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 n elutes in a low molecular weight fraction (complex III).

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

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

7 itochondrial ROS generation from respiratory complex III.

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

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

10 mpaired its protein-protein interaction with Complex III.

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

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

13 likely derived from semiquinone formation at complex III.

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

15 complex IV and no significant inhibition of complex III.

16 none protects by limiting electron flow into complex III.

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

18 nd the activity of mitochondrial respiratory complex III.

19 assembly of mitochondrial respiratory chain complex III.

20 e apparent inorganic phosphate activation of complex III.

21 eagents that inhibit cytochrome oxidase, not complex III.

22 binding site in Complex I and/or center o of Complex III.

23 nce maxima at 560 nm and not associated with complex III.

24 arding the mechanism of electron transfer by complex III.

25 ecreases the OCR by inhibiting mitochondrial complex III.

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

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

28 measures maximal oxidative capacity through complex III.

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

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

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

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

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

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

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

36 Complex III activity measured by cytochrome c reduction

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

38 The absence of cytochrome b and complex III activity was also associated with increased

39 n the Finnish patients with GRACILE syndrome complex III activity was within the normal range, implyi

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

41 Decreased complex III activity, evident as early as 6 h after trea

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

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

44 , did not alter mitochondrial respiration or complex III activity.

45 sulfur protein (ISP) and cytochrome c(1)) of complex III, addition of succinate reduced heme b(H) fol

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

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

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

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

50 its members of the electron transport chain, complex III and cytochrome c oxidase.

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

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

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

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

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

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

57 increases in ATP recovery and activities of complex III and IV in mitochondria after SI/RO.

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

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

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

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

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

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

64 ivity, while assembly mutants of respiratory complex III and the F0F1-ATPase were less inhibited.

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

66 mmunoreactivity toward the Rieske protein of complex III and the percentage of mutant mtDNA: immunopo

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

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

69 cidosis associated with severe deficiency of complex III and who responded to therapy with menadione

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

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

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 ity of inner membrane-associated respiratory complexes III and IV to exogenously added cytochrome c.

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

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

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

85 Complexes III and IV were purified from Saccharomyces ce

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

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

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

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

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

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

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

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

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

95 red for assembly of respiratory-chain enzyme complexes III and IV.

96 e respiratory supercomplexes from individual complexes III and IV.

97 and oligomycin (inhibitors of mitochondrial complexes III and V, respectively) on chondrocyte mitoch

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

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

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

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

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

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

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

105 leted SMP containing </=0.06 mol of Q/mol of complex III, and Q-replenished SMP.

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

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

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

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

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

111 ve oxygen species generated at mitochondrial complex III are the initiators of the hypoxic signal.

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

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

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

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

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

117 b of ubiquinol: cytochrome c oxidoreductase (complex III, bc1 complex) has been studied in bovine hea

118 iquinol:cytochrome c oxidoreductase complex (complex III, bc1 complex) were studied in bovine heart s

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

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

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

122 eacted poorly with antibodies to subunits of complex III but reacted normally with antibodies to subu

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

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

125 H or succinate was added to SMP inhibited at complex III by antimycin and energized by ATP, the bis-h

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

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

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

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

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

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

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

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

134 Complex III contained eight molecules of cardiolipin, an

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

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

137 Complex I inhibitors, center o inhibitors of Complex III, cyanide, oligomycin A, and coenzyme Q analo

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

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

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

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

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

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

144 with a respiratory deficiency and a specific complex III defect.

145 hereas decreases occurred in 2 patients with Complex III defects (approximately 20%).

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

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

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

149 ntolerance and myoglobinuria associated with complex III deficiency in muscle.

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

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

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

153 tingly, the British and Turkish patients had complex III deficiency, whereas in the Finnish patients

154 four patients), and biochemical evidence of complex III deficiency.

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

156 enotypes and mitochondrial respiratory chain complex III deficiency.

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

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

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

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

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

162 Complex II as well as center i inhibitors of Complex III enhanced 4HPR-induced hydroperoxide producti

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

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

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

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

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

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

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

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

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

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

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

174 reported on the electron transfer pathway of complex III in bovine heart submitochondrial particles (

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

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

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

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

179 The formation of complex III in vivo is also shown to be essential and co

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

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

182 GSH, endogenous ROS generated at respiratory complex III induce MPT independently of Bcl-2.

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

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

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

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

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

188 hown that (i) when SMP were treated with the complex III inhibitor myxothiazol (or MOA-stilbene or st

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

190 Only when the complex III inhibitor was antimycin, and the high potent

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

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

193 value increased approximately 8-fold by the complex III inhibitor, antimycin A.

194 In contrast, antimycin A, an MRC complex III inhibitor, enhanced 4HPR-induced ROS generat

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

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

197 inhibition occurred following treatment with complex III inhibitors and the alternative oxidase inhib

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

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

200 bate to reduce the high potential centers of complex III (iron-sulfur protein and cytochromes c + c1)

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

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

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

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

205 ealed that the activity of respiratory chain complex III is reduced by C2-ceramide with half-maximum

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

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

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

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

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

211 cytochrome c1 and the iron-sulfur protein of complex III (ISP).

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

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

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

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

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

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

218 ssociated with the cytosolic form of the AHR complex, (iii) ligand binding directly activates this ki

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

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

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

222 st degree of inhibition at I mol each/mol of complex III monomer.

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

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

225 Accordingly, complex III mutant cells also showed decreased proteasom

226 Other complex III mutations inhibit complex I function either

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

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

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

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

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

232 releasing reactive oxygen species (ROS) from complex III of the electron transport chain (ETC).

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

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

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

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

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

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

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

240 We conclude that complex III of the mitochondrial ETC acts as the hypoxic

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

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

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

244 ly inhibited by antimycin A, an inhibitor of complex III of the respiratory chain.

245 of these results on the path of electrons in complex III, on oxidant-induced extra cytochrome b reduc

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

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

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

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

250 0.12-0.20] nmol x [min x mg protein](-1) by complex III; P = .02).

251 by affecting a target between complex II and complex III, presumably coenzyme Q.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

276 cifically, V1 can be assembled directly from complex III (subunits E and G) with complex IV (subunits

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

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

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

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

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

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

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

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

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

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

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

288 myxothiazol are stoichiometric inhibitors of complex III (ubiquinol-cytochrome c oxidoreductase), exe

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

296 reactive oxygen species (ROS) generation at Complex III, which causes accumulation of HIF-1alpha pro

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

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

299 mplex I of the ETC with rotenone (100 nM) or complex III with myxothiazol (100 nM) did not cause vaso

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