ライフサイエンスコーパス: carbonyl cyanide

1 otocol was validated with the model compound carbonyl cyanide 3-chlorophenylhydrazone (CCCP) and used

2 The mitochondrial stressor carbonyl cyanide 3-chlorophenylhydrazone (CCCP) promotes

3 ane potential to be effectively inhibited by carbonyl cyanide 3-chlorophenylhydrazone (CCCP), a disru

4 sults including treatment with the uncoupler carbonyl cyanide 3-chlorophenylhydrazone (CCCP), express

5 tment of AGS cells with a mitophagy inducer, carbonyl cyanide 3-chlorophenylhydrazone (CCCP), resulte

6 H+-transporting ionophores nigericin/K+ and carbonyl cyanide 3-chlorophenylhydrazone inhibit the tra

7 wild-type signal sequence; sodium azide and carbonyl cyanide 3-chlorophenylhydrazone treatments indi

8 sium ionophore valinomycin, the protonophore carbonyl cyanide 3-chlorophenylhydrazone, and HCl.

9 n contrast, a proton motive force inhibitor, carbonyl cyanide 3-chlorophenylhydrazone, increased the

10 id not change in the presence of colistin or carbonyl cyanide 3-chlorophenylhydrazone, suggesting tha

11 vity to mitochondrial stressors rotenone and carbonyl cyanide 3-chlorophenylhydrazone, without any al

12 The addition of carbonyl-cyanide-3-chlorophenylhydrazone, monensin, bref

13 In the presence of oligomycin and low carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone (F

14 transport chain, as confirmed by addition of carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone an

15 NMDA-induced NO increase was abolished with carbonyl cyanide 4-(trifluoromethoxy)phenyl-hydrazone an

16 Zinquin fluorescence was unaffected by carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FC

17 Valinomycin, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FC

18 in the presence of cyanide or the uncoupler carbonyl cyanide 4-trifluoromethoxyphenylhydrazone (FCCP

19 ression of BTN1 or the presence of ionophore carbonyl cyanide m-chlorophenil hydrazone (CCCP) causes

20 ss genes by the respiratory chain uncoupler, carbonyl cyanide m-chlorophenyl hydrazine (CCCP).

21 ctivity was strongly inhibited by NH4(+) and carbonyl cyanide m-chlorophenyl hydrazine and was insens

22 rane after mitochondrial depolarization with carbonyl cyanide m-chlorophenyl hydrazine, a mitochondri

23 with experiments using the proton ionophore carbonyl cyanide m-chlorophenyl hydrazine, indicate that

24 hondrial oxidative phosphorylation uncoupler carbonyl cyanide m-chlorophenyl hydrazone (2 microM) als

25 Pretreatment with the protonophore carbonyl cyanide m-chlorophenyl hydrazone (CCCP) prevent

26 Here, we report that both carbonyl cyanide m-chlorophenyl hydrazone (CCCP) treatme

27 The effects of carbonyl cyanide m-chlorophenyl hydrazone (CCCP), an inh

28 Herein, carbonyl cyanide m-chlorophenyl hydrazone (CCCP)-induced

29 After addition of carbonyl cyanide m-chlorophenyl hydrazone (CCCP, 1-2 mic

30 Carbonyl cyanide m-chlorophenyl hydrazone (CCCP; 5 micro

31 nol (CEP), calcimycin (a Ca2+ ionophore) and carbonyl cyanide m-chlorophenyl hydrazone (CCCP; a mitoc

32 It is eliminated by the protonophore carbonyl cyanide m-chlorophenyl hydrazone and is approxi

33 function induced by mitochondrial ionophore, carbonyl cyanide m-chlorophenyl hydrazone and other resp

34 other cells, mitochondrial depolarization by carbonyl cyanide m-chlorophenyl hydrazone did not induce

35 port, while the protonmotive-force-inhibitor carbonyl cyanide m-chlorophenyl hydrazone had no effect.

36 Although the uncoupler carbonyl cyanide m-chlorophenyl hydrazone inhibited AGT(

37 centrations (0.06 mg L(-1)) of the uncoupler carbonyl cyanide m-chlorophenyl hydrazone inhibited NTO

38 of Opa1 splice variants but does not affect carbonyl cyanide m-chlorophenyl hydrazone or apoptosis-i

39 ondria membrane potential with the uncoupler carbonyl cyanide m-chlorophenyl hydrazone or the release

40 Using carbonyl cyanide m-chlorophenyl hydrazone treatment, we

41 nsensitive to ATP or treatment with NH4Cl or carbonyl cyanide m-chlorophenyl hydrazone, indicating th

42 n those treated with TNF or uncoupling agent carbonyl cyanide m-chlorophenyl hydrazone, suggesting an

43 tochondria or parkin-mediated mitophagy upon carbonyl cyanide m-chlorophenyl hydrazone-induced mitoch

44 en the TM proton gradient was abolished with Carbonyl cyanide m-chlorophenyl hydrazone.

45 ut not after mitochondrial depolarization by carbonyl cyanide m-chlorophenyl hydrazone.

46 CCCP (carbonyl cyanide m-chlorophenyl), a protonophore uncoupl

47 tablished mitochondrial depolarizing agents, carbonyl cyanide m-chlorophenyl-hydrazine and niclosamid

48 a2+]c, were abolished by a proton ionophore, carbonyl cyanide m-chlorophenyl-hydrazone (CCCP), and by

49 polarizing mitochondria with antimycin A1 or carbonyl cyanide m-chlorophenyl-hydrazone, the stimulati

50 n response to global mitochondrial damage by carbonyl cyanide m-chlorophenylhydrazine (CCCP) requires

51 lectrochemical gradient by the protonophore, carbonyl cyanide m-chlorophenylhydrazone (CCCP) almost c

52 onditions, hypersensitivity to the uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) and mtDN

53 The uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) inhibite

54 h prolonged by mitochondrial inhibition with carbonyl cyanide m-chlorophenylhydrazone (CCCP) or Ruthe

55 model of mitophagy induced by an uncoupler, carbonyl cyanide m-chlorophenylhydrazone (CCCP) that Par

56 When carbonyl cyanide m-chlorophenylhydrazone (CCCP) was appl

57 of murine embryonic fibroblasts treated with carbonyl cyanide m-chlorophenylhydrazone (CCCP), a mitoc

58 ial electron transport chain complex II, and carbonyl cyanide m-chlorophenylhydrazone (CCCP), an unco

59 Driving-ion studies with phenamil, carbonyl cyanide m-chlorophenylhydrazone (CCCP), and dif

60 etween ST1710 and three ligands, salicylate, carbonyl cyanide m-chlorophenylhydrazone (CCCP), and eth

61 Gramicidin and carbonyl cyanide m-chlorophenylhydrazone (CCCP), antimic

62 itochondrial metabolic inhibitors, including carbonyl cyanide m-chlorophenylhydrazone (CCCP), antimyc

63 f the inhibitor of oxidative phosphorylation carbonyl cyanide m-chlorophenylhydrazone (CCCP), dinitro

64 After mitochondrial depolarization with carbonyl cyanide m-chlorophenylhydrazone (CCCP), Flag-gp

65 ssic uncoupler of oxidative phosphorylation, carbonyl cyanide m-chlorophenylhydrazone (CCCP), induced

66 ry, provoked by incubation of platelets with carbonyl cyanide m-chlorophenylhydrazone (CCCP), led to

67 Rotenone, thenoyltrifluoroacetone (TTFA), carbonyl cyanide m-chlorophenylhydrazone (CCCP), Mn(III)

68 gy) stimulated by a mitochondrial uncoupler, carbonyl cyanide m-chlorophenylhydrazone (CCCP), require

69 tivation due to the addition of protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP), which d

70 l store was estimated by releasing them with carbonyl cyanide m-chlorophenylhydrazone (CCCP).

71 estimated by counting the quanta released by carbonyl cyanide m-chlorophenylhydrazone (CCCP).

72 taneous nerve muscle preparations exposed to carbonyl cyanide m-chlorophenylhydrazone (CCCP, 2 M), ol

73 Depolarizing mitochondria with carbonyl cyanide m-chlorophenylhydrazone (CCCP, 5 microM

74 netic stress) and control cells treated with carbonyl cyanide m-chlorophenylhydrazone (metabolic stre

75 pumping into reticular stores), and 2 microM carbonyl cyanide m-chlorophenylhydrazone (uptake into mi

76 lusion of mitochondrial inhibitors (2 microM carbonyl cyanide m-chlorophenylhydrazone and 2 microM ol

77 Cu-Mb is inhibited by the uncoupling agents carbonyl cyanide m-chlorophenylhydrazone and methylamine

78 B. pertussis strains that were treated with carbonyl cyanide m-chlorophenylhydrazone and sodium arse

79 We found that in the absence of Parkin, carbonyl cyanide m-chlorophenylhydrazone induced the for

80 The electron transport uncoupler carbonyl cyanide m-chlorophenylhydrazone inhibited aceta

81 Loading of this store is prevented by carbonyl cyanide m-chlorophenylhydrazone or by antimycin

82 and release (tetraphenylphosphonium or TPP+, carbonyl cyanide m-chlorophenylhydrazone or CCCP, and ru

83 al sequence, was detected in the presence of carbonyl cyanide m-chlorophenylhydrazone or sodium azide

84 In the presence of the uncouplers carbonyl cyanide m-chlorophenylhydrazone or valinomycin,

85 translocation to mitochondria in response to carbonyl cyanide m-chlorophenylhydrazone treatment.

86 brid motor was inhibited by the protonophore carbonyl cyanide m-chlorophenylhydrazone under neutral a

87 ent and strongly stimulated by the uncoupler carbonyl cyanide m-chlorophenylhydrazone when no externa

88 t and was unaffected by the uncouplers CCCP (carbonyl cyanide m-chlorophenylhydrazone) and DNP (2,4-d

89 Since protonophores CCCP (carbonyl cyanide m-chlorophenylhydrazone) and DTHB (3,5-

90 tion rates in both cell lines, whereas CCCP (carbonyl cyanide m-chlorophenylhydrazone) stimulated the

91 , an uncoupler of oxidative phosphorylation (carbonyl cyanide m-chlorophenylhydrazone), a superoxide

92 ivity was inhibited by the proton ionophores carbonyl cyanide m-chlorophenylhydrazone, 2,4-dinitrophe

93 cold (50% at 4 degrees C), by protonophores (carbonyl cyanide m-chlorophenylhydrazone, 44%, and 2,4-d

94 in HIV-1 infectivity was observed only with carbonyl cyanide m-chlorophenylhydrazone, a compound whi

95 e of a membrane potential since inclusion of carbonyl cyanide m-chlorophenylhydrazone, a protonophore

96 Extended pretreatment of B cells with carbonyl cyanide m-chlorophenylhydrazone, an inhibitor o

97 Fbxl7 protects mitochondria from actions of carbonyl cyanide m-chlorophenylhydrazone, an inhibitor o

98 ligands of the EmrAB pump-2,4-dinitrophenol, carbonyl cyanide m-chlorophenylhydrazone, and carbonyl c

99 uch as rotenone, thenoyltrifluoroacetone, or carbonyl cyanide m-chlorophenylhydrazone, associated wit

100 or treatment with a mitochondrial ionophore, carbonyl cyanide m-chlorophenylhydrazone, initiates a st

101 tors of oxidative phosphorylation antimycin, carbonyl cyanide m-chlorophenylhydrazone, or oligomycin.

102 By using carbonyl cyanide m-chlorophenylhydrazone, we showed that

103 Unlike the protonophore carbonyl cyanide m-chlorophenylhydrazone, which activate

104 ol ROS bursts after high-dose treatment with carbonyl cyanide m-chlorophenylhydrazone.

105 ed through the addition of the protonophore, carbonyl cyanide m-chlorophenylhydrazone.

106 with a mitochondrial Ca2+ uptake inhibitor, carbonyl cyanide m-chlorophenylhydrazone.

107 g, was blocked by pretreatment with azide or carbonyl cyanide m-chlorophenylhydrazone; however, 10% o

108 inhibitor, bafilomycin A1, the protonophore carbonyl cyanide m-chorophenylhydrazone or the ionophore

109 nt strain by addition of a proton conductor, carbonyl cyanide m-chorophenylhydrazone.

110 r treatment with the mitochondrial uncoupler carbonyl cyanide m-methylhydrazone, because of protein m

111 ld-type cells poisoned with the protonophore carbonyl cyanide-m-chlorophenylhydrazone retained their

112 ly collapsed upon the addition of nigericin, carbonyl cyanide p-(tri-fluoromethoxy) phenyl-hydrazone,

113 arbonyl cyanide m-chlorophenylhydrazone, and carbonyl cyanide p-(trifluoro-methoxy)phenylhydrazone-wi

114 al inhibitor NaCN and mitochondria uncoupler carbonyl cyanide p-(trifluoromethoxy) phenyl hydrazone (

115 g dry weight; this increase was abolished by carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (F

116 fter addition of the mitochondrial uncoupler carbonyl cyanide p-(trifluoromethoxy)phenyl hydrazone (F

117 ere sensitive to the mitochondrial uncoupler carbonyl cyanide p-(trifluoromethoxy)phenyl-hydrazone (F

118 roM monensin (a Na+ ionophore) or 0.3 microM carbonyl cyanide p-(trifluoromethoxy)phenyl-hydrazone (F

119 etreatment with the mitochondrial inhibitors carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (1

120 The protonophore carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FC

121 ERK1 and ERK2 by the mitochondrial uncoupler carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FC

122 Exposure to the protonophore carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FC

123 with the role of mitochondrial Ca overload, carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone dec

124 of substrates/ADP or uncouplers (valinomycin/carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone) an

125 EMPO (TEMPOL) or the mitochondrial uncoupler carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone.

126 Inhibiting mitochondria by treatment with carbonyl cyanide p-(trifuoro-methoxy)phenylhydrazone, an

127 hree inhibitors of mitochondrial metabolism: carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol,

128 Carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol,

129 by treating cells with the proton uncoupler carbonyl cyanide p-chlorophenylhydrazone.

130 n of mitochondrial Ca2+ uptake with cyanide, carbonyl cyanide p-trifluoromethoxy-phenylhydrazone or R

131 Both 2,4-dinitrophenol (DNP) and carbonyl cyanide p-trifluoromethoxyphenyl hydrazone (FCC

132 e (P2X(7) receptor agonist), AG10, AG18, and carbonyl cyanide p-trifluoromethoxyphenyl hydrazone rapi

133 However, like the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxyphenyl hydrazone, tyr

134 perature (4 degrees C), the proton ionophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone (2.5

135 tochondrial inhibitor NaCN, or the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP

136 gh the coronary arteries with the uncoupler, carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP

137 Release of mitochondrial Ca(2+) by carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP

138 10 microm carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP

139 y ADP or when mitochondria were uncoupled by carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP

140 ent whose Ca2+ uptake was inhibited 82% with carbonyl cyanide p-trifluoromethoxyphenylhydrazone and K

141 In addition, the protonophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone only

142 Addition of carbonyl cyanide p-trifluoromethoxyphenylhydrazone or de

143 letion and treatment with potassium cyanide, carbonyl cyanide p-trifluoromethoxyphenylhydrazone, and

144 ucose depletion, by potassium cyanide, or by carbonyl cyanide p-trifluoromethoxyphenylhydrazone, whic

145 ximum respiration induced with either ADP or carbonyl cyanide p-trifluoromethoxyphenylhydrazone,alpha

146 Rotenone at 20 nM inhibited basal and carbonyl cyanide p-trifluoromethoxyphenylhydrazone-stimu

147 inuous superfusion with the uncoupling agent carbonyl cyanide-p-trifluoromethoxy-phenylhydrazone (1-3

148 Moreover, in the presence of carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP

149 The uncoupler carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP

150 ters that are pronounced under the action of carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP

151 th oxidative and glycolytic metabolism using carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP