ライフサイエンスコーパス: oligomycin

1 tion (rotenone, FCCP) and hyperpolarization (oligomycin).

2 reus was affected by the addition of FCCP or oligomycin.

3 rial respiratory antagonists antimycin A and oligomycin.

4 esistance to drugs such as cycloheximide and oligomycin.

5 43 in preparations exposed to either CCCP or oligomycin.

6 ne 123 (Rho 123), rotenone, antimycin A, and oligomycin.

7 ernal mitochondrial membrane potential using oligomycin.

8 carbonyl cyanide m-chlorophenylhydrazone, or oligomycin.

9 by the mitochondrial ATP-synthase inhibitor oligomycin.

10 s explaining the differential sensitivity to oligomycin.

11 ose responses, an effect that was blocked by oligomycin.

12 ed after acute inhibition of ATP synthase by oligomycin.

13 e energy metabolism modifiers, metformin and oligomycin.

14 sed sensitivity to the mitochondrial poison, oligomycin.

15 in A (5 nM), sodium o-vanadate (500 microM), oligomycin (1 microM), N-ethylmaleimide (100 microM), an

16 Blockade of the F0F1 ATPase by oligomycin (10 microm) had variable effects on myenteric

17 te mitochondrial Ca(2+) uptake combined with oligomycin (10microM) to prevent ATP depletion, we first

18 Oligomycin (2 microg) abolished the hypoxic response.

19 f all ages with inhibitors of ATP synthesis (oligomycin, 2,4-dinitrophenol, or 2-deoxyglucose) made t

20 Moreover, inhibition of OXPHOS with oligomycin, 2-deoxy glucose or BPTES all impeded heighte

21 vely), however, cyclosporin A (7 microg/ml), oligomycin (20 microg/ml), or carboxyatractyloside (25 m

22 Whereas application of FCCP plus oligomycin 2s after neuronal depolarization initiated mi

23 cyanide m-chlorophenylhydrazone (CCCP, 2 M), oligomycin (8 g x ml(-1)) or CCCP and oligomycin togethe

24 ated m/lEVs from donor BECs pre-treated with oligomycin A (OGM, mitochondria electron transport compl

25 2 inhibit mitochondrial function similar to oligomycin A and apoptolidin A, selective inhibitors of

26 Reduced SesB activity or depletion of ATP by oligomycin A could rescue the autophagic defect in Dcp-1

27 In this study, we obtained Oligomycin A Diels-Alder adducts with benzoquinone and N

28 wed that the Diels-Alder modification of the Oligomycin A diene system resulted in a complex antiprol

29 Furthermore, inhibition of Fo-ATPase by Oligomycin A induced docetaxel-mediated ROS generation i

30 Oligomycin A induced mitochondrial defects including col

31 Oligomycin A is a potent antibiotic and antitumor agent.

32 Thus, modification of the diene moiety of Oligomycin A is a promising strategy for developing nove

33 try is controlled by hydrogen bonding of the Oligomycin A side-chain isopropanol moiety with the carb

34 ured hippocampal neurons by using non-lethal oligomycin A treatment.

35 Meanwhile, Oligomycin A was more potent against myeloid leukemia ce

36 Oligomycin A, an Fo-ATPase inhibitor, eliminated docetax

37 center o inhibitors of Complex III, cyanide, oligomycin A, and coenzyme Q analogues decreased 4HPR-in

38 gy charge was well maintained by addition of oligomycin A, phosphocreatine, and creatine phosphokinas

39 n of Q-VD-OPh showed no protective effect on oligomycin A-induced mitochondrial dysfunction.

40 with these dendritic mitochondrial changes, oligomycin A-insulted neurons displayed spine loss and a

41 Such oligomycin A-mediated changes in dendritic spines were s

42 d lung carcinoma cell line A-549 compared to Oligomycin A.

43 in dendritic shaft and spines in response to oligomycin A.

44 In hypoxia mimicked by treating MDM with oligomycin (a mitochondrial ATP synthase inhibitor), bot

45 In contrast, oligomycin, a mitochondrial ATP synthase inhibitor, had

46 entiated by low concentrations (<5 ng/ml) of oligomycin, a mitochondrial inhibitor that blocks capaci

47 major carbon source, and that resistance to oligomycin, a mitochondrial inhibitor, is associated wit

48 s approximately 1000 times more sensitive to oligomycin, a specific inhibitor of the mitochondrial F(

49 gainst oxidative toxins (H2O2, rotenone, and oligomycin-A).

50 Oligomycin abolished the FCCP-induced rise in [Mg2+]i wi

51 tional changes, but both divalent cation and oligomycin addition evoked modest changes in LY fluoresc

52 m-chlorophenylhydrazone or by antimycin A1 + oligomycin, agents that are known to inhibit mitochondri

53 igomycin together than in those treated with oligomycin alone.

54 Antimycin and oligomycin also abrogated the ability of the ATP-hydroly

55 In mammalian cells, oligomycin also inhibited Bax-induced apoptosis and acti

56 an uncoupler or blocking ATP synthesis with oligomycin also stopped movement but did not alter morph

57 harmacological inhibitor of the proton pump, oligomycin, also partially abrogated the cytotoxic actio

58 r inhibitor of the electron-transport chain, oligomycin, also showed temporal correlation between the

59 ctose decreased ATP to <25% of basal values, oligomycin (an ATP synthase inhibitor) did not inhibit a

60 ient increase in Delta Psi(m) was blocked by oligomycin, an inhibitor of F(0)F(1-)ATPase that may hav

61 Depletion of ATP by oligomycin, an inhibitor of F0F1-ATPase, had similar eff

62 in lactate production following addition of oligomycin, an inhibitor of mitochondrial adenosine trip

63 ls were treated with the depolarizing agents oligomycin and antimycin A (OA) and subjected to cryo-fo

64 2Y-R enhanced neuroprotection was blocked by oligomycin and by Xestospongin C, inhibitors of the ATP

65 layed ATP hydrolysis activity that was fully oligomycin and inhibitor protein IF(1)-sensitive.

66 In the presence of oligomycin and low carbonyl cyanide 4-(trifluoromethoxy)

67 The remaining contacts between oligomycin and subunit c are primarily hydrophobic.

68 brane potential obtained by a combination of oligomycin and titration with a proton ionophore.

69 the mitochondrial F(1)F(0)-ATPase inhibitor oligomycin and translocation of cytochrome c.

70 h both oxidative phosphorylation (metformin, oligomycin) and beta-oxidation of fatty acids (etomoxir)

71 synthase (N, N'-dicyclohexylcarbodiimide and oligomycin) and incubation of cells in the dark stimulat

72 ed in resistance to the drugs cycloheximide, oligomycin, and 4-nitroquinoline N-oxide (4-NQO).

73 Respiratory complex inhibitors, FCCP and oligomycin, and a producer of reactive oxygen species (R

74 hout ruthenium red, carboxyatractyloside, or oligomycin, and at several levels of Mg2+ and P(i).

75 reatments include CCCP, antimycin, rotenone, oligomycin, and hypoxia.

76 was inhibited by diadenosine pentaphosphate, oligomycin, and UDP, suggesting the involvement of cell

77 Using three respiratory inhibitors, oligomycin, antimycin A, and cyanide, we find that polle

78 e treated rat cerebral cortical neurons with oligomycin, antimycin, or rotenone, which inhibit differ

79 nction induced by the ATP synthase inhibitor oligomycin as well as the electron transport chain inhib

80 chain activity, rise rapidly in response to oligomycin, as expected.

81 ed using rotenone, myxothiazol, antimycin A, oligomycin, ascorbate and the electron donor tetramethyl

82 We found that oligomycin at 100 ng/ml completely inhibits OXPHOS activ

83 20 nM), but not by the Fo-ATPase inhibitor, oligomycin (at up to 7 microg/ml).

84 Oligomycin B (5 microM) did not reduce the inhibition of

85 Oligomycin B (5 microM), which prevents mitchondrial ATP

86 However, an ATP-synthase inhibitor, oligomycin B, had no significant effect.

87 the product of an unannotated gene from the oligomycin BGC.

88 gion similar to that shown to participate in oligomycin binding by the F-ATPase.

89 in binding, and that this site resembles the oligomycin binding site of the F-ATPase.

90 The amino acid residues that form the oligomycin-binding site are 100% conserved between human

91 Prior genetics studies suggest that the oligomycin-binding site overlaps with the binding site o

92 Oligomycin binds to the surface of the c(10) ring making

93 es the pH gradient but not by valinomycin or oligomycin, both of which reduce the membrane potential

94 high-resolution (1.9 A) crystal structure of oligomycin bound to the subunit c(10) ring of the yeast

95 itochondrial complex inhibitors rotenone and oligomycin, but not by the cytosolic phospholipase A(2)

96 lide antibiotics (+)-rutamycin B (1) and (+)-oligomycin C (2) is described.

97 mpleted the synthesis of the rutamycin B and oligomycin C.

98 lete conversion of the major metabolite into oligomycin C.

99 itochondrial toxins rotenone, antimycin, and oligomycin can be transferred without conferring a DSU-s

100 MPPNP, and is not altered by the presence of oligomycin, carboxyatractyloside, or AP5A, used alone or

101 tion, and showed that selection in galactose-oligomycin caused a significant increase in the fraction

102 lly, MV from cells treated with antimycin or oligomycin contained less PPi and precipitated >50% more

103 stasis, including the protection afforded by oligomycin, could be reproduced by veratridine.

104 However, in the presence of oligomycin CSN response to Ba2+ was significant.

105 Oligomycin decreased the rate of rise of [Mg2+]i delayed

106 Treating PIP-FUCCI IECs with oligomycin demonstrates that inhibiting mitochondrial re

107 th the potentiometric dye, JC-1, revealed an oligomycin-dependent increase in mitochondrial membrane

108 , and PIP-H2A cells allow us to measure that oligomycin differentially lengthens S and G2/M phases ac

109 In glycolysis-dominant cells, oligomycin does not induce much energy stress as measure

110 We also demonstrate that the adaptation to oligomycin does not invoke activation of hypoxia-induced

111 on is consistent with our demonstrating that oligomycin elevated cellular [AMP] and selectively inhib

112 Application of FCCP plus oligomycin elevated resting [Ca(2+)]c in SNL L4 neurons

113 Inhibition of ATP synthase with oligomycin elevated ROS and f9a transcripts, while ROS i

114 demonstrated that the energy-depleting agent oligomycin enhanced both Rac1 activity and cell death.

115 bitors, rotenone, 3-NPA, antimycin, KCN, and oligomycin, exhibited concentration dependent toxicity i

116 dmium transporter), a short yeast MRP (Yor1p oligomycin exporter), and human CFTR channels.

117 Pretreatment of cells with 0.01 microM oligomycin for 45 min prior to addition of 50 microM H(2

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

119 oxygen species (ROS) (e.g., antimycin A and oligomycin) had a negative impact on CI and supercomplex

120 ylcyanide p-trifluoro-methoxyphenylhydrazone/oligomycin) had no effect on the size of Ca(2+) changes

121 Blocking antibodies and antagonists (oligomycin, IC(50) approximately 1.8 muM; piceatannol, I

122 energetic adaptation to the OXPHOS inhibitor oligomycin in a group of cancer cells.

123 Treatment with oligomycin increased, whereas FCCP decreased, DeltaPsi(m

124 r metabolic inhibition with deoxyglucose and oligomycin, indicating an energy-independent mode of ent

125 hondrial depolarization that was enhanced by oligomycin, indicating ATP synthase reversal.

126 was increased by the ATP synthase inhibitor oligomycin, indicating that barbiturates act by inhibiti

127 E2 was ineffective against KCN and oligomycin-induced cell death.

128 After AMPK activation is completed, oligomycin-induced increase of acetyl-CoA carboxylase ph

129 Finally, we found that oligomycin-induced ROS production was significantly (p <

130 In OXPHOS-dependent LKB1 wild type cells, oligomycin induces 5-8% ATP drops and transient AMPK act

131 In contrast, ADP plus oligomycin inhibited both permeabilities under all of th

132 These oligomycin inhibited mitochondria-modified electrodes we

133 rotenone or antimycin A in combination with oligomycin inhibited mitochondrial NO production.

134 increased oxygen utilization under basal and oligomycin-inhibited conditions.

135 icant reduction in the ratio of uncoupled to oligomycin-inhibited endogenous respiration observed in

136 Oligomycin-inhibited mitochondria-modified electrodes we

137 also assessed the effects of antimycin A and oligomycin (inhibitors of mitochondrial complexes III an

138 In a separate set of mice, oligomycin injection to block ATP generation decreased C

139 The increase in OCR was oligomycin-insensitive and contingent on cAMP-dependent

140 C208/L2 and the other atp22 mutants have oligomycin-insensitive F1-ATPase, suggesting that the le

141 ATPase activity was largely oligomycin-insensitive in these mitochondrial fractions.

142 effects, we found that salicylate increases oligomycin-insensitive respiration (state 4o) and direct

143 of the macrocyclic polyketides ossamycin and oligomycin involves catalysis by a novel spiroacetal cyc

144 ndent LKB1-null cells, no AMPK activation by oligomycin is detected, yet cells still show a similar a

145 ccurs rapidly in response to ATP (2 mM) when oligomycin is present.

146 evealed that the enzyme is also activated by oligomycin (K(1/2) approximately 16 nm).

147 Oligomycin largely reduced the increase in [Ca2+](m) by

148 mycin production and led to the isolation of oligomycin-like metabolites lacking the spiroacetal stru

149 Oligomycin may protect by preventing the consequent mito

150 Thus rotenone, myxothiazol, cyanide and oligomycin mimic the effects of hypoxia in that they all

151 of AH/Type-II neurons were hyperpolarized by oligomycin, most likely by activating ATP-dependent K+ c

152 (CAT), and the F1FO-ATP synthase inhibitor, oligomycin (OLIG), inhibited ureagenesis-induced respira

153 In the presence of oligomycin (Oligo), an F1F0-ATPase inhibitor, the decrea

154 yxothiazol, antimycin A, cyanide (CN(-)) and oligomycin on isolated carotid body type I cells.

155 l release in preparations treated with CCCP, oligomycin or CCCP and oligomycin together could result

156 th the mitochondrial ATP synthase inhibitors oligomycin or dicyclohexylcarbodiimide, which resulted i

157 presence of the combination of rotenone and oligomycin or in the presence of antimycin, which collap

158 Blocking mitochondrial ATP production with oligomycin or myxothiazol had no effect on excitability.

159 hed by ATP depletion (2 deoxy-D-glucose with oligomycin or perfusion of apyrase), can be restored wit

160 in the presence of the mitochondrial poison oligomycin or the glial toxin fluoroacetate.

161 Pase activity was not inhibited by vanadate, oligomycin, or nitrate, but was inhibited by relatively

162 (trifuoro-methoxy)phenylhydrazone, antimycin-oligomycin, or ruthenium red revealed that mitochondria

163 tors (erythro-9-[3-(2-hydroxynonyl)]adenine, oligomycin, ouabain, and thapsigargin) had no effect on

164 lar ATP synthesis was detected, whereas with oligomycin, piceatannol, and aurovertin (inhibitors of F

165 Rotenone, but not antimycin or oligomycin, prevented this effect, indicating that elect

166 The deletion of olmO abolished oligomycin production and led to the isolation of oligom

167 The mitochondrial ATP synthase inhibitor oligomycin protected cells against KA- but not NMDA-evok

168 ecule perturbagens (2-deoxyglucose, oxamate, oligomycin, rapamycin, and wortmannin), and a large numb

169 carbonylcyanide-m-chlorophenylhydrazone, or oligomycin reproduced this effect, as did generation of

170 f phenylalanine 670 (DeltaF670) in the yeast oligomycin resistance 1 gene (YOR1, an ABC transporter)

171 genic suppressing mutations that rescued the oligomycin resistance associated with this aberrant prot

172 isiae in our laboratory implicated the yeast oligomycin resistance gene (YOR1), a member of the ATP b

173 ng cassette (ABC) transporter Yor1p mediates oligomycin resistance in Saccharomyces cerevisiae.

174 udy, we demonstrate that Yrr1p also mediates oligomycin resistance through activation of the ATP-bind

175 processing and translation, which conferred oligomycin resistance to yeast.

176 ified on the basis of its ability to elevate oligomycin resistance when it was overproduced from a hi

177 ispensability, V-ATPase defective cells were oligomycin resistant, suggesting ATP synthase uncoupling

178 f two mutations corresponded to positions of oligomycin-resistant mutations in the c subunit of F(1)F

179 itochondrial toxins rotenone, antimycin, and oligomycin, respectively.

180 n 3 mM succinate, cyclosporin A and ADP plus oligomycin restored potential and calcium uptake.

181 Furthermore, prolonged (2-h) incubation with oligomycin resulted in an impaired ability to activate a

182 sly stereochemically undefined member of the oligomycin-rutamycin family.

183 arately, its peripheral stalk subunits b and oligomycin sensitive conferral protein.

184 ane segment (F0) of ATP synthase and restore oligomycin-sensitive ATPase activity in OSCP-depleted F1

185 recombinant protein was able to reconstitute oligomycin-sensitive ATPase activity to inner membrane v

186 ull mutant that displays partial recovery of oligomycin-sensitive ATPase and of respiratory competenc

187 ovine submitochondrial particles enriched in oligomycin-sensitive ATPase; (ii) the NH2 termini of f a

188 r the biogenesis of chloroplast ATP synthase oligomycin-sensitive chloroplast coupling factor.

189 Furthermore, acetylation of oligomycin-sensitive conferring protein at lysine-70 in

190 dditionally supported by the detection of an oligomycin-sensitive decrease in mitochondrial membrane

191 ated with 40+/-3% and 72+/-9% inhibitions of oligomycin-sensitive F(1)F(0) ATPase activity, respectiv

192 d to 5 mM lactate (but not pyruvate) with an oligomycin-sensitive increase in [ATP](c).

193 n addition to isolated hepatocytes increases oligomycin-sensitive oxygen consumption and maximal resp

194 ADP induced an oligomycin-sensitive transition from resting to phosphor

195 ADP promoted an oligomycin-sensitive transition from resting to phosphor

196 ATP hydrolysis by the oligomycin-sensitive, mitochondrial F(1)F(O)-ATPase was

197 Both activities were highly oligomycin-sensitive.

198 gnal has been fused to the C terminus of the oligomycin sensitivity conferral protein (OSCP) of the A

199 is ensured by robust attachment of both the oligomycin sensitivity conferral protein (OSCP) to the c

200 ciated with the dimeric ATP synthase and the oligomycin sensitivity conferral protein (OSCP), a compo

201 e mitochondria, the N-terminal domain of the oligomycin sensitivity conferral protein (OSCP-NT; resid

202 e mitochondria, the N-terminal domain of the oligomycin sensitivity conferral protein (OSCP-NT; resid

203 Its uppermost region interacts with the oligomycin sensitivity conferral protein, bound to the N

204 The oligomycin sensitivity conferring protein (OSCP) is an e

205 Earlier studies on oligomycin sensitivity conferring protein (OSCP) of bovi

206 The structure/function relationships of oligomycin sensitivity conferring protein (OSCP) of bovi

207 Here, we observe selective loss of the oligomycin sensitivity conferring protein (OSCP) subunit

208 l stalk, as well as F(0) subunits, including oligomycin sensitivity conferring protein, b, and c subu

209 e segment (F0) nor able to reconstitute high oligomycin sensitivity in depleted F1-F0 complexes.

210 inding site is not required for conferral of oligomycin sensitivity to the reconstituted F0F1 complex

211 reconstitute F1 with membranes and to confer oligomycin sensitivity to the same extent as wild-type O

212 Ca(2+) like CyPD itself, and that decreasing oligomycin sensitivity-conferring protein expression by

213 We show that CyPD binds the oligomycin sensitivity-conferring protein subunit of the

214 to Bz-423 binding its molecular target, the oligomycin sensitivity-conferring protein subunit of the

215 d specifically to purified recombinant b and oligomycin sensitivity-conferring protein subunits of th

216 However, as expected, nearly complete Tb1 or oligomycin sensitivity-conferring protein suppression wa

217 protein; and subunits a, b, c, and d, OSCP (oligomycin sensitivity-conferring protein), F6, and A6L,

218 e findings were obtained by silencing of the oligomycin sensitivity-conferring protein, a conserved s

219 DD44 is homologous to the oligomycin sensitivity-conferring protein, an essential

220 of mitochondrial Sirt3 substrates, MnSOD and oligomycin-sensitivity conferring protein (OSCP).

221 Rotenone, cyanide, myxothiazol and oligomycin significantly inhibited resting background K(

222 The mitochondrial ATP synthase inhibitor, oligomycin, significantly decreased IEC persistence and

223 , chemical perturbation of mitochondria with oligomycin similarly prevents degradation of Pim1p subst

224 ECV304 cells after treatment with azide and oligomycin suggesting that the dynamic regulation of res

225 ntly increased, but collapsed in response to oligomycin, suggesting that the mitochondrial membrane p

226 equired Mg2+ and was insensitive to ouabain, oligomycin, thapsigargin, or levamisole.

227 ctive culture conditions using galactose and oligomycin that elicited a pathological phenotype in T89

228 In culture, endogenous TAK1 was activated by oligomycin, the antidiabetic drug metformin, 5-aminoimid

229 Unexpectedly, in the presence of oligomycin, the magnitude of the glucose response was si

230 ization of SMP by uncoupling (or addition of oligomycin to inhibit ATP hydrolysis) resulted in furthe

231 1 h failed to hyperpolarize upon addition of oligomycin to inhibit their ATP synthesis.

232 metabolic uncoupler FCCP, in the presence of oligomycin (to prevent ATP depletion), reversibly suppre

233 n preparations treated with CCCP or CCCP and oligomycin together because mitochondrial Ca2+ buffering

234 ns treated with CCCP, oligomycin or CCCP and oligomycin together could result from a progressive elev

235 n preparations treated with CCCP or CCCP and oligomycin together than in those treated with oligomyci

236 2 M), oligomycin (8 g x ml(-1)) or CCCP and oligomycin together.

237 ch are required for normal cycloheximide and oligomycin tolerances, respectively.

238 mbrane endocytosis occurred at some CCCP- or oligomycin-treated nerve terminals after 120 or 180 min

239 For oligomycin-treated nerve terminals, a progressive elevat

240 By contrast, inhibition of the complex using oligomycin triggered broad metabolic changes, affecting

241 (F-ATPases), suggesting that bafilomycin and oligomycin utilize a similar binding site and mechanism

242 r proton translocation, forms an H-bond with oligomycin via a bridging water molecule but is otherwis

243 ATP synthase inhibition by oligomycin was also toxic in the presence of glutamate.

244 ed mode of mitochondrial ATP-synthase, since oligomycin was not effective and nonhydrolysable analogs

245 F-ATPase subunit a also confer resistance to oligomycin, we investigated whether the a subunit of the

246 o chemical stimuli (e.g., calcium chelation, oligomycin) were continuously and noninvasively monitore

247 TPase, including apoptolidin, ossamycin, and oligomycin, were shown to be among the top 0.1% most cel

248 uring 1 Hz stimulation, and were not seen in oligomycin, which blocks mitochondrial ATP synthesis wit

249 d minimally cytotoxic doses of antimycin and oligomycin, which both induced intracellular ATP depleti

250 evels, and can be mimicked by agents such as oligomycin, which inhibit ATP synthesis.

251 cyanide m-chlorophenylhydrazone and 2 microM oligomycin) while perfusing with > 2 microM Ca(2+) aboli