ライフサイエンスコーパス: antimycin

1 ed when complex III is damaged (simulated by antimycin).

2 approximately 235 micros, in the presence of antimycin).

3 o occur before half of the enzyme could bind antimycin.

4 r to that in the presence of ubiquinone plus antimycin.

5 t cell death upon treatment with rotenone or antimycin.

6 rapidly oxidized upon subsequent addition of antimycin.

7 bited partially by myxothiazol, much more by antimycin.

8 are altered when b oxidation is prevented by antimycin.

9 E2 induced neuroprotection against 3-NPA and antimycin.

10 erated and approached the rate obtained with antimycin.

11 ounts of superoxide except when inhibited by antimycin.

12 (-1)) as calculated from its displacement by antimycin.

13 [Fe(2+)] and aconitase inhibition caused by antimycin.

14 ficantly protected against 3-NPA (7.5mM) and antimycin (125 muM) induced cell death and was moderatel

15 edium containing the mitochondrial inhibitor antimycin A (1 microM) resulted in 75% depletion of cell

16 hondrial electron transport chain (mtETC) by antimycin A (AA) or the TCA cycle by monofluoroacetate (

17 Antimycin A (AA), a mitochondrial electron transport cha

18 tially killed by the mitochondrial inhibitor antimycin A (AA).

19 e mitochondrial electron transport inhibitor antimycin A (AA).

20 ease mitochondrial O2*- and H2O2 production (antimycin A (AntA), myxothiazol (Myx), or rotenone (Rot)

21 Antimycin A (antimycin), one of the first known and most

22 rotenone and pyridaben (IC50=2 to 3 nmol/L), antimycin A (IC50=13 nmol/L), and diphenyleneiodonium (I

23 l dysfunction evoked by acute treatment with antimycin A (mitochondrial complex III Qi site inhibitor

24 Antimycin A (mitochondrial complex III Qi site inhibitor

25 The respiratory inhibitor antimycin A also bound to the hydrophobic groove of rhBc

26 d-type yeast at mitochondrial complex III by antimycin A and (ii) in mutant strains lacking the entir

27 ATP depletion preconditioning (1 h of antimycin A and 2-deoxyglucose treatment followed by 1 h

28 The complete inhibition of respiration by antimycin A and cyanide excluded the presence of an alte

29 Respiration was sensitive to antimycin A and cyanide, and N,N,N',N'-tetramethyl-p-phe

30 Antimycin A and cyanide, which inhibit the distal region

31 Respiration was sensitive to antimycin A and cyanide.

32 tural basis for the high affinity binding of antimycin A and for phenotypes of inhibitor resistance.

33 ubjected to either ATP depletion (0.1 microM antimycin A and glucose deprivation) or hypoxia (1% O(2)

34 These findings led us to propose that antimycin A and HQNO mimic the presence of QH(2) and Q a

35 on in RAW 264.7 cells, which is inhibited by antimycin A and is absent in respiration-deficient rho0

36 with succinate as substrate was inhibited by antimycin A and malonate, but not by rotenone.

37 s of the two specific respiratory inhibitors antimycin A and myxothiazol were identified.

38 larly inhibitors of respiration complex III (antimycin A and myxothiazol), mimicked hypoxia in apopto

39 ondrial electron transport chain inhibitors, antimycin A and myxothiazol, selectively blocked TNF-alp

40 e; this process is specifically inhibited by antimycin A and NQNO.

41 We also assessed the effects of antimycin A and oligomycin (inhibitors of mitochondrial

42 enerate reactive oxygen species (ROS) (e.g., antimycin A and oligomycin) had a negative impact on CI

43 by the mitochondrial respiratory antagonists antimycin A and oligomycin.

44 atment of seedlings with the mETC inhibitors antimycin A and potassium cyanide under normoxia promote

45 The respiratory chain blockers antimycin A and rotenone (10 microm) had similar effects

46 e was unaffected by cyanide but sensitive to antimycin A and SHAM when succinate was added as the res

47 mined the effect of ATP depletion induced by antimycin A and substrate depletion on actin polymerizat

48 High-throughput screening identified Antimycin A as a small molecule that disrupted the ABCC4

49 mplex III of the electron transport chain by antimycin A attenuates the inhibitory effects of CO on l

50 ce and, perhaps most notably, generating the antimycin A C7-C8-C9 stereotriad in a single step using

51 In dissociated vagal neurons, antimycin A caused ROS-dependent PKC translocation to th

52 tochondrial electron transport chain blocker antimycin A decreased clonogenic survival and increased

53 The presence or absence of the Qi inhibitor antimycin A did not affect the binding of the Qo inhibit

54 oach to the core stereochemical triad of the antimycin A family.

55 leavage, myxothiazol hardly affected it, and antimycin A greatly enhanced it.

56 with saturating concentrations of cyanide or antimycin A had little effect during the first 20 min an

57 cking the respiratory chain with rotenone or antimycin A in combination with oligomycin inhibited mit

58 and superoxide production in the presence of antimycin A in wild type.

59 However, antimycin A increased excitability in nociceptive C-fibe

60 Antimycin A increased ROS production and decreased cell

61 luminescent lifetimes of the probe at longer Antimycin A incubation times which lay outside of the O2

62 ell culture for 16 h with H2O2, menadione or antimycin A induced an oxidative stress decreasing growt

63 In mouse dissociated vagal neurons, antimycin A induced Ca(2+) influx that was significantly

64 Using an HEK293 cell expression system, antimycin A induced concentration-dependent activation o

65 Cyanide and antimycin A inhibit electron transfer in the distal regi

66 Antimycin A is the most frequently used specific and pow

67 omplex I or II substrates in the presence of antimycin A markedly increased H2O2.

68 To analyze the effects of antimycin A on the maturation of secretory proteins, we

69 e in procyclic cells was inhibited 80-90% by antimycin A or cyanide, 15-19% by salicylhydroxamic acid

70 is observed when the complex is inhibited by antimycin A or inactivated by heat treatment or proteina

71 H2O2-dependent CEF was not sensitive to antimycin A or loss of PGR5, indicating that increased C

72 Treatment of MCF-7 cells with antimycin A or rotenone increased intracellular ROS prod

73 mitochondrial poisons cyanide, rotenone, and antimycin A prevented mitochondrial- but not paraquat-me

74 t myxothiazol blocks cyt b reduction whereas antimycin A promotes it, we propose that this second byp

75 he mitochondrial electron transport chain by antimycin A resulted in an immediate production of ethan

76 Antimycin A selectively induces apoptosis in cells overe

77 lex exhibited myxothiazol, stigmatellin, and antimycin A sensitive cyt c reductase activity and an EP

78 nhibitor antimycin A, and by the presence of antimycin A sensitive Qi semiquinone.

79 Antimycin A suppressed quenching, increasing the Hill co

80 at were 3 times faster and more sensitive to antimycin A than the mesophile control, Chlamydomonas ra

81 Using Antimycin A the ability of the probe to respond dynamica

82 ion of respiratory metabolism by addition of antimycin A to cells also increased Snf1 activity.

83 lial cells after treatment with menadione or antimycin A to induce intracellular reactive oxygen spec

84 Chinese hamster ovary cells and fluoride and antimycin A to mouse fibroblast cells.

85 hermore, coimmunoprecipitation studies after antimycin A treatment demonstrated that Tg stably associ

86 Blockage of oxidative phosphorylation by antimycin A treatment led to increased intracellular lev

87 proximal tubule cell line, ATP depletion by antimycin A treatment upregulated survivin expression th

88 nscriptional changes observed in response to antimycin A treatment.

89 methyl abolishes the induction of AOX1a upon antimycin A treatment.

90 (2) induced by exogenously added H(2)O(2) or antimycin A was lower in C33 cell lines overexpressing c

91 cell viability; however, the toxic effect of antimycin A was more pronounced in ethanol-fed hepatocyt

92 activity and saturation of complex III with antimycin A was obtained for wild type mitochondria cons

93 The optimal binding conformation of antimycin A was predicted from molecular docking of anti

94 ration of the complex III-specific inhibitor antimycin A was studied.

95 in A was predicted from molecular docking of antimycin A with the hBcl-2 model created by homology mo

96 dy the dynamic aspects of the interaction of antimycin A with the Q(i) site of the bacterial and bovi

97 of responses, at least three, to ethanol and Antimycin A within the mitochondrial population.

98 bstrate ubiquinone and with either the bound antimycin A(1) or NQNO were determined and refined.

99 with its first two isoprenoid repeats and an antimycin A(1) were identified in the Q(i) pocket of the

100 xy-D-glucose) and oxidative phosphorylation (antimycin A), transepithelial electrical resistance, a m

101 of the cyt bc(1) complex in the presence of antimycin A, a Q(i) site inhibitor, results in accumulat

102 Antimycin A, a specific inhibitor of the cytochrome bc1

103 In the presence of antimycin A, an immobile Fe/S protein mutant exhibited n

104 blocked and respiration totally inhibited by antimycin A, an inhibitor of complex III of the respirat

105 Likewise, administration of antimycin A, an inhibitor of mitochondrial complex III,

106 In contrast, antimycin A, an MRC complex III inhibitor, enhanced 4HPR

107 inhibit mitochondrial function; N2, 0.01 mM antimycin A, and 1 and 10 mM potassium cyanide (KCN).

108 a combination of inhibitors, uncouplers, and antimycin A, and by following the kinetic pattern of gen

109 dged by its ability to bind the Qi inhibitor antimycin A, and by the presence of antimycin A sensitiv

110 ng three respiratory inhibitors, oligomycin, antimycin A, and cyanide, we find that pollen tube growt

111 icyhydroxamic acid, unaffected by cyanide or antimycin A, and inhibited 40% or 75%, respectively, by

112 The activities were inhibited by flavone, antimycin A, and KCN but not by rotenone.

113 Cell death caused by H(2)O(2), antimycin A, and menadione was considerably suppressed i

114 ys, i.e., rhodamine 123 (Rho 123), rotenone, antimycin A, and oligomycin.

115 as 5-amino-imidazole-4-carboxamide riboside, antimycin A, and sodium azide inhibited cell growth and

116 hibition by rotenone, 3-nitropropionic acid, antimycin A, and sodium azide.

117 ors of the cytochrome bc1 complex, including antimycin A, and the redox properties of its b- and c-ty

118 In the presence of antimycin A, but absence of myxothiazol, the second and

119 erse forms of injury (hypoxia/reoxygenation, antimycin A, Ca2+ ionophore, amphotericin B, FeSO4, and

120 igated the effects of rotenone, myxothiazol, antimycin A, cyanide (CN(-)) and oligomycin on isolated

121 vity to added prooxidants such as menadione, antimycin A, H(2)O(2), and 4-hydroxynonenal was lower in

122 aerobic cells is enhanced in the presence of antimycin A, in thiol oxidants, or in strains that lack

123 methylurea and the second peak by ned-19 and antimycin A, indicating that NO synthesis is dependent o

124 Co-incubation with rotenone and antimycin A, inhibitors of mitochondrial electron transp

125 ion of mitochondrial function with rotenone, antimycin A, KCN, carbonylcyanide-m-chlorophenylhydrazon

126 as depleted to less than 10% of control with antimycin A, mRNA levels of BiP, ERp72, and grp94 were i

127 application of the mitochondrial inhibitors antimycin A, NaCN, rotenone, or C1CCP, or of the divalen

128 However, when challenged with antimycin A, neurons did respond with a larger increase

129 3-(3,4-dichlorophenyl)-1,1-dimethylurea and antimycin A, of pyruvate dehydrogenase, moniliformin, of

130 re investigated using rotenone, myxothiazol, antimycin A, oligomycin, ascorbate and the electron dono

131 organelles after incubation with either N2, antimycin A, or 1 mM KCN in comparison with their appear

132 at only respiration is impaired (as with N2, antimycin A, or 1 mM KCN) photoreceptor cells are resist

133 after short-term incubations with either N2, antimycin A, or 1 mM KCN.

134 Mitochondrial inhibitors, rotenone and antimycin A, reduced TPA-induced cell death in PKCdelta-

135 medium containing the respiration inhibitor antimycin A, suggesting that Hxs1 may not function as a

136 C as well at 30 degrees C in the presence of antimycin A, suggesting that SOD2p is the primary defenc

137 Rotenone or antimycin A, the respiratory electron transport blockers

138 When mitochondria were inhibited with antimycin A, there was only a modest (1.3-fold) increase

139 with the scavenger, tiron, and the inducer, antimycin A, were easily monitored demonstrating the fea

140 ation of AMPK by the AMP mimetic AICAR or by antimycin A, which blocks aerobic respiration and causes

141 as observed after treatment with rotenone or antimycin A, which both inhibit mitochondrial electron t

142 espiratory chain inhibitors stigmatellin and antimycin A, which inhibit Qo and Qi sites of respirator

143 ROS production was exacerbated by the use of antimycin A, which inhibited normal cytochrome electron

144 superoxide generation were studied, but only antimycin A, which inhibits complex III of the mitochond

145 s reactions are most notably observed as the antimycin A- or myxothiazol-resistant reduction of cyt c

146 n of NHE5 protected the cells from sustained antimycin A-induced acidification.

147 both TRPA1 and TRPV1 was required to abolish antimycin A-induced Ca(2+) influx in vagal neurons.

148 Rotenone prevented antimycin A-induced H2O2 production in mitochondria with

149 Antimycin A-induced hyperexcitability was dependent on m

150 Antimycin A-induced hyperexcitability was inhibited by t

151 n of PLA2 significantly reduced hypoxic- and antimycin A-induced injury (percentage of lactate dehydr

152 AtWRKY40 was found to be a repressor of antimycin A-induced mitochondrial retrograde expression

153 Antimycin A-induced nociceptor hyperexcitability was ind

154 tion of gamma-secretase similarly attenuated antimycin A-induced Notch-2 activation, upregulation of

155 ol (complex III Qo site inhibitor) inhibited antimycin A-induced TRPA1 activation, as did the reducin

156 GalAT activity was separated from antimycin A-insensitive NADH:cytochrome c reductase and

157 yl-p-phenylenediamine (TMPD) was oxidized by antimycin A-poisoned mitochondria.

158 The small increase in antimycin A-resistant cyt c reduction rate at high O(2)

159 However, SOD inhibited only 35% of antimycin A-resistant cyt c reduction, suggesting the pr

160 ncreasing O(2) tension 5-fold stimulated the antimycin A-resistant reduction by a small amount ( appr

161 g hcef1 with pgr5, which is deficient in the antimycin A-sensitive pathway for plastoquinone reductio

162 rotenone-insensitive, flavone-sensitive, and antimycin A-sensitive.

163 either XIAP or AIF attenuated both basal and antimycin A-stimulated levels of reactive oxygen species

164 he nuclear mutation frequencies obtained for antimycin A-treated cells as well as for rho(-) and rho(

165 e density gradient analysis revealed that in antimycin A-treated cells Tg associates into large macro

166 eration in the mitochondria of rotenone- and antimycin A-treated cells was observed and may contribut

167 2-hydroxyethidium in normally respiring and antimycin A-treated mitochondria and demonstrated that t

168 e treatments, a subset of these increased in antimycin A-treated samples.

169 complexes produce as much superoxide as does antimycin A-treated wild-type complex.

170 ffect was augmented by complex III inhibitor antimycin A.

171 vely stressed with the respiratory inhibitor antimycin A.

172 0% of the V(max) observed in the presence of antimycin A.

173 d by inhibition of mitochondrial function by antimycin A.

174 imately 8-fold by the complex III inhibitor, antimycin A.

175 tive oxygen species increase by rotenone and antimycin A.

176 ake that was completely inhibited by KCN and antimycin A.

177 ate constant of 250 s(-1) in the presence of antimycin A.

178 l membrane potential induced by H(2)O(2) and antimycin A.

179 rein, and a respiratory inhibitor (stage 3), Antimycin A.

180 transport chain, cyanide (CN), rotenone, or antimycin A.

181 iratory chain in the presence of rotenone or antimycin A.

182 ocytes treated with the Complex III blocker, antimycin A.

183 ersed by treatment with H(2)O(2), Co(2+), or antimycin A.

184 milar to BAK, ATP-depletion (induced by both antimycin-A and hypoxia) led to MLC dephosphorylation.

185 nse to prototypical mitochondrial stressors (antimycin-A, xanthine/xanthine oxidase).

186 rbonyl cyanide m-chlorophenylhydrazone or by antimycin A1 + oligomycin, agents that are known to inhi

187 nylcyanide m-chlorophenylhydrazone (CCCP) or antimycin A1 caused cytosolic [Ca(2+)] to rise to much h

188 inhibited by depolarizing mitochondria with antimycin A1 or carbonyl cyanide m-chlorophenyl-hydrazon

189 a between cytochrome b and c1 as occurs with antimycin A1.

190 The stereoselective synthesis of (+)-antimycin A1b has been accomplished in 12 linear steps a

191 xothiazol, MOA-stilbene, stigmatellin, or of antimycin added to SMP pretreated with ascorbate and KCN

192 m ISP to b, a reaction that was inhibited by antimycin (also by myxothiazol or MOA-stilbene as report

193 The inhibitors used were antimycin (an N-side inhibitor), beta-methoxyacrylate de

194 Chemical hypoxia was induced by antimycin, an oxidative phosphorylation inhibitor.

195 he Selwood data on filaricidal activities of antimycin analogues.

196 Antimycin and antimycin + oligomycin had the same effect

197 salicylamides were prepared as analogues of antimycin and assayed for activity at complex III of the

198 ignificant difference in interaction between antimycin and conserved amino acid residues in bovine an

199 The strong hydrogen bond between antimycin and conserved Asp-228 (bovine numeration) was

200 In addition, the distances between antimycin and conserved His-201 and Lys-227 were consist

201 was added to SMP inhibited at complex III by antimycin and energized by ATP, the bis-heme cytochrome

202 o studies using the known Qn site inhibitors antimycin and funiculosin showed little cross-resistance

203 itochondrial oxidative stress by exposure to antimycin and H(2)O(2) or utilizing mutants lacking mito

204 ed a complete loss of mtDNA upon exposure to antimycin and H(2)O(2).

205 n of respiratory competency upon exposure to antimycin and H(2)O(2).

206 Antimycin and myxothiazol are stoichiometric inhibitors

207 g under these conditions, assuming that both antimycin and myxothiazol markedly affect subunit b conf

208 Cardiolipin-free cytochrome bc(1) also binds antimycin and myxothiazol normally with the expected red

209 )-sites of the complex are inhibited by both antimycin and myxothiazol, the flash-induced kinetics of

210 dation of heme b(H), even in the presence of antimycin and myxothiazol.

211 by the well-known cyt bc1 complex inhibitors antimycin and myxothiazol.

212 ted when the particles are treated with both antimycin and myxothiazol.

213 ition of b reduction than the combination of antimycin and myxothiazol.

214 Antimycin and oligomycin also abrogated the ability of t

215 , we identified minimally cytotoxic doses of antimycin and oligomycin, which both induced intracellul

216 n isolated from these cells was inhibited by antimycin and rotenone, but not by malonate, while cytoc

217 rst time to reliably describe the binding of antimycin and shows that the intramolecular hydrogen bon

218 d considerable conformational flexibility of antimycin and significant mobility of antimycin, as a wh

219 t cytochrome b-c1 complex in the presence of antimycin and/or myxothiazol.

220 H, the de-epoxidation state, the presence of antimycin, and also the presence of dibucaine, a quenchi

221 tivity to the mitochondrial toxins rotenone, antimycin, and oligomycin, respectively.

222 Only when the complex III inhibitor was antimycin, and the high potential centers were in the ox

223 in the bc(1) complex are similar to those of antimycin, another inhibitor that binds to the Qn site o

224 mitochondrial toxins such as MPP+, azide and antimycin appeared to inhibit the catalytic activity of

225 ity of antimycin and significant mobility of antimycin, as a whole, inside the Q(i) pocket.

226 ence of 5 mmol/L succinate and 30 micromol/L antimycin, based on its detection as catalase-inhibitabl

227 and result from fluctuations of protein and antimycin between multiple conformational states of simi

228 of the yeast bc1 complex dimer by analyzing antimycin binding and heme bH reduction at center N in t

229 UHDBT binding are markedly diminished, while antimycin binding is unaffected, in the bc(1) complexes

230 We conclude that many of the differences in antimycin binding observed in high-resolution x-ray stru

231 esence of stigmatellin but did not slow down antimycin binding rates.

232 nomer are able to reach the b(H) heme at the antimycin-blocked site in the other.

233 the same rate in the absence or presence of antimycin bound at the Qi-site, and is the reaction limi

234 Two previous X-ray structures of antimycin bound to vertebrate bc1 complex gave conflicti

235 ndrial bc1 complex at 2.28 A resolution with antimycin bound, allows us for the first time to reliabl

236 d through center N, and only one molecule of antimycin can be bound at center N in the bc(1) dimer la

237 the inhibitors of oxidative phosphorylation antimycin, carbonyl cyanide m-chlorophenylhydrazone, or

238 alents of decyl-ubiquinol in the presence of antimycin corresponded to only half of that present in t

239 tochondrial inhibitors such as myxothiazole, antimycin, cyanide and rotenone.

240 n the presence of variable concentrations of antimycin decreased non-linearly and could only be fitte

241 It was also shown that antimycin did not inhibit electron transfer from b (b(H)

242 me, was abolished by the center N inhibitors antimycin, funiculosin, and ilicicolin H, but was unchan

243 tivity of these compounds approached that of antimycin in inhibitory potency and some showed growth r

244 was able to abolish the biphasic binding of antimycin in the presence of stigmatellin but did not sl

245 hibits UQO>- formation, completely inhibited antimycin induced O2(-)(radical) toward the intermembran

246 role of polyamine-dependent K(ATP) channels, antimycin-induced capillary cell death was markedly decr

247 These inhibitors also diminished the antimycin-induced hyperpolarization, as well as the anti

248 in-induced hyperpolarization, as well as the antimycin-induced intracellular calcium increase, which

249 This antimycin-induced reoxidation did not happen when Q-extr

250 eroxide generating activity in the intact or antimycin inhibited wild-type or mutant complexes.

251 a, we demonstrate a novel mechanism by which antimycin-inhibited complex III generates significant am

252 Superoxide production from antimycin-inhibited complex III in isolated mitochondria

253 lex III, we generated a kinetic model of the antimycin-inhibited Q(o) site.

254 by 0.4 mM tetramethyl-p-phenylenediamine in antimycin-inhibited uncoupled intact cells have given re

255 the Q-cycle hypothesis regarding the site of antimycin inhibition.

256 This cyanide- and antimycin-insensitive but hypoxia-sensitive pattern of p

257 The rate of antimycin-insensitive cytochrome c reduction was sensiti

258 roduction was closely related to the rate of antimycin-insensitive cytochrome c reduction.

259 Factors affecting antimycin-insensitive reduction of cytochrome c also aff

260 Mitochondrial inhibitors, rotenone, 3-NPA, antimycin, KCN, and oligomycin, exhibited concentration

261 Neither antimycin nor myxothiazol binding produces dramatic stru

262 center P, concentration-dependent binding of antimycin occurred only to half of the center N sites.

263 Antimycin and antimycin + oligomycin had the same effect as CCCP.

264 cyanide p-(trifuoro-methoxy)phenylhydrazone, antimycin-oligomycin, or ruthenium red revealed that mit

265 (1) complex, we have examined the effects of antimycin on the presteady state reduction kinetics of t

266 Antimycin A (antimycin), one of the first known and most potent inhib

267 trans-stilbenyl)acrylatc in combination with antimycin or 2-n-heptyl-4-hydroxyquinoline-N-oxide in co

268 idation of reduced b, is inhibited by either antimycin or myxothiazol (or 2-n-heptyl-4-hydroxyquinoli

269 Finally, MV from cells treated with antimycin or oligomycin contained less PPi and precipita

270 Rotenone, but not antimycin or oligomycin, prevented this effect, indicati

271 In the presence of N2, 0.01 mM antimycin, or 1 mM KCN, lactic acid production was linea

272 t cerebral cortical neurons with oligomycin, antimycin, or rotenone, which inhibit different elements

273 n of high potential heme b is observed in an antimycin- or antimycin plus myxothiazol-inhibited, asco

274 ntial heme b is observed in an antimycin- or antimycin plus myxothiazol-inhibited, ascorbate plus TMP

275 7 or Glu-270 were mutated, no longer exhibit antimycin-resistant oxygen uptake, indicating that these

276 xes in a ubiquinone-sufficient state exhibit antimycin-sensitive reduction of cytochromes b (both low

277 ted with substoichiometric concentrations of antimycin showed a red shift upon the addition of substr

278 When ubiquinone is present, antimycin slows the rate of cytochrome c(1) reduction by

279 Antimycin stimulated the ubiquinol-cytochrome c reductas

280 oxidation of Mito-HE monitored at 396 nm by antimycin-stimulated mitochondria was 30% slower than at

281 ISP/c1 to cytochrome b was inhibited more by antimycin than by the P-side inhibitors.

282 ed hepatocytes with H2O2 or inhibitors (e.g. antimycin) that cause increased H2O2 release from mitoch

283 Between 30 and 60 min after treatment with antimycin to deplete ATP in the presence of glycine to p

284 e of the Qo site because addition of MCLA to antimycin-treated cytochrome bc1 complex, in the presenc

285 Total cell Ca2+ levels in antimycin-treated or hypoxic tubules did not change, sug

286 O-2 production and cytochrome c reduction by antimycin-treated reductase decreased.

287 O-2 production and cytochrome c reduction by antimycin-treated reductase increased.

288 n transfer from succinate to cytochrome c by antimycin-treated reductase, in which approximately 99.7

289 % of the rate of b reduction by succinate in antimycin-treated SMP, where both b(H) and b(L) were con

290 hypoxia (short-term glucose deprivation and antimycin treatment), as evidenced by morphologic change

291 es of the isolated enzyme in the presence of antimycin under conditions that allow the first turnover

292 onyl cyanide m-chlorophenylhydrazone (CCCP), antimycin, valinomycin and azide.

293 the quinone reduction (Q(N)) site inhibitor antimycin, were determined.

294 otenone and oligomycin or in the presence of antimycin, which collapse the mitochondrial membrane pot

295 Antimycin, which increases steady-state levels of UQO>-

296 The remaining half of the bc1 complex bound antimycin with a slower rate that was independent of inh

297 eme bL at center P, all center N sites bound antimycin with fast and concentration-dependent kinetics

298 d be responsible for a weaker interaction of antimycin with the bacterial bc(1) complex.

299 published rate constants (determined without antimycin), with unknown rate constants allowed to vary,

300 on barriers, as well as from the mobility of antimycin within the Q(i) pocket.