ライフサイエンスコーパス: OXPHOS

1 OXPHOS activity was measured after immunologic activatio

2 OXPHOS activity, OXPHOS subunits, and assembly of subuni

3 OXPHOS capacity was comparable between groups when compl

4 OXPHOS complexes pose a unique challenge for cells becau

5 rd ER(lo)-IL6(hi)-Notch(hi) loop, activating OXPHOS, in the absence of ER activity.

6 OXPHOS activity, OXPHOS subunits, and assembly of subunits into OXPHOS co

7 ls of glycolysis, in the absence of adequate OXPHOS, may not be as beneficial for tumor growth as gen

8 , a large (>5-fold) direct activation of all OXPHOS complexes was required to simulate measured phosp

9 significant decreased in the activity of all OXPHOS complexes, in fully assembled complexes, in the a

10 Thus, HT induces an OXPHOS metabolic editing of luminal breast cancers, para

11 membrane potential, oxygen consumption, and OXPHOS on a signaling time scale.

12 To better understand genome coordination and OXPHOS recovery during mitochondrial dysfunction, we exa

13 n a global downregulation of Krebs cycle and OXPHOS gene expression, defective mitochondria, reduced

14 inducing transcription of the TCA cycle and OXPHOS genes carried by both nuclear and mitochondrial D

15 ly the existence of histone deacetylase- and OXPHOS-independent crosstalk between the proteins in the

16 Genetic disorders of FAO and OXPHOS are among the most frequent inborn errors of meta

17 Type 1 IFNs also induced increased FAO and OXPHOS in non-hematopoietic cells and were found to be r

18 Increased FAO and OXPHOS in response to type 1 IFNs was regulated by PPARa

19 ound to be responsible for increased FAO and OXPHOS in virus-infected cells.

20 metabolic program as well as glycolysis and OXPHOS, but IFN-gamma production could be reinstated by

21 , to quantify the activity of glycolysis and OXPHOS.

22 r the regulatory principle of glycolysis and OXPHOS.

23 duction due to inhibition of complex III and OXPHOS.

24 iogenesis, oxidative metabolic pathways, and OXPHOS proteins in SAT are downregulated in acquired obe

25 Further, the expression of NPRA, PGC1A, and OXPHOS genes was coordinately upregulated in response to

26 red to simulate measured phosphocreatine and OXPHOS responses to both moderate and severe intensity e

27 ion subsequently inhibits OCR/ECAR ratio and OXPHOS, and eventually upregulate epigenetics remodeling

28 e acting to coordinate protein synthesis and OXPHOS assembly events and thus the bioenergetic capacit

29 ctivation of mitochondrial transcription and OXPHOS by the KR mutant remained robust, further highlig

30 nt increased mitochondrial transcription and OXPHOS in vitro.

31 gy; OXPHOS complex activity; fully assembled OXPHOS complexes and their subunits; gene expression of

32 ells use p32 to regulate the balance between OXPHOS and glycolysis.

33 following ET (18 +/- 16 and 43 +/- 30%), but OXPHOS remained unaltered.

34 A heteroplasmy, UPR(mt) activation caused by OXPHOS defects propagates or maintains the deleterious m

35 nsion of protective CD8(+) T cells driven by OXPHOS and represents a pathway for the restoration of l

36 iciency and proton translocation mediated by OXPHOS complex I.

37 acyl-CoA substrates were not metabolized by OXPHOS-containing supercomplex fractions.

38 xygen uptake and fluxes of ATP production by OXPHOS (vOX), anaerobic glycolysis and creatine kinase i

39 )maximal oxidative phosphorylation capacity (OXPHOS), and mitochondrial dynamics, turnover, and plast

40 arity, fibre types and respiratory capacity (OXPHOS).

41 ition to regulating mitochondrial chaperone, OXPHOS complex assembly factor, and glycolysis genes, AT

42 ed families with Leigh syndrome and combined OXPHOS defects.

43 ndrial protein translation, causing combined OXPHOS enzyme deficiency and clinical disease.

44 kb1 have defective mitochondria, compromised OXPHOS, depleted cellular ATP, and altered cellular meta

45 We considered OXPHOS genes of six holometabolous insects and their ort

46 the assembly of two flavoprotein-containing OXPHOS complexes, and cell type specific.

47 to the sucrose gradient fractions containing OXPHOS supercomplexes in the presence of potassium cyani

48 In contrast, OXPHOS inhibition or PTP opening increased synthasome di

49 production via the tricarboxylic acid cycle, OXPHOS, and fatty acid oxidation; beta-catenin function

50 DPH deficiency protects mice from developing OXPHOS dysfunction and NASH caused by a HFD.

51 hat all OH-PBDEs tested were able to disrupt OXPHOS via either protonophoric uncoupling and/or inhibi

52 he environment have the potential to disrupt OXPHOS.

53 We conclude that mtDNA-driven OXPHOS dysfunction correlates with increased motility an

54 d synthesis of the mitochondrial-DNA-encoded OXPHOS polypeptides and were less tumorigenic in vivo.

55 otide substitutions in mitochondrial-encoded OXPHOS genes, a process known as compensatory co-adaptat

56 show that nuclear- and mitochondrial-encoded OXPHOS transcript levels do not increase concordantly.

57 s of mitochondrial, but not nuclear, encoded OXPHOS subunits.

58 this hypothesis by analyzing nuclear-encoded OXPHOS genes for signatures of positive selection as wel

59 gence in 4 of the 59 studied nuclear-encoded OXPHOS genes.

60 However, if the deletion genome is enriched, OXPHOS declines, resulting in cellular dysfunction.

61 Reducing equivalents from FAO enter OXPHOS at the level of complexes I and III.

62 Our findings reveal FAO, OXPHOS and PPARalpha as potential targets to therapeutic

63 surface exposed subunit of each of the five OXPHOS complexes and used for systematic immunoblotting

64 -expression of genes within each of the five OXPHOS enzyme complexes, showing a higher degree of comp

65 al DNA encodes several subunits critical for OXPHOS, the metabolic consequence of activating mitochon

66 g the efficiency of translation of mRNAs for OXPHOS and ribosomal proteins.

67 One of the most frequent OXPHOS defects in humans frequently associated with card

68 ity and they undergo a metabolic switch from OXPHOS to glycolysis, mimicking the clinical features fo

69 rotons on the kinetics of ATP synthesis from OXPHOS, anaerobic glycolysis and creatine kinase.

70 s from patients failed to induce glycolysis, OXPHOS, ATP production, GLUT1 expression, glucose entry,

71 In nonstressed KO hearts, OXPHOS gene expression and palmitoyl-carnitine-supported

72 ranscriptional program that enhanced hepatic OXPHOS.

73 weeks, we studied the liver for: histology; OXPHOS complex activity; fully assembled OXPHOS complexe

74 phosphorylation (OXPHOS), but precisely how OXPHOS meets the challenge of increased substrate oxidat

75 of predefined pathways from KEGG identified OXPHOS pathway involved in oxidative phosphorylation in

76 ssed a validated quadruple immunofluorescent OXPHOS (IHC) assay to detect CI deficiency in the diagno

77 ondrial content) or acquired (e.g., impaired OXPHOS capacity and plasticity).

78 the major ANT isoform only modestly impairs OXPHOS in HEK293 cells, indicating that the low levels o

79 In OXPHOS-dependent LKB1 wild type cells, oligomycin induce

80 In OXPHOS-dependent LKB1-null cells, no AMPK activation by

81 ver, it remained unclear why the decrease in OXPHOS occurs under these circumstances.

82 translation products, as well as defects in OXPHOS complex assembly observed in MTO1 deficient mice

83 atum is particularly sensitive to defects in OXPHOS possibly due to an increased reliance on OXPHOS f

84 d leading to endocrine therapy resistance in OXPHOS-dependent breast cancer.

85 ibution of LRP130 deacetylation to increased OXPHOS in fasted liver.

86 NP treatment increased OXPHOS protein expression, fat oxidation, and maximal re

87 l transcription is associated with increased OXPHOS activity, increased supercomplexes, and denser cr

88 biguanides, antidiabetic drugs that inhibit OXPHOS, when cancer cells are grown in low glucose or as

89 tor of activated STAT3, was found to inhibit OXPHOS activity in the mitochondria, resulting in inhibi

90 Nicotine and e-cigarette inhibited OXPHOS complex III accompanied by increased MitoROS, and

91 , and it is linked to disease, as inhibiting OXPHOS reduces the severity of murine colitis and psoria

92 oligomycin at 100 ng/ml completely inhibits OXPHOS activity in 1 h and induces various levels of gly

93 PHOS subunits, and assembly of subunits into OXPHOS complexes were normal in these mice.

94 Our data show that key OXPHOS regulators are required for optimal Treg function

95 in biochemical defect, affecting the largest OXPHOS component.

96 wal-deficient cancer cells, CD133(hi)/ER(lo)/OXPHOS(lo).

97 th the m.12955A > G mutation exhibited lower OXPHOS coupling respiration and adenosine triphosphate (

98 in the oxidative phosphorylation machinery (OXPHOS), which are the only complexes composed of protei

99 suggest a therapeutic role for manipulating OXPHOS in Th17-driven diseases.

100 ntent was accompanied by a decreased maximal OXPHOS capacity in the simvastatin-treated patients.

101 uvate oxidation carried out in mitochondria (OXPHOS), a phenomenon termed the Warburg effect, which i

102 Mitochondrial OXPHOS capacity was measured in permeabilized muscle fib

103 bes, NP induced PGC-1alpha and mitochondrial OXPHOS gene expression in a cyclic GMP-dependent manner.

104 in muscle Q(10) may attenuate mitochondrial OXPHOS capacity, which may be an underlying mechanism.

105 bjects with defective combined mitochondrial OXPHOS-enzyme deficiencies, identified a total of nine d

106 tivity of complex I within the mitochondrial OXPHOS chain.

107 PGC-1alpha targets such as the mitochondrial OXPHOS genes.

108 nd tissue-specific deficiency of one or more OXPHOS complexes.

109 We identified mice with increased mucosal OXPHOS complex activities and levels of ATP.

110 Multiple OXPHOS defects and decreased mtDNA copy number (40%) wer

111 orylation (OXPHOS) defects, but there was no OXPHOS deficiency in fibroblasts from either subject, de

112 other recent advance is the discovery of non-OXPHOS complex proteins that appear to adhere to and sea

113 Although nuclear OXPHOS genes are typically highly conserved, we found si

114 -1 was required to limit the accumulation of OXPHOS transcripts during mitochondrial stress, which re

115 enerates lethal ROS via forced activation of OXPHOS.

116 teome to increase the levels and activity of OXPHOS protein complexes, leading to rescue of the bioen

117 fully assembled complexes, in the amount of OXPHOS subunits, and in gene expression of mitochondrial

118 With the purpose of analysing the effects of OXPHOS dysfunction in cancer cells and the molecular pla

119 Inborn errors of OXPHOS function are termed primary mitochondrial disorde

120 lexes and their subunits; gene expression of OXPHOS subunits; oxidative and nitrosative stress; and o

121 t manner, which was followed by induction of OXPHOS activity.

122 rmined here how acute (30 min) inhibition of OXPHOS affected cytosolic GLC homeostasis.

123 found that this is because of inhibition of OXPHOS by NO and that the switch to glycolysis is a surv

124 In contrast, pharmacological inhibition of OXPHOS expression and function inhibits ANT-dependent AD

125 Inhibition of OXPHOS impaired both Tcon and Treg cell function compare

126 Inhibition of OXPHOS induced a twofold increase in Vsteady-state and g

127 n (OXPHOS) with sensitivity to inhibition of OXPHOS.

128 rane potential are seen upon introduction of OXPHOS substrates into the nanofluidic channel.

129 Levels of OXPHOS subunits were coordinately increased in liver mit

130 Both in the absence and presence of OXPHOS inhibitors, GLC was consumed at near maximal rate

131 steady-state) in the absence and presence of OXPHOS inhibitors.

132 factor in the tissue-specific regulation of OXPHOS and fine tuning of mitochondrial translation accu

133 ied to mitochondria, so the co-regulation of OXPHOS genes remains largely unexplored.

134 1alpha or Sirt3, which are key regulators of OXPHOS, abrogated Treg-dependent suppressive function an

135 e a similar overall pattern of repression of OXPHOS and FAO genes as WT-TAC.

136 ced mitochondrial function and repression of OXPHOS and FAO genes.

137 were accompanied by coordinate repression of OXPHOS and peroxisome proliferator-activated receptor (P

138 Restoration of OXPHOS Complex I inhibitor-induced miR-663 expression by

139 , expression of EV mtRNA, and restoration of OXPHOS.

140 Mechanistically, the essential role of OXPHOS in Th17 cells results from their limited capacity

141 rial myopathy correlate with the severity of OXPHOS dysfunction, as indicated by the level of impaire

142 We show that stimulation of OXPHOS, inhibition of the PTP, or deletion of CypD incre

143 tion of complex III activity, suppression of OXPHOS, and ATP depletion.

144 ation to orchestrate the timely synthesis of OXPHOS complexes, representing an unappreciated regulato

145 e MRPS34 protein levels and the synthesis of OXPHOS subunits encoded by mtDNA.

146 wered abundance of Complexes I, IV, and V of OXPHOS.

147 with mitochondria and their consequences on OXPHOS.

148 ed, as was the effect of STAT3 inhibition on OXPHOS activity and mast cell function.

149 HOS possibly due to an increased reliance on OXPHOS function in this area and differences in response

150 Because the kidney relies on OXPHOS for metabolic homeostasis, we hypothesized that a

151 e observed for the first time that, not only OXPHOS genes as a group co-express, but there is a co-ex

152 Patients with deficiencies of either FAO or OXPHOS often show clinical and/or biochemical findings i

153 ee of these four genes, as well as six other OXPHOS genes, contain amino acid substitutions between N

154 ound that each-step activation of particular OXPHOS complexes, NADH supply and glycolysis, and strong

155 cancer cells may grow and survive persistent OXPHOS suppression through an as yet unidentified regula

156 Boosting residual oxidative phosphorylation (OXPHOS) activity can partially correct these failures.

157 ing in a burst of oxidative phosphorylation (OXPHOS) activity.

158 ned mitochondrial oxidative phosphorylation (OXPHOS) and activated mitochondrial permeability transit

159 ic acid cycle and oxidative phosphorylation (OXPHOS) and decreased production of adenosine triphospha

160 ciations favoring oxidative phosphorylation (OXPHOS) and FAO, while fission in TE cells leads to cris

161 rol mechanisms of oxidative phosphorylation (OXPHOS) and glycolysis during work transitions in human

162 idation (FAO) and oxidative phosphorylation (OXPHOS) are key pathways involved in cellular energetics

163 sed by defects in oxidative phosphorylation (OXPHOS) are severe, often lethal, conditions.

164 ted mitochondrial oxidative phosphorylation (OXPHOS) as the major pathway required for optimal prolif

165 rial proteins and oxidative phosphorylation (OXPHOS) bioenergetic function in these mice.

166 thy impair muscle oxidative phosphorylation (OXPHOS) by distinct mechanisms: the former by restrictin

167 and mitochondrial oxidative phosphorylation (OXPHOS) capacity were measured in simvastatin-treated pa

168 e subunits of the oxidative phosphorylation (OXPHOS) chain.

169 the mitochondrial oxidative phosphorylation (OXPHOS) complex, so mitochondrial dysfunction could cont

170 g glycolysis) and oxidative phosphorylation (OXPHOS) complexes and (2) glycolytic inhibition by proto

171 led the levels of oxidative phosphorylation (OXPHOS) complexes and respiration, resulting in the prod

172 components of the oxidative phosphorylation (OXPHOS) complexes.

173 s inhibited their oxidative phosphorylation (OXPHOS) complexes.

174 encode essential oxidative phosphorylation (OXPHOS) components.

175 y showed combined oxidative phosphorylation (OXPHOS) defects, but there was no OXPHOS deficiency in f

176 ted with combined oxidative phosphorylation (OXPHOS) deficiencies.

177 Neuronal oxidative phosphorylation (OXPHOS) deficiency has been associated with a variety of

178 DNA) mutations in oxidative phosphorylation (OXPHOS) deficiency.

179 e pathogenesis of oxidative phosphorylation (OXPHOS) dysfunction as found in mice fed a high-fat diet

180 ls, mitochondrial oxidative phosphorylation (OXPHOS) dysfunction has been shown to promote migration,

181 including lowered oxidative phosphorylation (OXPHOS) efficiency, increased mitochondrial superoxide p

182 e cells depend on oxidative phosphorylation (OXPHOS) for energy and cytokine production.

183 scent T cells use oxidative phosphorylation (OXPHOS) for energy production, and effector T cells (Tef

184 hondrial mass and oxidative phosphorylation (OXPHOS) function.

185 itially abrogates oxidative phosphorylation (OXPHOS) generating self-renewal-deficient cancer cells,

186 GC1A) and several oxidative phosphorylation (OXPHOS) genes in human skeletal muscle.

187 rol mitochondrial oxidative phosphorylation (OXPHOS) in acute myeloid leukemia (AML) cells.

188 cluding defective oxidative phosphorylation (OXPHOS) in cancer inhibit apoptosis by modulating ROS pr

189 of mitochondrial oxidative phosphorylation (OXPHOS) in mast cell exocytosis was recently suggested b

190 ls with different oxidative phosphorylation (OXPHOS) inhibitors showed that compounds known to genera

191 Oxidative phosphorylation (OXPHOS) is a vital process for energy generation, and is

192 The mitochondrial oxidative phosphorylation (OXPHOS) is critical for energy (ATP) production in eukar

193 Impaired oxidative phosphorylation (OXPHOS) is implicated in several metabolic disorders.

194 Mitochondrial oxidative phosphorylation (OXPHOS) is under the control of both mitochondrial (mtDN

195 rom glycolytic to oxidative phosphorylation (OXPHOS) metabolism and has been associated with increase

196 ial and inhibited oxidative phosphorylation (OXPHOS) of RPE cells.

197 flux through the oxidative phosphorylation (OXPHOS) pathway, usually without alterations in mitochon

198 in animals is the oxidative phosphorylation (OXPHOS) pathway, which depends on the tight interaction

199 dels do not cause oxidative phosphorylation (OXPHOS) perturbations.

200 nce suggests that oxidative phosphorylation (OXPHOS) plays a crucial role during cancer progression.

201 and mitochondrial oxidative phosphorylation (OXPHOS) protein levels.

202 nstantly adapt to oxidative phosphorylation (OXPHOS) suppression resulting from hypoxia or mitochondr

203 by defects in the oxidative phosphorylation (OXPHOS) system are susceptible to cardiac involvement.

204 components of the oxidative phosphorylation (OXPHOS) system encoded by the mitochondrial genome.

205 complexes of the oxidative phosphorylation (OXPHOS) system in different organs or tissues are quanti

206 ysfunction of the oxidative phosphorylation (OXPHOS) system is a major cause of human disease and the

207 nits of the human oxidative phosphorylation (OXPHOS) system is carried out by mitochondrial ribosomes

208 ic acid cycle and oxidative phosphorylation (OXPHOS) system.

209 ive mitochondrial oxidative phosphorylation (OXPHOS) system.

210 t subunits of the oxidative phosphorylation (OXPHOS) system.

211 A "switch" from oxidative phosphorylation (OXPHOS) to aerobic glycolysis is a hallmark of T cell ac

212 r metabolism from oxidative phosphorylation (OXPHOS) to glycolysis.

213 duction away from oxidative phosphorylation (OXPHOS) toward glycolysis during malignant progression,

214 utilization, and oxidative phosphorylation (OXPHOS) were determined.

215 on mitochondrial oxidative phosphorylation (OXPHOS) with sensitivity to inhibition of OXPHOS.

216 bility to disrupt oxidative phosphorylation (OXPHOS), an essential process in energy metabolism.

217 TP concentration, oxidative phosphorylation (OXPHOS), and glycolysis pathways in T cells were decreas

218 on mitochondrial oxidative phosphorylation (OXPHOS), BRSKs, CDC25B/C, MAP/Tau, Wee1 and epigenetics

219 te flux depend on oxidative phosphorylation (OXPHOS), but precisely how OXPHOS meets the challenge of

220 lt of an impaired oxidative phosphorylation (OXPHOS), especially complex V.

221 mRNAs involved in oxidative phosphorylation (OXPHOS), mammalian mitochondria contain a dedicated set

222 gy production via oxidative phosphorylation (OXPHOS), mitochondria are essential for nutrient and oxy

223 ed glycolysis and oxidative phosphorylation (OXPHOS), required for cytokine production.

224 o support FAO and oxidative phosphorylation (OXPHOS), suggesting that lipids must be synthesized to g

225 sult in defective oxidative phosphorylation (OXPHOS), via loss of complex I activity and assembly in

226 on, mitochondrial oxidative phosphorylation (OXPHOS), wound healing, and gel contraction at different

227 idation (FAO) and oxidative phosphorylation (OXPHOS).

228 cal disruption of oxidative phosphorylation (OXPHOS).

229 enes important to oxidative phosphorylation (OXPHOS).

230 nt ATP synthesis, oxidative phosphorylation (OXPHOS).

231 rom inhibition of oxidative phosphorylation (OXPHOS).

232 bic glycolysis to oxidative phosphorylation (OXPHOS).

233 ltiple defects in oxidative phosphorylation (OXPHOS).

234 is essential for oxidative phosphorylation (OXPHOS).

235 is essential for oxidative phosphorylation (OXPHOS).

236 eptor-independent oxidative phosphorylation (OXPHOS).

237 result in reduced oxidative phosphorylation (OXPHOS).

238 d (TCA) cycle and oxidative phosphorylation (OXPHOS).

239 the first step in oxidative phosphorylation (OXPHOS).

240 are part of the 'oxidative phosphorylation' (OXPHOS) pathway.

241 uring post-natal development and progressive OXPHOS dysfunction in time course analyses in control mi

242 ecause balanced ATFS-1 accumulation promoted OXPHOS complex assembly and function, our data suggest t

243 ssed in some cancers is capable of promoting OXPHOS.

244 e deleterious mtDNA in an attempt to recover OXPHOS activity by promoting mitochondrial biogenesis an

245 LS1 inhibition by the drug CB-839 can reduce OXPHOS, leading to leukemic cell proliferation arrest an

246 The anti-miR-663 reduced OXPHOS complex activity and increased in vitro cellular

247 mitochondrial function that included reduced OXPHOS, fatty acid oxidation (FAO), and ATP production.

248 d mitochondrial transcription that regulates OXPHOS in fasted liver and may explain how fasted liver

249 In our mouse model, MTO1-related OXPHOS deficiency can be bypassed by feeding a ketogenic

250 red cybrids grown under conditions requiring OXPHOS activity for survival.

251 ld-type, but not mutagenized, C1qbp restored OXPHOS protein levels and mitochondrial enzyme activitie

252 seudofirmus OF4, might facilitate its robust OXPHOS at pH 10.5, where the bulk protonmotive (PMF) for

253 of neuronal populations undergoing the same OXPHOS deficiency to determine their relative susceptibi

254 amide gel electrophoresis (BNGE) to separate OXPHOS complexes and supercomplexes followed by Western

255 of mitochondrial polypeptides, and a severe OXPHOS assembly defect.

256 ltered gene expression patterns under severe OXPHOS deficiency comparing several mouse models, that w

257 phosphate (ATP) and reactive oxygen species, OXPHOS complex activity, and epithelial cell proliferati

258 cific manner associated with tissue-specific OXPHOS defects.

259 t (KO) mice were treated to either stimulate OXPHOS or open the PTP.

260 lly diverse microtubule inhibitors stimulate OXPHOS transcription while suppressing reactive oxygen s

261 osomes and oxidative phosphorylation system (OXPHOS) complexes seems to be less affected.

262 rly of the oxidative phosphorylation system (OXPHOS), occurs in neurodegeneration, it is postulated t

263 Taken together, we demonstrate here that OXPHOS inhibition increases steady-state GLC uptake and

264 Thus ANTs and the OXPHOS machinery physically interact and functionally co

265 In this study, we determined the OXPHOS disruption potential of 18 OH-PBDE congeners repo

266 of ERRalpha or ERRgamma is required for the OXPHOS burst in both human and mouse cells, respectively

267 ensitive to low glucose are defective in the OXPHOS upregulation that is normally caused by glucose l

268 lucose metabolism through alterations in the OXPHOS-to-glycolysis balance.

269 e for both proteins in the regulation of the OXPHOS activity.

270 ate and lower levels of some proteins of the OXPHOS complex suggesting a role for PKCdelta in the reg

271 al genomes, to investigate activities of the OXPHOS complex.

272 unological investigation on the ratio of the OXPHOS complexes in different tissues of Arabidopsis tha

273 and the decreased stability/activity of the OXPHOS complexes, were probably caused by the lower amou

274 ranslation system, and protein levels of the OXPHOS machinery in the obese compared with the lean co-

275 esized that the nuclear-encoded genes of the OXPHOS pathway are under strong selective pressure to co

276 easurements for the protein complexes of the OXPHOS system and comparative 2D blue native/SDS PAGE an

277 we study the bioenergetic adaptation to the OXPHOS inhibitor oligomycin in a group of cancer cells.

278 Under the OXPHOS suppression, AMP-activated protein kinase (AMPK)

279 tochondria leads to perturbations within the OXPHOS complexes, generating more reactive oxygen specie

280 ased substrate oxidation by increasing their OXPHOS efficiency.

281 d glycolysis genes, ATFS-1 bound directly to OXPHOS gene promoters in both the nuclear and mitochondr

282 ctanoyl-CoA provided reducing equivalents to OXPHOS-containing supercomplex fractions, no accumulatio

283 in the mitochondrial DNA (mtDNA), leading to OXPHOS deficiency, mostly due to mtDNA depletion.

284 itochondrial DNA gene expression, leading to OXPHOS dysfunction.

285 tedly, we identify a new response pathway to OXPHOS dysfunction in which the intra-mitochondrial synt

286 xpression, shifting the Warburg phenotype to OXPHOS and inhibiting glioblastoma multiforme growth and

287 One mechanism by which cells respond to OXPHOS dysfunction is by activating the mitochondrial un

288 ifying tumours with increased sensitivity to OXPHOS inhibitors.

289 itochondrial function in cancer cells toward OXPHOS that restricts their malignant phenotype.

290 rowth by redirecting their metabolism toward OXPHOS.

291 imulates respiratory recovery by fine-tuning OXPHOS expression to match the capacity of the suboptima

292 ibition of myofibroblast differentiation via OXPHOS pathway.

293 put into the Q intersection [maximal ex vivo OXPHOS capacity]), a decreased (p < 0.01) capacity was o

294 visiae during mitochondrial biogenesis, when OXPHOS complexes are synthesized.

295 onse that serves to maintain ATP levels when OXPHOS is inhibited.

296 ittle is known about the mechanisms by which OXPHOS activity could be altered.

297 n's disease, which have been associated with OXPHOS defects.

298 ochondria that is physically associated with OXPHOS supercomplexes and promotes metabolic channeling.

299 te mitochondrial genomes of 41 families with OXPHOS deficiency were screened for mutations.

300 Several FAO enzymes co-migrated with OXPHOS supercomplexes in different patterns in the gels.