ライフサイエンスコーパス: carbonyl cyanide

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 Using carbonyl cyanide m-chlorophenyl hydrazone treatment, we

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 Carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol,

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

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

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

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

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

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

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

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

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

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

124 10 microm carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP

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

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

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

128 Addition of carbonyl cyanide p-trifluoromethoxyphenylhydrazone or de

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

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

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

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

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

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

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