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

1 thways, skewing osteoclast metabolism toward oxidative phosphorylation.

2 ffective against cancer types that depend on oxidative phosphorylation.

3 ogether with glucose-FA 'shared fuelling' of oxidative phosphorylation.

4 by decreasing oxygen delivery and inhibiting oxidative phosphorylation.

5 pplementing NAD+ for glycolysis and NADH for oxidative phosphorylation.

6 tochondria generate most cellular energy via oxidative phosphorylation.

7 a metabolically quiescent state dependent on oxidative phosphorylation.

8 s the mitochondrial inner membrane and power oxidative phosphorylation.

9 esulting in changes in respiration rates and oxidative phosphorylation.

10 was associated with increased glycolysis and oxidative phosphorylation.

11 cl-xL expression and increased mitochondrial oxidative phosphorylation.

12 a loss in hepatocytes promotes autophagy and oxidative phosphorylation.

13 sses, the tricarboxylic acid (TCA) cycle and oxidative phosphorylation.

14 lls, ATP is generated both by glycolysis and oxidative phosphorylation.

15 metabolic transition from glycolysis toward oxidative phosphorylation.

16 lomics upregulated glycolysis and suppressed oxidative phosphorylation.

17 ficiency and a switch between glycolysis and oxidative phosphorylation.

18 the mutant strain indicative of dysregulated oxidative phosphorylation.

19 uding up-regulation of genes associated with oxidative phosphorylation.

20 me essential for DNA repair, glycolysis, and oxidative phosphorylation.

21 s to meet ATP demand in the face of impaired oxidative phosphorylation.

22 erent compartments requires the induction of oxidative phosphorylation.

23 PTCD1 is required for ATP generation through oxidative phosphorylation.

24 type downregulating mTOR, IL-8 signaling and oxidative phosphorylation.

25 lycolytic metabolism without a depression of oxidative phosphorylation.

26 glycolysis, and after NTC increasingly used oxidative phosphorylation.

27 es a subset of genes which are essential for oxidative phosphorylation.

28 t arise largely from electron leakage during oxidative phosphorylation.

29 ination of elevated glycolysis and increased oxidative phosphorylation.

30 ves rise to augmented aerobic glycolysis and oxidative phosphorylation.

31 s, producing most of the cellular energy via oxidative phosphorylation.

32 ients with effects on NF-kappaB activity and oxidative phosphorylation.

33 reases oxygen radicals through inhibition of oxidative phosphorylation.

34 o AML rely on amino acid metabolism to drive oxidative phosphorylation.

35 rcomplex destabilization and inefficiency of oxidative phosphorylation.

36 versus oxidation of NADH to generate ATP by oxidative phosphorylation.

37 d mitochondrial proteins and did not improve oxidative phosphorylation.

38 been proposed as a master regulator of tumor oxidative phosphorylation.

39 opy number and the abundance of proteins for oxidative phosphorylation.

40 paratively increased role for non-glycolytic oxidative phosphorylation.

41 enetic machinery needed for local control of oxidative phosphorylation.

42 y targets tumour cells that are dependent on oxidative phosphorylation.

43 t antigenic stimulation impaired ADP-coupled oxidative phosphorylation.

44 y reprogram to favor aerobic glycolysis over oxidative phosphorylation.

45 ismal survival through exquisite coupling of oxidative phosphorylation, a prominent ROS-producing pat

46 o shift between glycolysis and mitochondrial oxidative phosphorylation according to energy demands.

47 thway analysis demonstrated association with Oxidative Phosphorylation (adjusted P < 0.05).

48 shift in the balance between glycolysis and oxidative phosphorylation and activation of the unfolded

49 ulation in human and mouse were enriched for oxidative phosphorylation and adipogenesis.

50 rentially expressed genes were implicated in oxidative phosphorylation and adipogenesis.

51 ocesses involved, such as citric acid cycle, oxidative phosphorylation and ATP-providing arginine dei

52 INK1-KO-PBMCs showed significantly increased oxidative phosphorylation and basal glycolysis compared

53 nced by down-regulation of genes involved in oxidative phosphorylation and by impaired oxygen consump

54 d to diverse processes including chemotaxis, oxidative phosphorylation and carbon and nitrogen metabo

55 ion into Th1 and Th17 subsets with increased oxidative phosphorylation and decreased NF-kappaB activa

56 uce a strong innate immune response; rather, oxidative phosphorylation and extracellular matrix-recep

57 nd allograft rejection but downregulation of oxidative phosphorylation and fatty acid metabolism path

58 reprogramming of tumor metabolism involving oxidative phosphorylation and fatty acid oxidation (FAO)

59 2 inhibition, and partial inhibition of both oxidative phosphorylation and fatty acid oxidation using

60 to mitochondria inner membranes, to suppress oxidative phosphorylation and fatty acid oxidation, ther

61 ate adenocarcinoma consumes citrate to power oxidative phosphorylation and fuel lipogenesis, enabling

62 ion of levels associated with each hallmark; oxidative phosphorylation and G(2)-M checkpoint were ass

63 mes and identified nuclear genes involved in oxidative phosphorylation and glycolysis (OXPHOG) as a c

64 Multiple myeloma relies on both oxidative phosphorylation and glycolysis following acqui

65 miR-294 enhanced oxidative phosphorylation and glycolysis in Neonatal ven

66 The approaches described include restoring oxidative phosphorylation and glycolysis, increasing ins

67 G) have been used to study the inhibition of oxidative phosphorylation and glycolysis, respectively,

68 lomic profile that reflects a combination of oxidative phosphorylation and glycolysis.

69 metabolism given that Cryptosporidium lacks oxidative phosphorylation and glycolytic enzymes are not

70 mune-challenged or aged macrophages restored oxidative phosphorylation and homeostatic immune respons

71 zed by a peroxynitrite-dependent decrease of oxidative phosphorylation and increased glycolysis and g

72 Statistical analyses revealed higher oxidative phosphorylation and lipid metabolism in respon

73 ith glycolysis and inverse correlations with oxidative phosphorylation and lysosomal gene expression,

74 ther antibacterial agents exhibited impaired oxidative phosphorylation and metabolic shifts to glycol

75 supporting glycolytic activity and promoting oxidative phosphorylation and mitochondrial H(+) and pho

76 a/ERRalpha signalling, and downregulation of oxidative phosphorylation and mitochondrial proteostasis

77 m, which has directed research interest into oxidative phosphorylation and muscle bioenergetics.

78 e bd oxidase, which are jointly required for oxidative phosphorylation and mycobacterial viability.

79 Aldehydes are by-products of increased oxidative phosphorylation and nucleotide synthesis in ca

80 Fetal thyroid hormone deficiency reduced oxidative phosphorylation and prevented the prepartum up

81 Male-selective DEGs were linked to oxidative phosphorylation and protein/molecule metabolis

82 R and found that genes linked to metabolism, oxidative phosphorylation and proteolysis were significa

83 lic studies showed a significant decrease in oxidative phosphorylation and RNA-seq data revealed a si

84 K revealed that breast cancer cells utilized oxidative phosphorylation and signaling by Akt to a grea

85 least in part, by BRB-induced impairment of oxidative phosphorylation and the associated increment o

86 is coupled to the generation of ATP-that is, oxidative phosphorylation and the production of metaboli

87 These genes were associated with enhanced oxidative phosphorylation and upregulation of transcript

88 to our knowledge, to regulate mitochondrial oxidative phosphorylation and, with miR-488-3p, represen

89 gnaling in osteoclast progenitors decreases "oxidative phosphorylation" and the expression of mitocho

90 at regulates intracellular Ca(2+) signaling, oxidative phosphorylation, and apoptosis.

91 chondria fragmentation, attenuates efficient oxidative phosphorylation, and decreases EC function.

92 nscriptomic changes related to inflammation, oxidative phosphorylation, and fatty acid metabolism pat

93 e was dependent on glycolysis, mitochondrial oxidative phosphorylation, and fatty acid metabolism, wh

94 cells have increased (i) mitochondrial mass, oxidative phosphorylation, and fatty acid oxidation; (ii

95 e in HIF-1alpha protein levels, reduction in oxidative phosphorylation, and increased glycolysis.

96 s Foxp3 expression, shifts metabolism toward oxidative phosphorylation, and increases survival and su

97 xidative stress, disruption of mitochondrial oxidative phosphorylation, and permeability transition,

98 pid oxidation, glycolysis, and mitochondrial oxidative phosphorylation are common strategies to cope

99 s are upregulated, whereas those involved in oxidative phosphorylation are downregulated.

100 hanisms regulating trophoblast mitochondrial oxidative phosphorylation are largely unknown.

101 udies support the notion that glycolysis and oxidative phosphorylation are rheostats in immune cells

102 etal cardiomyocytes shift from glycolysis to oxidative phosphorylation around the time of birth.

103 Pathway analysis revealed mitochondrial oxidative phosphorylation as the top pathway upregulated

104 Inhibitors of glycolysis and oxidative phosphorylation as well as mitochondrial uncou

105 ycle control, mitochondrial dysfunction, and oxidative phosphorylation, as well as down-regulated gen

106 synthesizing proteins that are essential for oxidative phosphorylation (ATP generation).

107 ncreased ATP synthesis through glycolysis or oxidative phosphorylation, but dependent on ME1-produced

108 ono-alkyl lipophilic cations (MALCs) inhibit oxidative phosphorylation by affecting NADH oxidation in

109 Mitochondria maintain oxidative phosphorylation by creating a membrane potenti

110 role of WTp53 in suppressing pyruvate-driven oxidative phosphorylation by inducing PUMA.

111 ings, however, suggest that cancers maintain oxidative phosphorylation capacity and that the role of

112 way, cytokine-cytokine receptor interaction, oxidative phosphorylation, cardiac muscle contraction, A

113 Inherited disorders of oxidative phosphorylation cause the clinically and genet

114 ow that CDNs decrease oxygen consumption and oxidative phosphorylation, cause a metabolic switch to g

115 This compromised oxidative phosphorylation, causing severe oxidative stre

116 ounced down-regulation in gene expression of oxidative phosphorylation, cell adhesion, and DNA replic

117 d a post-LVAD dissociation of glycolysis and oxidative-phosphorylation characterized by induction of

118 ic atrophy 1], and MFN 2 [mitofusin 2]), and oxidative phosphorylation (citrate synthase and electron

119 n skeletal muscle correlates positively with oxidative phosphorylation Complex I, sirtuin 3 and succi

120 vated receptor gamma coactivator 1-alpha and oxidative phosphorylation complex II and III were signif

121 ng the AAA+ protease, LonP1, and subunits of oxidative phosphorylation, complex V (ATP synthase).

122 bited by the drug, while activities of other oxidative phosphorylation complexes (III and V) were not

123 ression of PGC-1alpha restores mitochondrial oxidative phosphorylation complexes and mitigates cell d

124 ance of specific nuclear-encoded subunits in oxidative phosphorylation complexes I and V increased in

125 ndrial transcripts, and normal activities of oxidative phosphorylation complexes I through V.

126 itive charge to associate with mitochondrial oxidative phosphorylation complexes in a manner that is

127 , it is likely that the dense packing of the oxidative phosphorylation complexes in the cristae membr

128 al mitochondrial translation and assembly of oxidative phosphorylation complexes that are critical fo

129 ar mitochondrial DNA-encoded subunits of the oxidative phosphorylation complexes were altered in the

130 optic atrophy type 1, and components of the oxidative phosphorylation complexes.

131 he synthesis of 13 essential subunits of the oxidative phosphorylation complexes.

132 nd a compensatory upregulation of unaffected oxidative phosphorylation components.

133 we show that 4HNE decreases cell number and oxidative phosphorylation (control, 388.1+/-23.54 versus

134 WT) hearts, but there were no differences in oxidative phosphorylation coupling efficiency or membran

135 plex I and complex II), leak respiration and oxidative phosphorylation coupling.

136 fatal infantile cardiomyopathy and multiple oxidative phosphorylation defects.

137 We demonstrate signatures of oxidative phosphorylation deficiency for common mtDNA va

138 using IMC, providing an accurate measure of oxidative phosphorylation deficiency for complexes I-V a

139 However as neurons become oxidative phosphorylation dependent, mitophagy is severe

140 -mediated increases in SC levels and reduces oxidative phosphorylation-dependent ATP production.

141 Ultimately, this led to deficient oxidative phosphorylation, diminishing nicotinamide aden

142 les characterized by elevated glycolysis and oxidative phosphorylation, distinct from ATM from lean m

143 ights the function of mitochondrial genes in oxidative phosphorylation, DNA repair and the cell cycle

144 Pharmacological inhibition of oxidative phosphorylation dramatically attenuated metast

145 that FMRP deficiency results in inefficient oxidative phosphorylation during the neurodevelopment an

146 oxylic acid cycle, electron transport chain, oxidative phosphorylation, elevated oxygen consumption,

147 r predicted mitochondrial function, of which oxidative phosphorylation emerged as the top-most enrich

148 ithelial-to-mesenchymal (EMT), stemness, and oxidative phosphorylation-enriched gene sets.

149 ochondrial complex I powers ATP synthesis by oxidative phosphorylation, exploiting the energy from ub

150 lassified as being involved in regulation of oxidative phosphorylation, extracellular matrix formatio

151 olving acute downregulation of mitochondrial oxidative phosphorylation, fatty acid metabolism, calciu

152 ake were also enriched for genes involved in oxidative phosphorylation, fatty acid metabolism, peroxi

153 es typically rely on aerobic glycolysis over oxidative phosphorylation for energy.

154 CLL cells rely on oxidative phosphorylation for their bioenergetics, parti

155 n a normal surveillance state, microglia use oxidative phosphorylation for their energy supply, but r

156 ms, most notably the regulated uncoupling of oxidative phosphorylation from ATP generation by uncoupl

157 ical pathway analysis showed upregulation of oxidative phosphorylation genes indicative of mitochondr

158 enes were down-regulated in the RV and while oxidative phosphorylation genes were activated.

159 ession of most nuclear-encoded mitochondrial oxidative phosphorylation genes, improve mitochondrial f

160 at S811 or T826 stimulates the expression of oxidative phosphorylation genes, increasing cellular oxy

161 -regulation of nuclear-encoded mitochondrial oxidative phosphorylation genes, trigger a ROS-JNK retro

162 rigin T cells appeared quiescent, expressing oxidative phosphorylation genes.

163 e are the first to report characteristics of oxidative phosphorylation, H(2)O(2) production, activity

164 hifting between glycolysis and mitochondrial oxidative phosphorylation has been implicated in macroph

165 s to generate ATP via glycolysis rather than oxidative phosphorylation, has fostered the misconceptio

166 ovided by interlinked analysis revealed that oxidative phosphorylation, hypersensitive response, DNA

167 Inhibition of mitochondrial oxidative phosphorylation in activated T cells was suffi

168 Given the universality of oxidative phosphorylation in aerobic biology, the iron c

169 ay and uncover a role of FBXW7 in regulating oxidative phosphorylation in B-cell malignancies.

170 d effect on mitochondrial tRNA stability and oxidative phosphorylation in differentiated cells.

171 umor metabolism was strongly shifted towards oxidative phosphorylation in EP300 downregulated tumors.

172 itiated low-grade inflammation and increased oxidative phosphorylation in liver and adipose tissues.

173 ch demonstrates the functional importance of oxidative phosphorylation in metastasis and highlights i

174 Cardiac ATP production primarily depends on oxidative phosphorylation in mitochondria and is dynamic

175 P, most of which is produced from glucose by oxidative phosphorylation in mitochondria, complemented

176 al pH values and is not necessary for robust oxidative phosphorylation in mitochondria.

177 ignificant increase in complex I-facilitated oxidative phosphorylation in mutant muscle.

178 Like c-Myc, IRE1alpha-XBP1 also promotes oxidative phosphorylation in NK cells.

179 gulation of MEIS1 promotes the maturation of oxidative phosphorylation in perinatal cardiomyocytes.

180 ria, and hence may have an important role in oxidative phosphorylation in terminally differentiated c

181 Oxidative phosphorylation in the presence of substrates

182 an interplay between PARP and mitochondrial oxidative phosphorylation in TNBC that comes into play i

183 ransport Chain (ETC) proteins and stimulates oxidative phosphorylation in trophoblast and that ETC pr

184 Muscle capacity for oxidative phosphorylation increased primarily after birt

185 ure to UVB radiation decreased mitochondrial oxidative phosphorylation, increased glycolysis and the

186 To enhance the chemotherapeutic efficacy and oxidative phosphorylation inhibition, we developed a mit

187 ysis inhibitor) plus 2,4-dinitrophenol (DNP; oxidative phosphorylation inhibitor).

188 Mito-LND, a tumor-selective inhibitor of oxidative phosphorylation, inhibits mitochondrial bioene

189 ain driver of allogeneic T cell-driven GVHD, oxidative phosphorylation is a main driver of Treg suppr

190 We have observed that oxidative phosphorylation is also increased.

191 cellular adenosine triphosphate levels while oxidative phosphorylation is moderately affected.

192 A metabolic transition from glycolysis to oxidative phosphorylation is often associated with diffe

193 nalized approach to intervention focusing on oxidative phosphorylation is pivotal in this condition.

194 The influence of carbon metabolism on oxidative phosphorylation is poorly understood in mycoba

195 We have previously demonstrated that oxidative phosphorylation is required for the survival o

196 n of ATM within mitochondria and its role in oxidative phosphorylation is still unknown.

197 n of mitochondria is the synthesis of ATP by oxidative phosphorylation, known as mitochondrial bioene

198 a reveal that loss of ATP production through oxidative phosphorylation limits T cell proliferation an

199 is indispensable for proper function of the oxidative phosphorylation machinery.

200 nificant downregulation of genes involved in oxidative phosphorylation, mammalian target of rapamycin

201 coincided with an increase in glycolysis and oxidative phosphorylation measured with Seahorse technol

202 Interference with both oxidative phosphorylation (metformin, oligomycin) and be

203 n-regulated genes included those involved in oxidative phosphorylation, mitochondrial dysfunction, nu

204 96 overlapping DEGs at both ages involved in oxidative phosphorylation, mitochondrial function, and c

205 RV failure showed lower oxidative phosphorylation (moderate RV hypertrophy, 287.

206 in a multitude of AF relevant pathways like oxidative phosphorylation or RhoA (Ras homolog gene fami

207 vitro models, with M2 macrophages utilizing oxidative phosphorylation (OX PHOS) and M1 macrophages u

208 Among those, only the complexes of oxidative phosphorylation (OXPHOS) affected the CL compo

209 nel to mitochondria is essential for optimal oxidative phosphorylation (OXPHOS) and ATP production.

210 Mitochondrial oxidative phosphorylation (OXPHOS) and cellular workload

211 e ESCs particularly rely on elevated FAO for oxidative phosphorylation (OXPHOS) and energy production

212 R) are widely used proxies for mitochondrial oxidative phosphorylation (OXPHOS) and glycolytic rate i

213 enhances activity of complex IV, increasing oxidative phosphorylation (OXPHOS) and NAD(+) generation

214 -transformed mouse fibroblasts also increase oxidative phosphorylation (OXPHOS) by nearly two-fold an

215 ybrid phenotype in which both glycolysis and oxidative phosphorylation (OXPHOS) can be utilized.

216 Reduced placental oxidative phosphorylation (OXPHOS) capacity measured in

217 ed the folding and function of mitochondrial oxidative phosphorylation (OXPHOS) complex II and IV sub

218 both nuclear- and mitochondrial-DNA encoded oxidative phosphorylation (OxPhos) components were incre

219 This resulted in the engagement of oxidative phosphorylation (OXPHOS) driven by elevated fa

220 metabolism phenotypes between glycolysis and oxidative phosphorylation (OXPHOS) during tumorigenesis

221 n higher mitochondrial respiratory capacity, oxidative phosphorylation (OXPHOS) efficiency, and a con

222 echanisms shape the biogenesis of multimeric oxidative phosphorylation (OXPHOS) enzyme in mitochondri

223 mutant UM tumors into two subgroups based on oxidative phosphorylation (OXPHOS) gene expression sugge

224 Il22ra2 deficiency favors downregulation of oxidative phosphorylation (OXPHOS) genes in an IL-22-dep

225 For decades, these reductions in oxidative phosphorylation (OxPhos) have been presumed to

226 beta-oxidation, that leads to a reduction of oxidative phosphorylation (OxPHOS) in acute myeloid leuk

227 A) cycle in mediating lipid accumulation and oxidative phosphorylation (OXPHOS) in the mitochondria.

228 the combination of HK2(shRNA) knockdown, an oxidative phosphorylation (OXPHOS) inhibitor diphenylene

229 e ATP level in the ER is readily depleted by oxidative phosphorylation (OxPhos) inhibitors and that E

230 e, we report that glucose metabolism through oxidative phosphorylation (OXPHOS) is the predominant bi

231 SCZ glutamatergic neurons, show dysregulated Oxidative Phosphorylation (OxPhos) related gene expressi

232 opic AR expression reduced the expression of oxidative phosphorylation (OXPHOS) subunits.

233 focused on understanding how glycolysis and oxidative phosphorylation (OxPhos) support proliferation

234 play an important role in dysfunction of the oxidative phosphorylation (OXPHOS) system in renal oncoc

235 e the insect stage utilizes a cost-effective oxidative phosphorylation (OxPhos) to generate ATP, whil

236 metabolic reprogramming from a predominantly oxidative phosphorylation (OXPHOS) to glycolysis to moun

237 the sensor to detect a metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis was dem

238 Certain subtypes of cancer cells require oxidative phosphorylation (OXPHOS) to survive.

239 Targeting oxidative phosphorylation (OXPHOS) with BDQ and simultan

240 icroscopically in the 1840s, but the idea of oxidative phosphorylation (OXPHOS) within mitochondria d

241 ATP is produced during oxidative phosphorylation (OXPHOS), a metabolic pathway

242 sis, the tricarboxylic acid (TCA) cycle, and oxidative phosphorylation (Oxphos), and those that consu

243 cells have elevated levels of glycolysis and oxidative phosphorylation (OXPHOS), in comparison to nai

244 onas aeruginosa produces toxins that disrupt oxidative phosphorylation (OXPHOS), resulting in UPR(mt)

245 d by monitoring the expression of drivers of oxidative phosphorylation (OXPHOS), the rates of utiliza

246 abolism, Tricarboxylic acid (TCA) cycle, and Oxidative Phosphorylation (OXPHOS), which redirected the

247 Here, we use multiple oxidative phosphorylation (OXPHOS)-competent and incompe

248 lating gene expression signatures related to oxidative phosphorylation (OxPhos).

249 red for energy generation processes, such as oxidative phosphorylation (OXPHOS).

250 abolism and ATP generation via mitochondrial oxidative phosphorylation (OXPHOS).

251 ymes crucial for heme synthesis, uptake, and oxidative phosphorylation (OXPHOS).

252 ssion of key elements of the Krebs cycle and oxidative phosphorylation (OXPHOS).

253 EC-specific upregulation of genes related to oxidative phosphorylation (OxPhos).

254 tored hepatic calcium retention capacity and oxidative phosphorylation parameters and reduced liver d

255 those involved in ATP production through the oxidative phosphorylation pathway and those involved in

256 ch in the metabolism with upregulation of 34 oxidative phosphorylation pathway proteins and 18 tricar

257 erocyte population enriched for genes within oxidative phosphorylation pathways.

258 they selectively utilized EIF2 signaling and oxidative phosphorylation pathways.

259 s, inflammasome activation and mitochondrial oxidative phosphorylation pathways.

260 Chemical inhibition of ATP synthesis by oxidative phosphorylation phenocopied the growth defect

261 Oxidative phosphorylation produces ATP, but it is also a

262 High levels of FAO promoted mitochondrial oxidative phosphorylation, production of reactive oxygen

263 ranscripts from mitochondrial genes encoding oxidative phosphorylation protein complexes, whereas nuc

264 The heterogeneous expression of oxidative phosphorylation proteins and resulting respira

265 Mitochondrial biogenesis and oxidative phosphorylation proteins were upregulated thro

266 in mitochondrial iron and reduced levels of oxidative phosphorylation proteins.

267 Trophoblast oxidative phosphorylation provides energy for active tra

268 l electron transfer chain complex I-mediated oxidative phosphorylation rate but did not decrease coup

269 e levels of calcium overload can cause lower oxidative phosphorylation rates.

270 impairs ETC II activity, thereby inhibiting oxidative phosphorylation, reducing production of ATP, a

271 red expression of mitochondrial dynamics and oxidative phosphorylation regulatory proteins, and mitoc

272 ified a clear CO signature dominated with 23 oxidative phosphorylation-related genes (FDR <10%).

273 s impacted by genomic alterations, including oxidative phosphorylation-related metabolism, protein tr

274 Only when neurons are oxidative phosphorylation reliant the extent of mitochon

275 from bacteria to humans, that associate with oxidative phosphorylation supercomplexes.

276 Bcl2l13 promotes adipogenesis by increasing oxidative phosphorylation, suppressing apoptosis, and pr

277 the consumption of O(2) by the mitochondrial oxidative phosphorylation system (OXPHOS) to produce ene

278 ae that contain the protein complexes of the oxidative phosphorylation system.

279 Oxidative phosphorylation, the primary source of cellula

280 ges rely on the tricarboxylic acid cycle and oxidative phosphorylation; thus, factors that affect mac

281 rophages and dendritic cells is shifted from oxidative phosphorylation to aerobic glycolysis, which i

282 en TCA cycle activity exceeds the ability of oxidative phosphorylation to convert mitochondrial redox

283 Beige adipocytes depend on mitochondrial oxidative phosphorylation to drive thermogenesis.

284 for PGC1alpha in mediating glutamine-driven oxidative phosphorylation to facilitate the invasive gro

285 ate a shift in mitochondrial metabolism from oxidative phosphorylation to glycolysis in human hearts

286 The metabolic switch from oxidative phosphorylation to glycolysis is required for

287 ecause of a shift in glucose metabolism from oxidative phosphorylation to lactate production for ener

288 diates a mitochondrial metabolic switch from oxidative phosphorylation to superoxide production in re

289 hages, which involves a metabolic shift from oxidative phosphorylation toward glucose consumption.

290 nce Category <= 2) and mitochondrial maximal oxidative phosphorylation utilizing substrate for comple

291 covered that combination therapies targeting oxidative phosphorylation via the thioredoxin reductase

292 The reliance of multiple myeloma cells on oxidative phosphorylation was caused by intercellular mi

293 nce for primary dysfunction of mitochondrial oxidative phosphorylation was detected in the brainstem

294 Impaired oxidative phosphorylation was observed at early disease

295 l and spare respiratory capacities driven by oxidative phosphorylation were largely unchanged.

296 Several of these (ribosome biogenesis, oxidative phosphorylation) were identified in our prior

297 Adipocytes predominantly utilize oxidative phosphorylation, whereas osteoblasts use glyco

298 regulate the balance between glycolysis and oxidative phosphorylation, which is critical in highly d

299 g, this increases glycolysis disengaged from oxidative phosphorylation with mitochondrial fragmentati

300 res induction of IRF4, MYC-target genes, and oxidative phosphorylation, with the loss of CD62L expres