ライフサイエンスコーパス: complex III

1 ccinate cytochrome c reductase (complex II + complex III).

2 65 (complex I), 0.425 (complex II) and 0.34 (complex III).

3 (complex I), 584 nm (complex II) and 642 nm (complex III).

4 stabilization of complex I in the absence of complex III.

5 t shuttles electrons from complex I or II to complex III.

6 table semiquinone mediated by the Q cycle of complex III.

7 owth in cancer cells that lack mitochondrial complex III.

8 measures maximal oxidative capacity through complex III.

9 d the maximum rates achieved by complex I or complex III.

10 miting the electron flow from complex I into complex III.

11 kdown of the iron-sulfur protein, Rieske, in complex III.

12 protein (ISP), a subunit of the respiratory Complex III.

13 ent growth is the Q(o) site of mitochondrial complex III.

14 itochondrial ROS generation from respiratory complex III.

15 As a consequence, superoxide is produced at complex III.

16 t (ALR) strain, mt-Nd2(c) increases ROS from complex III.

17 complexes I and IV and had reduced levels of complex III.

18 mpaired its protein-protein interaction with Complex III.

19 n species (ROS) generation at the Qo site of complex III.

20 port to complex I and through the Q cycle in complex III.

21 likely derived from semiquinone formation at complex III.

22 rial respiratory chain complexes I and II to complex III.

23 complex IV and no significant inhibition of complex III.

24 none protects by limiting electron flow into complex III.

25 nd the activity of mitochondrial respiratory complex III.

26 assembly of mitochondrial respiratory chain complex III.

27 ograde signal originating from mitochondrial complex III.

28 lavoprotein dehydrogenase interacts with ETC complex III.

29 Psd1 support the intrinsic functionality of complex III.

30 l Complex I defects by donating electrons to Complex III.

31 tion, [Pi] does not modulate the activity of complex III.

32 e apparent inorganic phosphate activation of complex III.

33 ecreases the OCR by inhibiting mitochondrial complex III.

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

35 cytochrome bc complex, now named alternative complex III (ACIII), which has been purified from C. aur

36 n, imeglimin inhibits complex I and restores complex III activities, suggesting an increase in fatty

37 heral neuropathy, impaired respiratory chain complex III activity and aberrant mitochondrial ultrastr

38 ecreased mitochondrial GSH levels by 40% and complex III activity by approximately 20%, and it increa

39 Biochemical assays revealed inhibition of complex III activity in BITC-treated MDA-MB-231 cells as

40 n complexes I and IV with a mild decrease of complex III activity in skeletal and cardiac muscle.

41 Complex III activity measured by cytochrome c reduction

42 y, pharmacological treatments that inhibited complex III activity significantly promoted the formatio

43 ite in the complex III subunit, Qcr7, impair complex III activity similar to PSD1 deletion.

44 eurological and metabolic decline, decreased complex III activity, and increased production of reacti

45 duction, which correlated with inhibition of complex III activity, suppression of OXPHOS, and ATP dep

46 nd membrane permeability and the decrease in complex III activity.

47 lysis in Caenorhabditis elegans reveals that complex III affects supercomplex I.III.IV formation by a

48 offer insights into the assembly process of Complex III and allow mapping of human disease-associate

49 ild-type Htt exhibited a reduced activity of complex III and an increased activity of complex IV.

50 have major defects, mutant mitochondria lack complex III and are characterized by a compromised ultra

51 sed in parasites, ATO inhibits mitochondrial complex III and cell respiration.

52 A supermolecular complex between complex III and complex IV of the mitochondrial ETS dete

53 hat included NADH dehydrogenase, alternative complex III and cytochrome oxidase.

54 EPR largely detected superoxide generated at complex III and effluxed outward.

55 heightened ROS production in ALR.mt(NOD) to complex III and identified complex I as the site of elev

56 The formation of complex III and its interaction with additional cytosoli

57 ific requirement for mitochondrial PE in MRC complex III and IV activities but not for their formatio

58 substrates as well as by salutary changes in Complex III and IV activities.

59 ing heme oxygenase-1 (Hmox1), which disrupts complex III and IV of the respiratory chain and lowers t

60 Inhibition of complex III and IV resulted in a similar increase in MAO

61 anthropoid ETC genes that encode subunits of Complex III and IV, and the electron carrier molecule cy

62 and expression of the mitochondrial proteins Complex III and IV, consistent with a defect in mitochon

63 nvolving ROS production due to inhibition of complex III and OXPHOS.

64 Respiratory chain complex III and possibly cytochrome b function are essen

65 er insight into the agostic preference(s) of complex III and the observed exchange processes.

66 tem connecting the mitochondrial respiratory complex III and the production of Htt aggregates.

67 Despite the decreased mitochondrial area, complex III and V expression increased in debanding comp

68 Furthermore, different subunits from complex III and V of the electron transfer chain were he

69 est that therapeutic interventions targeting complex III and/or proteasome could ameliorate the progr

70 shed enzymatic activity of respiratory chain complexes (III and IV) and a reduction in the rate of ox

71 ctivities of other oxidative phosphorylation complexes (III and V) were not affected.

72 r reduced steady-state levels of subunits of complexes III and IV as well as of the assembled complex

73 Complexes III and IV associate to form a supercomplex th

74 The opposing surfaces of complexes III and IV differ considerably from those repo

75 Complexes III and IV genes show high homology ranging fr

76 xidative phosphorylation and the activity of complexes III and IV in IFM from aged hearts to rates pr

77 yed a supercomplex composed of homodimers of complexes III and IV in the former case but only the ind

78 cardiolipin is essential for association of complexes III and IV into a supercomplex in intact yeast

79 stance between cytochrome c binding sites of complexes III and IV is about 6 nm, which supports propo

80 on in electron shuttling between respiratory complexes III and IV is alternative to its role in apopt

81 hetic enzymes, and mitochondrial respiratory complexes III and IV was elevated in asthmatic lung samp

82 -state levels of nuclear-encoded subunits of complexes III and IV were also significantly decreased.

83 ression of CL synthase) approximately 90% of complexes III and IV were observed as individual homodim

84 Complexes III and IV were purified from Saccharomyces ce

85 losing cytochrome-based electron transport (complexes III and IV).

86 s of the assembled mitochondrial respiratory complexes III and IV, and also cyanide-sensitive oxygen

87 of electrons enter at complex I, go through complexes III and IV, and are finally delivered to oxyge

88 degradation was selective for components of complexes III and IV, because little effect was observed

89 drial intermembrane electron shuttle between complexes III and IV, can, upon binding with an anionic

90 ase in the level of two respiratory enzymes, complexes III and IV, led to their repression.

91 th aging, there is a decrease in activity of complexes III and IV, which account for the decrease in

92 ns involved in the structure and function of complexes III and IV, which form the terminal segment of

93 e respiratory supercomplexes from individual complexes III and IV.

94 ocked from passage to oxygen via respiratory complexes III and IV.

95 by reference to the known stoichiometries of complexes III and IV.

96 Cytochrome bc(1) complex (complex III) and cytochrome c oxidase complex (complex I

97 The yeast bc1 complex (complex III) and cytochrome oxidase (complex IV) are mos

98 by stigmatellin, indicating its origin from complex III, and by piericidin, demonstrating the import

99 e to the formation of complex I, complex II, complex III, and coenzyme Q [11-14].

100 upercomplex consisting of complex I, dimeric complex III, and complex IV (I1III2IV1).

101 f antimycin A, an inhibitor of mitochondrial complex III, and constitutive activation of mitochondria

102 al defect of mitochondrial respiratory chain complex III, and explores the impact of a distinct magne

103 of complex I, subunits core 1 and core 2 of complex III, and the mitochondrial DNA-encoded subunit I

104 tors, particularly inhibitors of respiration complex III (antimycin A and myxothiazol), mimicked hypo

105 However, we find that when complex I and complex III are inhibited and succinate concentration is

106 l reactive oxygen species (ROS) generated at complex III are required for TGF-beta-induced gene expre

107 electron transporter and cyt c reduction by Complex III are strongly inhibited.

108 ource of adaphostin-induced ROS and identify complex III as a potential target for antineoplastic age

109 This provides a direct link between complex III as the main source of ROS and its role in de

110 -induced cytochrome c reduction, identifying complex III as the site of inhibition by this agent.

111 A decrease in Complex III assembly was detected in the adult patient's

112 sequences of the interactions of these three complex III-associated genes could influence reproductiv

113 the electron transport chain at the level of complex III, attenuated mitochondrial outer membrane per

114 lex III, suggesting that other components of complex III besides the UQO- can cause O2(-)(radical) ge

115 rial localization of TTC19 and its link with complex III biogenesis.

116 idized CL in cardiomyocytes treated with the Complex III blocker, antimycin A.

117 We show that the absence of complex III blocks complex I biogenesis by preventing th

118 Cancer cells that lack mitochondrial complex III but can regenerate NAD+ by expression of the

119 Instead, inhibitors of complex III (but not complex I) of the mitochondrial ele

120 ty of free ubiquinone between complex II and complex III, but not inside supercomplexes.

121 blocked in wild-type yeast at mitochondrial complex III by antimycin A and (ii) in mutant strains la

122 I, inhibited complex II and interfered with complex III by maintaining the substrate, CYT-C in a red

123 pound 8a was shown to bind at the Qi site of complex III by red-shift titration of the bc1 complex.

124 Our data indicate that Complex III can release superoxide to both sides of the

125 when TTC19 is absent they accumulate within complex III, causing its structural and functional impai

126 ve ultrastructural changes and by defects in Complex III (CIII) activity, coenzyme Q (CoQ) biosynthes

127 We fed KD to mice with respiratory chain complex III (CIII) deficiency and progressive hepatopath

128 port chain deficiencies involving defects in complex III (CIII) or complex IV (CIV).

129 Here we measured the DeltaPsi generated by complex III (CIII) to discriminate between these possibi

130 found solely in an SC with cytochrome bc(1) (complex III, CIII).

131 R381C-A) as an important assembly factor for complex III, complex IV, and their supercomplexes.

132 blocked in microvessels after knockdown of a complex III component and after mitochondria-targeted ca

133 Complex III contained eight molecules of cardiolipin, an

134 Cytochrome b, a central catalytic subunit of complex III, contains two heme bs.

135 ference in complex II content or activity or complex III content.

136 d reduction in the steady-state abundance of complex III could be attributed to cytochrome c (1) bein

137 l interfaces of CLs on the respiratory chain complex III (cytochrome bc(1), CIII).

138 nous mitochondrial complex I (ubiquinone) or complex III (cytochrome c) electron acceptors, but was i

139 on system, in particular the cytochrome bc1 (complex III)-cytochrome c oxidase (complex IV) supercomp

140 istinct homoplasmic mutation in a subunit of complex III, cytochrome b.

141 KG to form a bicyclic Fe(IV)-peroxyhemiketal complex; (iii) decarboxylation of this complex concomita

142 ctb-1 suppresses a nuclear encoded complex III defect, isp-1, without improving complex III

143 ractions, whereas mutations in patients with complex III deficiency alter ATP-binding residues, as de

144 rome) to profound multisystem organ failure (complex III deficiency and the GRACILE syndrome).

145 he Bjornstad syndrome, BCS1L mutations cause complex III deficiency and the GRACILE syndrome, which i

146 However, only mutations associated with complex III deficiency increased mitochondrial content,

147 ies provided evidence to support this model: complex III deficiency mutations prevented ATP-dependent

148 rial proteins was performed in patients with complex III deficiency without a molecular genetic diagn

149 d families who had a leukoencephalopathy and complex III deficiency.

150 enotypes and mitochondrial respiratory chain complex III deficiency.

151 Rieske iron-sulfur protein of mitochondrial complex III did not have increased levels of ROS nor was

152 Additionally, ROS generated at complex III did not sensitise mitochondria to mPTP openi

153 rate that TTC19 binds to the fully assembled complex III dimer, i.e., after the incorporation of the

154 wo Rieske iron-sulfur cluster domains in the complex III dimer, one is resolved, indicating that this

155 succinate/malate-fueled ROS production from complex III due to activation of malic enzyme by increas

156 s expand an additional link of mitochondrial complex III dysfunction in Parkinson's disease.

157 of UQO>- (ubisemiquinone at the Qo site) in complex III, enhanced both H2O2 generation from the matr

158 respiratory supercomplex composed of dimeric complex III flanked on each side by one monomeric comple

159 t of the existing atomic x-ray structures of complex III from yeast and complex IV from bovine heart

160 by the dissociation of TRAF6-TAK1-TAB1-TAB2 (complex III) from IRAK and consequent translocation of c

161 complex III defect, isp-1, without improving complex III function.

162 e no abnormalities observed in complex II or complex III function.

163 s in the IM is critical for cytochrome bc(1) complex (III) function and mutations predicted to disrup

164 of the keratin IF network via mitochondrial complex III-generated reactive oxygen species.

165 Genetically disrupting mitochondrial complex III-generated ROS production attenuated TGF-beta

166 novel mechanism by which antimycin-inhibited complex III generates significant amounts of ROS in the

167 Each target considered as complex III has some specific reason for requiring bRo5

168 n available samples from patients; decreased complex III holocomplex was observed in fibroblasts from

169 hich rearranges to form the HOO-HOOO + H(2)O complex; (iii) HOO-HOOO rearranges to HOOH-OOO, which su

170 capacity of the ubiquinol oxidation site in complex III in generating ROS does not differ between th

171 peroxide production from antimycin-inhibited complex III in isolated mitochondria first increased to

172 ablation of mitochondrial respiratory chain complex III in mice results in the development of fatal

173 bc (1) complexes (cyt bc (1)), also known as complex III in mitochondria, are components of the cellu

174 ive-assembly model in which the main role of complex III in SCs is to provide a structural and functi

175 normal enzymatic activities of complex I and complex III in staurosporine-treated 143B.TK(-) osteosar

176 Loss of complex III in T(reg) cells increased DNA methylation as

177 TPases that is necessary for the assembly of complex III in the mitochondria.

178 sed serine phosphorylation of FeS protein in complex III, increased threonine phosphorylation of COX

179 el simulations show that ROS production from complex III increases exponentially with membrane potent

180 dependent complex I and duroquinol-dependent complex III-induced oxygen consumption whereas Mito(12)-

181 ptors, (ii) accumulating in the nuclear pore complexes, (iii) inhibiting nucleocytoplasmic traffickin

182 : (a) complex II inhibition by atpenin A5 or complex III inhibition by stigmatellin that results in s

183 This effect of complex III inhibition on the Htt aggregates appeared to

184 ed MitoROS, and this effect was augmented by complex III inhibitor antimycin A.

185 Anti-mycin A (20 mumol/L), a complex III inhibitor known to generate ROS, decreased I

186 species was attenuated by the mitochondrial complex III inhibitor stigmatellin (20 nM) when given at

187 ion was completely blocked by myxothiazol (a complex III inhibitor) and 3-mercaptopropionate (an inhi

188 as abolished by myxothiazol, a mitochondrial complex III inhibitor, and glutathione peroxidase 1 (GPX

189 Myxothiazol, a complex III inhibitor, has similar effects in normoxic m

190 It is interesting that both hypoxia and complex III inhibitors ameliorated cisplatin-induced p53

191 Tc) loss-of-function mutants and respiratory complex III inhibitors showed that CYTc acts as the in v

192 have established that a link exists between Complex III integrity and the labile mitochondrial zinc

193 A portion of the superoxide generated at complex III is also released into the mitochondrial inte

194 Therefore, we propose that complex III is central for MRC maturation and SC formati

195 tion after PTP opening can be sustained when complex III is damaged (simulated by antimycin).

196 These results suggest that if complex III is damaged during ischemia, PTP opening may

197 increased oxidative damage in diabetes, and complex III is one of the sources of increased superoxid

198 We tested whether mitochondrial Complex III is required for the ROS signaling and vasoco

199 d pharmacologic evidence that the Qo site of complex III is required for the transduction of hypoxic

200 Model simulations predict that complex III is responsible for more ROS production durin

201 In mitochondria, complex III is the principal site for ROS generation dur

202 his mechanism, and we propose that a dianion complex (III) is formed reversibly from the initial 1,3-

203 or complex II-mediated respiratory activity, complex III+IV respiratory activity or complex IV activi

204 Respiratory complexes III, IV and V are formed by components of both

205 Variation in amounts concerning complexes III, IV and V was less pronounced in different

206 ndence of the kinetics of NADH oxidation via complexes III, IV, and cytochrome c on the concentration

207 onents of the electron transport chain (ETC) complexes III, IV, and V, and destabilizing sarcoendopla

208 uster of mitochondrial protein components of complexes III, IV, and V.

209 Bypassing mitochondrial complex III/IV deficiencies with Alternative oxidase (AO

210 e elevation of ceramide, which could inhibit complex III, leading to increased reactive oxygen specie

211 This complex III-mediated modulation of Htt aggregates was al

212 The central position of the active complex III monomer between complex I and IV in the resp

213 m complex I to complex IV through the active complex III monomer in the mammalian supercomplex.

214 through the mitochondrial respiratory chain complex III (MRC-cIII), thereby generating high levels o

215 Also, a complex III mtDNA mutation, ctb-1, inhibits complex I fu

216 Accordingly, complex III mutant cells also showed decreased proteasom

217 Other complex III mutations inhibit complex I function either

218 oxidatively modified DNA, electron transport complex III, nitrotyrosine, and mitochondrial superoxide

219 rs to be a stoichiometric subunit neither of complex III nor of complex IV.

220 site for H(2)O(2) as the ubiquinone cycle at complex III of mitochondria by using various inhibitors

221 e generation of reactive oxygen species from complex III of mitochondria.

222 cute hypoxia induces superoxide release from Complex III of smooth muscle cells.

223 he addition of antioxidants or inhibition of complex III of the electron transport chain by antimycin

224 the presence of respiratory substrates, (c) complex III of the electron transport chain is centrally

225 tein subunit of cytochrome c oxidoreductase (complex III of the electron transport chain).

226 rally thought to be located in complex I and complex III of the electron transport chain.

227 dase activity and electron leak occurring at complex III of the electron transport chain.

228 t cells containing mutations in complex I or complex III of the ETC, in patient-derived renal carcino

229 ) is the hinge protein for the multi-subunit complex III of the mitochondrial electron transport chai

230 tudied, but only antimycin A, which inhibits complex III of the mitochondrial electron transport chai

231 reased reactive oxygen species - produced at complex III of the mitochondrial electron transport chai

232 ROS produced by complex III of the mitochondrial electron-transport chai

233 tion by major sources, the NADPH oxidases or Complex III of the mitochondrial respiratory chain, H2O2

234 ve oxygen species (ROS) due to inhibition of complex III of the mitochondrial respiratory chain.

235 ues of antimycin and assayed for activity at complex III of the mitochondrial respiratory chain.

236 n, which has a known role in the assembly of Complex III of the mitochondrial respiratory chain.

237 nd decreased the activity of UCP1, UCP3, and complex III of the respiratory chain alongside with UCP2

238 two subunits of Complex I, three subunits of Complex III, one subunit of Complex IV, and one subunit

239 tochondrial respiration in cells harboring a complex III or IV deficiency as well as in transmitochon

240 , whereas alternative oxidase (AOX) bypassed complex III or IV inhibition.

241 We suggest that critical amounts of complexes III or IV are required in order for supercompl

242 eneration of the NAD+ and FAD cofactors, and complex III oxidizes ubiquinol back to ubiquinone, which

243 0.12-0.20] nmol x [min x mg protein](-1) by complex III; P = .02).

244 ogically inhibiting electron transport chain complex III production of ROS prevented activation of PI

245 f UQCRC1, another oxidative damage-sensitive complex III protein, did not significantly alter cellula

246 on fitness due to the interactions of three complex III proteins of the electron transport system in

247 The functional asymmetry of complex III provides strong evidence for directed electr

248 quinone in the outer quinone-binding site in complex III (Q(o)).

249 Antimycin A (mitochondrial complex III Qi site inhibitor) had no effect on the exci

250 te treatment with antimycin A (mitochondrial complex III Qi site inhibitor) preferentially activated

251 Myxothiazol (complex III Qo site inhibitor) inhibited antimycin A-ind

252 I flavin site, complex I electron backflow, complex III QO site, and electron transfer flavoprotein

253 ant BCS1L proteins disrupted the assembly of complex III, reduced the activity of the mitochondrial e

254 ncreases in [NADH] elevate ubiquinol-related complex III reduction beyond the optimal range for ROS g

255 Disruption of complex III renders cells sensitive to H(2)O(2) but not

256 inhibit Qo and Qi sites of respiratory chain complex III, respectively, blocked ROS production, prese

257 revents the accessibility of cytochrome c to complex III, resulting in the production of reactive oxy

258 ring hyperammonaemia, leak of electrons from complex III results in oxidative modification of protein

259 n both patients, and biochemical analysis of Complex III revealed normal respiratory chain enzyme act

260 logically promoting electron transport chain complex III ROS production activated PI 3-kinase indepen

261 T cell activation through the production of complex III ROS.

262 ubunits proposed as putative oxygen sensors (Complex III's Rieske Fe-S center and COX4i2 [cytochrome

263 Our data on Complex III show direct extramitochondrial release of su

264 T(reg) cells deficient in complex III showed decreased expression of genes associa

265 imum capacity (e.g. the outer quinol site in complex III (site IIIQo) has a very high capacity in rat

266 and cytochrome c on the concentration of the complex III-specific inhibitor antimycin A was studied.

267 Mice that lack mitochondrial complex III specifically in T(reg) cells displayed a los

268 In addition, while inhibition of complex III stimulated O2*- production, Ca2+ reduced the

269 plex IV subunits appeared sequestered within complex III subassemblies, leading to defective complex

270 11 and complex IV 7B subunits, but increased complex III subunit 9 in young adult mice.

271 We demonstrate that cells deficient in the complex III subunit cytochrome b, which are respiratory

272 RNA interference of the complex III subunit Rieske iron sulfur protein in the cy

273 o disrupt a conserved PE-binding site in the complex III subunit, Qcr7, impair complex III activity s

274 hrome b with assembly factors and structural complex III subunits.

275 k most parsimoniously placed at the level of complex III, suggesting candidate gene loci for autism w

276 othiazol alone enhanced H2O2 production from complex III, suggesting that other components of complex

277 and reduced content of respiratory complex I/complex III supercomplexes.

278 ns in virus particles and large biomolecular complexes; (iii) supports a connection between mechanica

279 has a major role in stabilizing the dimeric complex; (iii) the b (6) f complex is stabilized by inco

280 The trimethoxy complex (III), the (1)H NMR spectrum of which was observ

281 For complex III, the slightly red-shifted electronic transit

282 The locus of superoxide production in Complex III, the ubiquinol oxidation site, is situated i

283 get of inhibition changes from mitochondrial complex III to complex I.

284 plex IV subunit COX7a switching contact from complex III to complex I.

285 Thus, T(reg) cells require mitochondrial complex III to maintain immune regulatory gene expressio

286 redox state of the Q pool, and inhibition of complex III to prevent QH(2) oxidation via the Q cycle.

287 I) from IRAK and consequent translocation of complex III to the cytosol.

288 rose nonfermenting-type chromatin remodeling complex, (iii) transcription coactivator activity, and (

289 molecular interactions between mitochondrial complexes III (ubiquinol-cytochrome c reductase; cyt. bc

290 o CL biosynthesis was reduced in respiratory complexes III (ubiquinol:cytochrome c oxidoreductase) an

291 on and duroquinol to assess the flux through complex III; uncoupled duroquinol oxidation measures max

292 Complex III was found to release O2(-)(radical) into the

293 of the Rieske iron-sulfur protein (RISP) of Complex III was generated.

294 was consistent with the Q-cycle mechanism of complex III, we generated a kinetic model of the antimyc

295 ne oxidoreductase 1 (NQO1) and mitochondrial complex III were identified as the major enzymes involve

296 ntly reduced, whereas levels and activity of complex III were normal or up-regulated.

297 sing cancer cells deficient in mitochondrial complex III, which highlights the necessity of ubiquinon

298 Electron transfer from complex I to complex III, which requires quinones, is severely depres

299 tween respiratory activity and saturation of complex III with antimycin A was obtained for wild type

300 have a destabilized cytochrome c reductase (Complex III) without any effects on Complexes IV or V.