ライフサイエンスコーパス: OXPHOS

1 OXPHOS activity, OXPHOS subunits, and assembly of subuni

2 OXPHOS complexes pose a unique challenge for cells becau

3 OXPHOS requires O(2) as the final electron acceptor, but

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

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

6 t not mitochondrial matrix Ca(2+), may adapt OXPHOS to workload by adjusting the rate of pyruvate sup

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

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

9 inimal phenotypic changes and does not alter OXPHOS.

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

11 tic homeostasis of both OXPHOS-competent and OXPHOS-defective cells, with Ca(2+) regulation of alphaK

12 in these cells, we used OXPHOS-competent and OXPHOS-defective cells.

13 ndent autophagy in both OXPHOS-competent and OXPHOS-defective cells.

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

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

16 OXPHOS supercomplexes were destabilized, and OXPHOS enzymatic activities were reduced in AR-expressin

17 and decreased phosphorylation efficiency and OXPHOS coupling efficiency in both species, which may se

18 and decreased phosphorylation efficiency and OXPHOS coupling efficiency, which may serve to augment n

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

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

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

22 e regulation to balance their glycolysis and OXPHOS activities.

23 metabolic state in which both glycolysis and OXPHOS can be used.

24 phenotype and targeting both glycolysis and OXPHOS is necessary to eliminate their metabolic plastic

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

26 lls have low activity of both glycolysis and OXPHOS.

27 robust and rapid increases in glycolysis and OXPHOS.

28 , to quantify the activity of glycolysis and OXPHOS.

29 r the regulatory principle of glycolysis and OXPHOS.

30 Targeting heme metabolism and OXPHOS may be an effective strategy to combat lung cance

31 n the lung by inhibiting heme metabolism and OXPHOS.

32 ingly, we found activated mitobiogenesis and OXPHOS with significant increase of H2O2, sharply contra

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

34 tabolism through both lactate production and OXPHOS is necessary for normal osteoclastogenesis.

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

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

37 DPI was replaceable by the FDA-approved OXPHOS inhibitor metformin (MET), both for synthetic let

38 t transcriptional PGC-1alpha targets such as OXPHOS or gluconeogenic genes.

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

40 Conversely, depletion of COX6B2 attenuates OXPHOS and collapses mitochondrial membrane potential le

41 ch induced SIRT1-dependent autophagy in both OXPHOS-competent and OXPHOS-defective cells.

42 maintaining bioenergetic homeostasis of both OXPHOS-competent and OXPHOS-defective cells, with Ca(2+)

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

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

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

46 iciency and proton translocation mediated by OXPHOS complex I.

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

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

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

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

51 ed families with Leigh syndrome and combined OXPHOS defects.

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

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

54 uces aerobic glycolysis without compromising OXPHOS, but nonetheless diminishes osteoclast differenti

55 in mitochondrial translation and consequent OXPHOS deficiency, without affecting mitochondrial RNA l

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

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

58 These results reveal that Na(+) controls OXPHOS function and redox signalling through an unexpect

59 ly, impairing mitochondrial fusion decreased OXPHOS but did not deplete ATP levels.

60 In cells with defective OXPHOS, reductive carboxylation replaces oxidative metab

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

62 to pneumococcal pneumonia by downregulating OXPHOS genes and increasing glycolysis in macrophages.

63 metabolism and fatty acid oxidation to drive OXPHOS, thereby providing a means for LSCs to circumvent

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

65 ontrols up to 85% of maximal pyruvate-driven OXPHOS rates, mediated by the activity of the complete M

66 gh reducing mitochondrial respiration (i.e., OXPHOS), which in turn triggers reversible pluripotent q

67 sfunction, including respiratory efficiency, OXPHOS subunits, and complex amount and assembly.

68 chondrial biogenesis, which further elevated OXPHOS.

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

70 ted heme flux and function underlie enhanced OXPHOS and tumorigenicity of NSCLC cells.

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

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

73 y suggests a general function of the MOF/FAO/OXPHOS axis in regulating cell fate determination in ste

74 The inhibition of FAO/OXPHOS also induces quiescence in naive human ESCs.

75 tic products to the mitochondrial matrix for OXPHOS.

76 Ca(2+) cannot be the exclusive mechanism for OXPHOS control.

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

78 ch enables validation of ECAR resulting from OXPHOS versus glycolysis, and expression of metabolic fl

79 absence of miR-142, DCs fail to switch from OXPHOS and show reduced production of proinflammatory cy

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

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

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

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

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

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

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

87 Whereas autophagic flux in OXPHOS-competent cells promoted cell survival, it was im

88 of alphaKGDH and impaired autophagic flux in OXPHOS-defective cells resulted in pronounced cell death

89 s promoted cell survival, it was impaired in OXPHOS-defective cells because of inhibition of autophag

90 revealed downregulation of genes involved in OXPHOS.

91 safety profile, eliminates aspartate only in OXPHOS-incompetent tumors, and prevents their growth and

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

93 shuttle (MAS)-dependent substrate supply in OXPHOS responses to changing Ca(2+) concentrations in is

94 Increased OXPHOS dependency is frequently a hallmark of cancer ste

95 uated inflammatory gene expression increased OXPHOS pathway genes and had potentially clinically impo

96 t that cell proliferation requires increased OXPHOS as supported by mitochondrial fusion.

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

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

99 hondrial gas pedal." Its implementation into OXPHOS control models integrates seemingly contradictory

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

101 in biochemical defect, affecting the largest OXPHOS component.

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

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

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

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

106 n of matrix dehydrogenases, thereby matching OXPHOS substrate supply to ATP demand.

107 t had some distinct effects on mitochondrial OXPHOS capacity between species, but the capacity of com

108 is reliance of cancer cells on mitochondrial OXPHOS pathways could offer an actionable therapeutic ta

109 tivity of complex I within the mitochondrial OXPHOS chain.

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

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

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

113 Consistent with these observations, OXPHOS supercomplexes were destabilized, and OXPHOS enzy

114 enerates lethal ROS via forced activation of OXPHOS.

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

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

117 Thus, the assembly of OXPHOS complexes induces CL remodeling, which, in turn,

118 lutarate (aKG) esters elicits rapid death of OXPHOS-deficient cancer cells by elevating intracellular

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

120 Inborn errors of OXPHOS function are termed primary mitochondrial disorde

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

122 an overview of the structure and function of OXPHOS complexes, their biological functions in cancer,

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

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 The knockdown of OXPHOS expression had the same effect on CL as the knock

129 ls and models, as well as the limitations of OXPHOS as drug targets.

130 ults demonstrate that distinct mechanisms of OXPHOS exist in chRCC and renal oncocytoma and that expr

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

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

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

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

135 ties of AMPK and HIF-1, master regulators of OXPHOS and glycolysis, respectively, with the activities

136 1alpha or Sirt3, which are key regulators of OXPHOS, abrogated Treg-dependent suppressive function an

137 As such, the relevance of OXPHOS status and role of CI mutations in chRCC remain u

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 However, sequestration of OXPHOS components in cristae membranes necessitates a re

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

143 o focus on the current development status of OXPHOS inhibitors and potential therapeutic strategies t

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

145 activators, help to coordinate synthesis of OXPHOS catalytic subunits by the mitoribosomes with both

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

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

148 lation (OXPHOS), the rates of utilization of OXPHOS/glycolysis in response to metabolic stress, and m

149 with mitochondria and their consequences on OXPHOS.

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

151 nt UM cell lines also showed OXPHOS(high) or OXPHOS(low) subgroups.

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

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

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

155 the complexes of oxidative phosphorylation (OXPHOS) affected the CL composition.

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

157 ntial for optimal oxidative phosphorylation (OXPHOS) and ATP production.

158 Mitochondrial oxidative phosphorylation (OXPHOS) and cellular workload are tightly balanced by th

159 elevated FAO for oxidative phosphorylation (OXPHOS) and energy production.

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 for mitochondrial oxidative phosphorylation (OXPHOS) and glycolytic rate in cell metabolism studies.

163 ex IV, increasing oxidative phosphorylation (OXPHOS) and NAD(+) generation.

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

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

166 sts also increase oxidative phosphorylation (OXPHOS) by nearly two-fold and mitochondrial coupling ef

167 th glycolysis and oxidative phosphorylation (OXPHOS) can be utilized.

168 Reduced placental oxidative phosphorylation (OXPHOS) capacity measured in situ was observed despite n

169 of mitochondrial oxidative phosphorylation (OXPHOS) complex II and IV subunits, dampened reactive ox

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 encode essential oxidative phosphorylation (OXPHOS) components.

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

174 ted with combined oxidative phosphorylation (OXPHOS) deficiencies.

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

176 the engagement of oxidative phosphorylation (OXPHOS) driven by elevated fatty acid oxidation (FAO), r

177 en glycolysis and oxidative phosphorylation (OXPHOS) during tumorigenesis and metastasis.

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

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

180 iratory capacity, oxidative phosphorylation (OXPHOS) efficiency, and a consequential increase in cell

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

182 sis of multimeric oxidative phosphorylation (OXPHOS) enzyme in mitochondria from the yeast Saccharomy

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

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

185 hondrial mass and oxidative phosphorylation (OXPHOS) function.

186 ubgroups based on oxidative phosphorylation (OXPHOS) gene expression suggesting metabolic heterogenei

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

188 downregulation of oxidative phosphorylation (OXPHOS) genes in an IL-22-dependent manner.

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

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

191 accumulation and oxidative phosphorylation (OXPHOS) in the mitochondria.

192 NA) knockdown, an oxidative phosphorylation (OXPHOS) inhibitor diphenyleneiodonium (DPI), and a fatty

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

194 etabolism through oxidative phosphorylation (OXPHOS) is the predominant bioenergetic pathway to suppo

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

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

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

198 and mitochondrial oxidative phosphorylation (OXPHOS) protein levels.

199 the expression of oxidative phosphorylation (OXPHOS) subunits.

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

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

202 ysfunction of the oxidative phosphorylation (OXPHOS) system in renal oncocytoma, but are less frequen

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

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

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

206 m a predominantly oxidative phosphorylation (OXPHOS) to glycolysis to mount an immunogenic response.

207 abolic shift from oxidative phosphorylation (OXPHOS) to glycolysis was demonstrated in embryos by an

208 cer cells require oxidative phosphorylation (OXPHOS) to survive.

209 Targeting oxidative phosphorylation (OXPHOS) with BDQ and simultaneously inhibiting substrate

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

211 , but the idea of oxidative phosphorylation (OXPHOS) within mitochondria did not appear until the 193

212 s produced during oxidative phosphorylation (OXPHOS), a metabolic pathway coupling electron transfer

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

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

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

216 of glycolysis and oxidative phosphorylation (OXPHOS), in comparison to naive T-cells.

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

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

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

220 xins that disrupt oxidative phosphorylation (OXPHOS), resulting in UPR(mt) activation.

221 ion of drivers of oxidative phosphorylation (OXPHOS), the rates of utilization of OXPHOS/glycolysis i

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

223 (TCA) cycle, and Oxidative Phosphorylation (OXPHOS), which redirected the TNBC metabolism to mitocho

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

225 , we use multiple oxidative phosphorylation (OXPHOS)-competent and incompetent cancer cell pairs to d

226 he main driver of oxidative phosphorylation (OXPHOS).

227 d upregulation of oxidative phosphorylation (OXPHOS).

228 cal disruption of oxidative phosphorylation (OXPHOS).

229 bic glycolysis to oxidative phosphorylation (OXPHOS).

230 ltiple defects in oxidative phosphorylation (OXPHOS).

231 is essential for oxidative phosphorylation (OXPHOS).

232 is essential for oxidative phosphorylation (OXPHOS).

233 eptor-independent oxidative phosphorylation (OXPHOS).

234 result in reduced oxidative phosphorylation (OXPHOS).

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

236 the first step in oxidative phosphorylation (OXPHOS).

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

238 e Krebs cycle and oxidative phosphorylation (OXPHOS).

239 enes important to oxidative phosphorylation (OXPHOS).

240 rocesses, such as oxidative phosphorylation (OXPHOS).

241 via mitochondrial oxidative phosphorylation (OXPHOS).

242 esis, uptake, and oxidative phosphorylation (OXPHOS).

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

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

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

246 We reveal that by promoting OXPHOS, mitofusins enable spermatogonial differentiation

247 eases the levels of two regulators promoting OXPHOS, MYC and MCL1, and effectively alleviates tumor h

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

249 hile silencing CLPP was sufficient to reduce OXPHOS capacity, membrane potential, and promoted mitoch

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

251 ges from Il22ra2(-/-) mice displayed reduced OXPHOS gene expression upon infection with S. pneumoniae

252 CI mutations, was the main cause for reduced OXPHOS in chRCC.

253 tes or germ cells in vivo results in reduced OXPHOS subunits and activity.

254 ion of the UPR(mt) with methacycline reduced OXPHOS capacity, while silencing CLPP was sufficient to

255 +) acts as a second messenger that regulates OXPHOS function and the production of reactive oxygen sp

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

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

258 o directly inhibit mitochondrial respiration/OXPHOS.

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

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

261 sis of BAP1 mutant UM cell lines also showed OXPHOS(high) or OXPHOS(low) subgroups.

262 cific manner associated with tissue-specific OXPHOS defects.

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

264 ly, CycT acts via multiple modes to suppress OXPHOS.

265 ochondrial oxidative phosphorylation system (OXPHOS) to produce energy.

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

267 lopment of combination therapies that target OXPHOS and glycolysis.

268 Thus, targeting OXPHOS is a promising strategy to treat various cancers.

269 These findings demonstrate that OXPHOS deficiency caused by either hypoxia or mutations,

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

271 bolomics, and molecular analyses showed that OXPHOS(high) BAP1 mutant UM cells utilize glycolytic and

272 The OXPHOS system is composed of large, multiprotein complex

273 In addition, the OXPHOS uses O(2) to produce reactive oxygen species that

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

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

276 We hypothesize that protein crowding in the OXPHOS system imposes packing stress on the lipid bilaye

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

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

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

280 ent state of knowledge about assembly of the OXPHOS complexes in land plants.

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

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

283 complex, it was the global impairment of the OXPHOS system that altered CL and at the same time short

284 Suppressing the OXPHOS function might also influence the tumor microenvi

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

286 egy against cancer cells regardless of their OXPHOS status.

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

288 itochondrial DNA gene expression, leading to OXPHOS dysfunction.

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

290 creased reliance upon glycolysis relative to OXPHOS was demonstrated in embryos as they developed fro

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

292 bolism during development and in response to OXPHOS inhibition as a model system for monitoring metab

293 rowth by redirecting their metabolism toward OXPHOS.

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

295 t, during NMP, there was marked upregulation OXPHOS genes, but also of a number of immune and inflamm

296 lating bioenergetics in these cells, we used OXPHOS-competent and OXPHOS-defective cells.

297 ibition of myofibroblast differentiation via OXPHOS pathway.

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

299 nd nucleotide biosynthesis pathways, whereas OXPHOS(low) BAP1 mutant UM cells employ fatty acid oxida

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