ライフサイエンスコーパス: oligomycin

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

2 rial respiratory antagonists antimycin A and oligomycin.

3 esistance to drugs such as cycloheximide and oligomycin.

4 43 in preparations exposed to either CCCP or oligomycin.

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

6 carbonyl cyanide m-chlorophenylhydrazone, or oligomycin.

7 by the mitochondrial ATP-synthase inhibitor oligomycin.

8 ernal mitochondrial membrane potential using oligomycin.

9 s explaining the differential sensitivity to oligomycin.

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

11 ed after acute inhibition of ATP synthase by oligomycin.

12 e energy metabolism modifiers, metformin and oligomycin.

13 sed sensitivity to the mitochondrial poison, oligomycin.

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

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

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

17 Oligomycin (2 microg) abolished the hypoxic response.

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

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

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

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

22 2 inhibit mitochondrial function similar to oligomycin A and apoptolidin A, selective inhibitors of

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

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

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

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

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

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

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

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

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

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

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

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

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

36 igomycin together than in those treated with oligomycin alone.

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

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

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

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

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

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

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

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

45 2Y-R enhanced neuroprotection was blocked by oligomycin and by Xestospongin C, inhibitors of the ATP

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 20 nM), but not by the Fo-ATPase inhibitor, oligomycin (at up to 7 microg/ml).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 These oligomycin inhibited mitochondria-modified electrodes we

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

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

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

108 Oligomycin-inhibited mitochondria-modified electrodes we

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

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

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

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

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

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

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

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

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

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

119 Oligomycin may protect by preventing the consequent mito

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 Both activities were highly oligomycin-sensitive.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 1 h failed to hyperpolarize upon addition of oligomycin to inhibit their ATP synthesis.

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

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

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

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

200 2 M), oligomycin (8 g x ml(-1)) or CCCP and oligomycin together.

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

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

203 For oligomycin-treated nerve terminals, a progressive elevat

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

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

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

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

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

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

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

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

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

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

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