ライフサイエンスコーパス: antimycin A

1 ffect was augmented by complex III inhibitor antimycin A.

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

3 tive oxygen species increase by rotenone and antimycin A.

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

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

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

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

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

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

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

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

12 vely stressed with the respiratory inhibitor antimycin A.

13 0% of the V(max) observed in the presence of antimycin A.

14 d by inhibition of mitochondrial function by antimycin A.

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

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

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

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

19 Antimycin A, a specific inhibitor of the cytochrome bc1

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

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

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

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

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

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

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

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

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

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

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

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

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

33 Antimycin A and cyanide, which inhibit the distal region

34 Respiration was sensitive to antimycin A and cyanide.

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

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

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

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

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

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

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

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

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

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

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

46 by the mitochondrial respiratory antagonists antimycin A and oligomycin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 nt of cultured thyroid epithelial cells with antimycin A greatly inhibited ( > 90%) the secretion of

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

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

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

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

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

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

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

84 Antimycin A increased ROS production and decreased cell

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

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

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

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

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

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

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

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

93 Antimycin A-induced hyperexcitability was dependent on m

94 Antimycin A-induced hyperexcitability was inhibited by t

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

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

97 Antimycin A-induced nociceptor hyperexcitability was ind

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

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

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

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

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

103 Antimycin A is the most frequently used specific and pow

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

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

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

107 Antimycin A (mitochondrial complex III Qi site inhibitor

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

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

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

111 3-(3,4-dichlorophenyl)-1,1-dimethylurea and antimycin A, of pyruvate dehydrogenase, moniliformin, of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Antimycin A selectively induces apoptosis in cells overe

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

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

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

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

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

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

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

138 Antimycin A suppressed quenching, increasing the Hill co

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

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

141 Rotenone or antimycin A, the respiratory electron transport blockers

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

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

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

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

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

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

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

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

150 2-hydroxyethidium in normally respiring and antimycin A-treated mitochondria and demonstrated that t

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

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

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

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

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

156 nscriptional changes observed in response to antimycin A treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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