phosphorylation, a process that is suppressed

45 Furthermore, we show that the continuous oxidative phosphorylation activity is important for vira

46 effects on basal transmission, inhibition of oxidative phosphorylation alone depressed recovery from

47 rons, ATP production by either glycolysis or oxidative phosphorylation alone sustained basal evoked s

48 mosome inactivation and of genes involved in oxidative phosphorylation, alongside reduction in absolu

49 ic cellular processes such as glycolysis and oxidative phosphorylation also contribute to the shaping

50 oxic conditions; 51% of the energy came from oxidative phosphorylation and 49% came from glycolysis.

51 As the major coenzyme in fuel oxidation and oxidative phosphorylation and a substrate for enzymes si

52 tabolic pathways demonstrated alterations in oxidative phosphorylation and ABC transporters, suggesti

53 ucose-deprived melanoma cells depend on both oxidative phosphorylation and acetate metabolism for cel

54 and through the regulation of TCR-activated oxidative phosphorylation and aerobic glycolysis.

55 on of this protein as an electron carrier in oxidative phosphorylation and as a peroxidase that react

56 l fragmentation leading to decreased rate of oxidative phosphorylation and ATP levels.

57 he accumulation of misfolded SDHB, impairing oxidative phosphorylation and ATP production while activ

58 We found that NLRX1 regulates oxidative phosphorylation and cell integrity, whereas lo

59 mplicated in the regulation of mitochondrial oxidative phosphorylation and cellular metabolism.

60 We found impairments in oxidative phosphorylation and changes in TCA cycle metab

61 mitochondria, which results in impairment of oxidative phosphorylation and compromised recovery of th

62 ory profiling (measurements of mitochondrial oxidative phosphorylation and determination of its coupl

63 ls is underpinned by increased mitochondrial oxidative phosphorylation and enhanced glycolysis.

64 and MTP18 expression, which lead to reduced oxidative phosphorylation and enhanced mitochondrial fus

65 ical assays with isolated GTs indicated that oxidative phosphorylation and ethanolic fermentation wer

66 e-B cells exhibited significant decreases in oxidative phosphorylation and glycolysis, indicating tha

67 by supporting a developmental switch toward oxidative phosphorylation and GSIS at the transition to

68 uggest that subsequent return to reliance on oxidative phosphorylation and increasing spare respirato

69 oint connecting glycolysis and mitochondrial oxidative phosphorylation and is important for maintaini

70 mic organelles that generate energy (ATP) by oxidative phosphorylation and mediate key cellular proce

71 ibosome, phagocytosis, lysosome, proteasome, oxidative phosphorylation and metabolic pathways.

72 n was associated with induction of genes for oxidative phosphorylation and mitochondrial biogenesis i

73 (+) cells are characterized by: (i) impaired oxidative phosphorylation and mitochondrial complex I, I

74 p canonical pathway in both Jo-1 and IBM was oxidative phosphorylation and mitochondrial dysfunction.

75 tial melastatin 1 intronic region, regulates oxidative phosphorylation and mitochondrial energy metab

76 ociated with energy metabolism, particularly oxidative phosphorylation and mitoribosomal protein prod

77 N28 binds to mRNAs of proteins important for oxidative phosphorylation and modulates protein abundanc

78 hese events were associated with TH-mediated oxidative phosphorylation and NAD(+) production and sugg

79 his identified altered transcript levels for oxidative phosphorylation and oxidative stress genes.

80 changes in mitochondrial pathways, including oxidative phosphorylation and oxidative stress.

81 es, a striking upregulation of mitochondrial oxidative phosphorylation and perturbation of lipid meta

82 mutation on intrinsic apoptosis, shuts down oxidative phosphorylation and reduces ATP levels in glio

83 (T-ALL) cells are characterized by increased oxidative phosphorylation and robust ATP production.

84 ed to integrate the biophysical processes of oxidative phosphorylation and ROS generation.

85 e mitofusin protein MFN2, leading to reduced oxidative phosphorylation and ROS production.

86 in turn aggravates cyst growth by inhibiting oxidative phosphorylation and stimulating proliferation

87 Increased oxidative phosphorylation and subcellular ATP accumulati

88 dehydrogenase (SDH) is at the crossroads of oxidative phosphorylation and the tricarboxylic acid cyc

89 production of reactive oxygen species during oxidative phosphorylation and were enhanced by expressio

90 the regulation of mitochondrial translation, oxidative phosphorylation, and a number of metabolic pat

91 etic pathways, including aerobic glycolysis, oxidative phosphorylation, and fatty acid metabolism, we

92 ficantly decreased lipid droplets, decreased oxidative phosphorylation, and increased apoptosis.

93 ddC treatment inhibited mtDNA replication, oxidative phosphorylation, and induced cytotoxicity in a

94 This limits glycolysis, increases oxidative phosphorylation, and is essential for neutroph

95 he primary function is electron shuttling in oxidative phosphorylation, and is exerted by the so-call

96 rtionally more upon anaerobic glycolysis and oxidative phosphorylation, and less upon PCr breakdown.

97 volved in the regulation of metabolic genes, oxidative phosphorylation, and mitochondrial biogenesis.

98 UT1) levels, leading to elevated glycolysis, oxidative phosphorylation, and suppression of basal auto

99 gE activation aligned with processes such as oxidative phosphorylation, angiogenesis, and the p53 pat

100 metabolites involved in lipid metabolism and oxidative phosphorylation are altered, and perturbations

101 nearly, mitochondrial membrane potential and oxidative phosphorylation are highest at intermediate ce

102 Glycolysis and oxidative phosphorylation are the fundamental pathways o

103 rmacological inhibition of glutaminolysis or oxidative phosphorylation arrests the lytic cycle of the

104 display heterogeneity in using glycolysis or oxidative phosphorylation as an energy source.

105 ative reliance on the usage of glycolysis or oxidative phosphorylation as ATP sources for sperm motil

106 ial O2()/H2O2 generation that do not inhibit oxidative phosphorylation, as tools to characterize the

107 c miR-29b-1/a-regulated GO processes include oxidative phosphorylation, ATP metabolism, and apoptosis

108 sult of their ability to produce ATP through oxidative phosphorylation, buffer cytoplasmic calcium, r

109 hondria that harbor the protein complexes of oxidative phosphorylation, but how cristae are formed, r

110 chondrial functions such as ATP synthesis by oxidative phosphorylation, Ca(2+) dynamics, and respirat

111 Either glycolysis or oxidative phosphorylation can fuel low-frequency synapti

112 d not increase mitochondrial respiration and oxidative phosphorylation capacities.

113 resting mitochondrial activity, (sub)maximal oxidative phosphorylation capacity (OXPHOS), and mitocho

114 ndrial translation, which results in reduced oxidative phosphorylation capacity and increased ROS lev

115 ly in brains of R6/2 and WT mice, suggesting oxidative phosphorylation capacity and respiratory coupl

116 tion coupling, mitochondrial biogenesis, and oxidative phosphorylation capacity.

117 Inherited disorders of oxidative phosphorylation cause the clinically and genet

118 to fine-tune the expression and activity of oxidative phosphorylation complex I in excess light, whi

119 o the respirasome supercomplex consisting of oxidative phosphorylation complexes I, III, and IV.

120 a is restricted to a few key subunits of the oxidative phosphorylation complexes that are synthesized

121 Defects in mitochondrial oxidative phosphorylation complexes, altered bioenergeti

122 phobic proteins required for assembly of the oxidative phosphorylation complexes.

123 he MDD group, gray matter Pi, a regulator of oxidative phosphorylation, correlated positively with se

124 Oxidative phosphorylation defects in human tissues are o

125 Blocking bacterial metabolism by inhibiting oxidative phosphorylation did not affect WLBU2 killing c

126 dosis and sideroblastic anemia (MLASA) is an oxidative phosphorylation disorder, with primary clinica

127 ssion is marked by accelerated metabolic and oxidative phosphorylation, drug metabolism, fatty acid m

128 annels following inhibition of mitochondrial oxidative phosphorylation during hypoxia and by mitochon

129 cation efficiency rather than to mismatch or oxidative phosphorylation dysfunction.

130 mall number of biochemical pathways, notably oxidative phosphorylation, enriched in proteins vulnerab

131 l zonation of both glycogen synthase and the oxidative phosphorylation enzymes meant that the build-u

132 r energy from aerobic glycolysis rather than oxidative phosphorylation even in the presence of oxygen

133 Neurons depend on oxidative phosphorylation for energy generation, whereas

134 oxygen to generate ATP via the mitochondrial oxidative phosphorylation for its phototransduction and

135 Oxidative phosphorylation, fueled by either glycolysis o

136 hat S-OPA1 alone without L-OPA1 can maintain oxidative phosphorylation function as judged by growth i

137 infection, while inhibition of the cellular oxidative phosphorylation function significantly suppres

138 We found increased oxidative phosphorylation gene expression at the onset o

139 also marked downregulation of mitochondrial oxidative phosphorylation genes resulting in diminished

140 of Ucp1, Ppargc1a (encoding PGC-1alpha), and oxidative phosphorylation genes.

141 atients also exhibit decreased expression of oxidative phosphorylation genes.

142 A and regulate metabolic sensors to increase oxidative phosphorylation, glycolysis, and fatty acid sy

143 ving at the limits of cellular streamlining, oxidative phosphorylation has been lost: energy is obtai

144 lar metabolic activity towards glycolysis or oxidative phosphorylation in 3D Caco-2 models of colorec

145 s and can be leveraged to selectively target oxidative phosphorylation in AML.

146 functional evidence for an essential role of oxidative phosphorylation in cancer.

147 ive glycolytic metabolism and suppression of oxidative phosphorylation in CD8(+) T cells, achieved by

148 development of a drug combination targeting oxidative phosphorylation in M. tuberculosis.

149 nergy phosphate metabolism and regulation of oxidative phosphorylation in MDD patients.

150 Inhibition of oxidative phosphorylation in MDMs prevented the modulato

151 UQCRC2, and COX7A2, actively participated in oxidative phosphorylation in mitochondrial dysfunction a

152 udies have reported defects in mitochondrial oxidative phosphorylation in patients with ASD, the role

153 m trypanosomes, decreased ATP production via oxidative phosphorylation in procyclic form and affected

154 In accordance, real-time measurements of oxidative phosphorylation in response to deguelin treatm

155 increase proteins involved in mitochondrial oxidative phosphorylation in response to Dex.

156 owed that NK cells upregulate glycolysis and oxidative phosphorylation in response to either IL-2 or

157 oles for mitochondrial enzyme COX10-mediated oxidative phosphorylation in T cell quiescence exit.

158 odor transduction relies on ATP generated by oxidative phosphorylation in the dendrite and glycolytic

159 in sources of ATP production, glycolysis and oxidative phosphorylation, in fueling presynaptic functi

160 ed that the protein levels and activities of oxidative phosphorylation increased during vaccinia viru

161 through apparent reductions in mitochondrial oxidative phosphorylation, increases in substrate level

162 olic inputs that couple carbon catabolism to oxidative phosphorylation is a primary cause of growth p

163 ing of ATP generation between glycolysis and oxidative phosphorylation is central to cellular bioener

164 ux of respiration; (2) the time hierarchy of oxidative phosphorylation is given by phosphorylation su

165 erves neuronal ATP levels, particularly when oxidative phosphorylation is impaired, such as in neuron

166 Oxidative phosphorylation is the major cellular energy-p

167 Although mitochondrial physiology, including oxidative phosphorylation, is also important for efficie

168 d (TCA) cycle, electron transport chain, and oxidative phosphorylation, leading to a switch from ferm

169 and aging are associated with defects in the oxidative phosphorylation machinery (OXPHOS), which are

170 e mitochondrial electron transport chain and oxidative phosphorylation machinery at the stage of the

171 successful integration into Complex V of the oxidative phosphorylation machinery.

172 d proteins indicate defects in mitochondrial oxidative phosphorylation machinery.

173 We have recently observed that oxidative phosphorylation-mediated ATP production is ess

174 mitant down-regulation of genes required for oxidative phosphorylation, mitochondrial biogenesis, and

175 contribution probably encompasses defects of oxidative phosphorylation, mitochondrial turnover (mitop

176 ent bone marrow samples revealed an enhanced oxidative phosphorylation mRNA signature.

177 ver, the short 5' untranslated region of the oxidative phosphorylation mRNAs contributed to the trans

178 This study revealed that oxidative phosphorylation mRNAs were translationally upr

179 involved in a range of processes, including oxidative phosphorylation, neuropeptide biogenesis, and

180 Neither oxidative phosphorylation nor glycolytic activity, corre

181 phenotype with the ability to switch between oxidative phosphorylation or glycolysis.

182 that certain cancer cells display increased oxidative phosphorylation or high metabolically active p

183 An impaired ability to select substrates for oxidative phosphorylation, or metabolic inflexibility, i

184 Boosting residual oxidative phosphorylation (OXPHOS) activity can partiall

185 his enzyme results in dampened mitochondrial oxidative phosphorylation (OXPHOS) and activated mitocho

186 rt chain (ETC) complex associations favoring oxidative phosphorylation (OXPHOS) and FAO, while fissio

187 ic phenotype of cells characterized by mixed oxidative phosphorylation (OxPhos) and fermentative glyc

188 The basic control mechanisms of oxidative phosphorylation (OXPHOS) and glycolysis during

189 Mitochondrial disorders affecting oxidative phosphorylation (OxPhos) are caused by mutatio

190 tem metabolic disorders caused by defects in oxidative phosphorylation (OXPHOS) are severe, often let

191 ase and mitochondrial myopathy impair muscle oxidative phosphorylation (OXPHOS) by distinct mechanism

192 (mitochondrial DNA, mtDNA) encode essential oxidative phosphorylation (OXPHOS) components.

193 ed genes, have been associated with combined oxidative phosphorylation (OXPHOS) deficiencies.

194 DPH oxidase (NADPHox) in the pathogenesis of oxidative phosphorylation (OXPHOS) dysfunction as found

195 mitochondrial dysfunction including lowered oxidative phosphorylation (OXPHOS) efficiency, increased

196 These cells depend on oxidative phosphorylation (OXPHOS) for energy and cytoki

197 While quiescent T cells use oxidative phosphorylation (OXPHOS) for energy production

198 HT initially abrogates oxidative phosphorylation (OXPHOS) generating self-renew

199 that glutamine levels control mitochondrial oxidative phosphorylation (OXPHOS) in acute myeloid leuk

200 tochondrial dysfunctions including defective oxidative phosphorylation (OXPHOS) in cancer inhibit apo

201 Oxidative phosphorylation (OXPHOS) is a vital process fo

202 ative importance of lactate fermentation and Oxidative Phosphorylation (OxPhos) is debated.

203 ae structure and intracristal space (ICS) to oxidative phosphorylation (oxphos) is not well understoo

204 CcO promotes the switch from glycolytic to oxidative phosphorylation (OXPHOS) metabolism and has be

205 endogenous Abeta in our models do not cause oxidative phosphorylation (OXPHOS) perturbations.

206 However, recent evidence suggests that oxidative phosphorylation (OXPHOS) plays a crucial role

207 the synthesis of the core components of the oxidative phosphorylation (OXPHOS) system encoded by the

208 Dysfunction of the oxidative phosphorylation (OXPHOS) system is a major cau

209 mtDNA)-encoded protein subunits of the human oxidative phosphorylation (OXPHOS) system is carried out

210 cells increase glycolysis at the expense of oxidative phosphorylation (oxphos) to generate sufficien

211 Basal ATP concentration, oxidative phosphorylation (OXPHOS), and glycolysis pathw

212 s and its subsequent effect on mitochondrial oxidative phosphorylation (OXPHOS), BRSKs, CDC25B/C, MAP

213 amount, probably as a result of an impaired oxidative phosphorylation (OXPHOS), especially complex V

214 slate the 13 mtDNA-encoded mRNAs involved in oxidative phosphorylation (OXPHOS), mammalian mitochondr

215 r critical function in energy production via oxidative phosphorylation (OXPHOS), mitochondria are ess

216 iency in AIF is known to result in defective oxidative phosphorylation (OXPHOS), via loss of complex

217 still compatible with uncompromised maximal oxidative phosphorylation (oxphos), whereas lower maxima

218 myofibroblast differentiation, mitochondrial oxidative phosphorylation (OXPHOS), wound healing, and g

219 ase phenotype by showing multiple defects in oxidative phosphorylation (OXPHOS).

220 hondrial electron transport is essential for oxidative phosphorylation (OXPHOS).

221 membrane, an activity that is essential for oxidative phosphorylation (OXPHOS).

222 tDNA promoting estrogen receptor-independent oxidative phosphorylation (OXPHOS).

223 itochondrial complex I can result in reduced oxidative phosphorylation (OXPHOS).

224 es of the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS).

225 unit enzyme that catalyzes the first step in oxidative phosphorylation (OXPHOS).

226 by increased fatty acid oxidation (FAO) and oxidative phosphorylation (OXPHOS).

227 ic but also by pharmacological disruption of oxidative phosphorylation (OXPHOS).

228 n hypoxic cells from anaerobic glycolysis to oxidative phosphorylation (OXPHOS).

229 lism [increasing glycolysis while decreasing oxidative phosphorylation (oxphos)] or a metabolic ampli

230 ased levels of enzymes that are part of the 'oxidative phosphorylation' (OXPHOS) pathway.

231 unit B (SDHB) was nearly depleted in glucose oxidative phosphorylation pathway however certain enzyme

232 hat encodes genes necessary for the complete oxidative phosphorylation pathway including Complex I, d

233 regulation of cell cycle, mitochondrial, and oxidative phosphorylation pathway transcripts at 24 h po

234 bunits of complexes I, III, IV, and V in the oxidative phosphorylation pathway.

235 sis and increased expression of genes in the oxidative phosphorylation pathway.

236 (PDH) activity, suggesting impairment of the oxidative phosphorylation pathway.

237 d an enrichment of downregulated genes among oxidative phosphorylation pathways.

238 rs, focusing on glycolytic and mitochondrial oxidative phosphorylation pathways.

239 e associated with a compensatory increase in oxidative phosphorylation per mitochondrion.

240 contrary to previous models of regulation of oxidative phosphorylation, [Pi] does not modulate the ac

241 ealed a decreased abundance in ribosomal and oxidative phosphorylation proteins in obesity, and a nor

242 ake signaling pathways as well as changes in oxidative phosphorylation proteins were examined.

243 Oxidative phosphorylation provides most of the ATP that

244 Hypoxia and inhibitors of mitochondrial oxidative phosphorylation reduced AMPK-sensitive K(+) cu

245 sphorylation function as judged by growth in oxidative phosphorylation-requiring media, respiration m

246 of the enzymes mediating beta-oxidation and oxidative phosphorylation resulted in excess fats being

247 Myc signaling in parallel with mitochondrial oxidative phosphorylation, resulting in suppression of n

248 tochondrial dysfunction, particularly of the oxidative phosphorylation system (OXPHOS), occurs in neu

249 ns into this smallest protein complex of the oxidative phosphorylation system (which is not so small

250 teracts with components of the mitochondrial oxidative phosphorylation system, in particular the cyto

251 s that are essential for the function of the oxidative phosphorylation system, which is composed of f

252 tDNA) that encodes essential subunits of the oxidative phosphorylation system.

253 mitochondrial DNA and the biogenesis of the oxidative phosphorylation system.

254 As increased, particularly those involved in oxidative phosphorylation that are responsible for cellu

255 importance for the bioenergetic machinery of oxidative phosphorylation that is required for tumor ini

256 Remarkably, the proteins of oxidative phosphorylation, the cellular-energy-generatin

257 of non-fermentable carbon sources but not in oxidative phosphorylation; the mutant did not exhibit ma

258 erived exosomes (CDEs) inhibit mitochondrial oxidative phosphorylation, thereby increasing glycolysis

259 activated increase fatty acid oxidation and oxidative phosphorylation; these metabolic changes are c

260 ming of carbohydrate metabolic pathways from oxidative phosphorylation to accelerated glycolysis.

261 tuberculosis infection induced a shift from oxidative phosphorylation to aerobic glycolysis in macro

262 A shift in macrophage metabolism from oxidative phosphorylation to aerobic glycolysis is a req

263 Rapidly proliferating cells switch from oxidative phosphorylation to aerobic glycolysis plus glu

264 ents with sepsis, we found that a shift from oxidative phosphorylation to aerobic glycolysis was an i

265 T cells to undergo metabolic remodeling from oxidative phosphorylation to aerobic glycolysis, during

266 aggressive cancers is the reprogramming from oxidative phosphorylation to aerobic glycolysis, referre

267 ith idiopathic PAH, confirming a switch from oxidative phosphorylation to aerobic glycolysis.

268 ing real-time analysis of minute shifts from oxidative phosphorylation to anaerobic glycolysis, an ea

269 ary to the Warburg hypothesis, AML relies on oxidative phosphorylation to generate adenosine triphosp

270 d cellular signaling results in a shift from oxidative phosphorylation to glycolysis as the preferred

271 The switch from oxidative phosphorylation to glycolysis in proliferating

272 ion, macrophages shift from producing ATP by oxidative phosphorylation to glycolysis while also incre

273 e in mitochondrial DNA content, and required oxidative phosphorylation to meet their bioenergetic nee

274 The relative contributions of glycolysis and oxidative phosphorylation to neuronal presynaptic energy

275 The ability of oxidative phosphorylation to precisely set and maintain

276 the NAD(+)-to-NADH ratio, which reflects the oxidative phosphorylation-to-glycolysis ratio and/or the

277 ggests that glycolysis in the cilia and knob oxidative phosphorylation together fuel chemotransductio

278 s a shift of neuronal energy metabolism from oxidative phosphorylation toward aerobic glycolysis, als

279 nactivation triggers a metabolic switch from oxidative phosphorylation towards glycolysis and enhance

280 zed by common upregulation of cell cycle and oxidative phosphorylation transcriptional programs.

281 , indicating that these cells relied more on oxidative phosphorylation upon treatment.

282 ards glycolysis using potassium cyanide, and oxidative phosphorylation using hydrogen peroxide, emplo

283 Disruption of mitochondrial oxidative phosphorylation (using biguanides) led to a co

284 on that regulate diverse processes including oxidative phosphorylation, vesicle traffic, and the unfo

285 ATP generation is not only accomplished by oxidative phosphorylation via the pmf, but also by subst

286 roliferator-activated receptor signaling and oxidative phosphorylation was detected when moving from

287 Although oxidative phosphorylation was not compromised in the pah

288 Functional impairment of oxidative phosphorylation was then demonstrated by compa

289 nner membrane dynamics, cristae remodelling, oxidative phosphorylation, was post-translationally clea

290 e absence of TRAF3, anaerobic glycolysis and oxidative phosphorylation were increased in B cells with

291 Elevated levels of oxidative phosphorylation were required to support both

292 degree of metabolic plasticity, switched to oxidative phosphorylation when glycolysis was impaired.

293 undergo a metabolic shunt from glycolysis to oxidative phosphorylation, where defective machinery, as

294 resynaptic demands are met preferentially by oxidative phosphorylation, which can be maintained by bu

295 s to specifically block CDCP1-driven FAO and oxidative phosphorylation, which contribute to TNBC migr

296 ith phospholipids and uncouple mitochondrial oxidative phosphorylation, which initiates biochemical c

297 activity, leading to increased PDC flux and oxidative phosphorylation with attenuated cancer cell pr

298 on similar to Yy1 loss, thus further linking oxidative phosphorylation with late-gestation intestinal

299 Aging impairs mitochondrial oxidative phosphorylation, with a greater role played by

300 ndosymbiotic origin that are responsible for oxidative phosphorylation within eukaryotic cells.