ライフサイエンスコーパス: CCCP

1 CCCP (5 microM) reduced the magnitude of the [Ca2+]c tra

2 CCCP (a protonophore; 1 microm) and rotenone (an electro

3 CCCP (carbonyl cyanide m-chlorophenyl), a protonophore u

4 CCCP abolished spontaneously occurring transient Ca(2+)-

5 CCCP application to naive cells did not block the ACh-in

6 CCCP augmented peak tetanic and submaximum [Ca2+]i and f

7 CCCP inhibited the increase in mitochondrial [Ca2+].

8 CCCP per se did not induce apoptosis or release of proap

9 CCCP releases fewer quanta after stimulation than from u

10 CCCP-induced mitochondrial fragmentation leads to Mfn2 a

11 In the absence of IP(3), CCCP had no effect on the cytosolic Ca(2+) levels.

12 a2+ concentration, [Ca2+]m) rose slowly in a CCCP-sensitive manner during and for about 3 s after dep

13 RUND-1 and CCCP-1 colocalize with RAB-2 at the Golgi, and rab-2, ru

14 that are supported by the binding of DNA and CCCP to the N and C termini of VceR, respectively.

15 e mutant to growth inhibition by ethanol and CCCP at pH 7; ethanol was not excluded, however, from th

16 on was shown to be induced by gramicidin and CCCP, agents known to dissipate the proton motive force,

17 lizing ionophore combinations (nigericin and CCCP) or digitonin.

18 proteins: RUND-1, a RUN domain protein, and CCCP-1, a coiled-coil protein.

19 In the absence of SITS and CCCP, dehydration was limited by the diffusional Cl- per

20 t did prevent cell death following TRAIL and CCCP exposure.

21 ntimycin + oligomycin had the same effect as CCCP.

22 R is a dimer in the absence of DNA but binds CCCP with a Hill co-efficient of 4, implying that it has

23 th the phosphor-inactivation of GSK-3beta by CCCP and by the induction of PRC by the GSK-3 inhibitor

24 ed the phosphor-inactivation of GSK-3beta by CCCP, a result consistent with the ability of Akt to pho

25 peration of the Na(+)-NQR was accelerated by CCCP, inhibited by valinomycin, and completely arrested

26 enes that require PRC for their induction by CCCP.

27 p62 seemed to affect autophagy induction by CCCP.

28 y 86Rb+ uptake; this uptake was inhibited by CCCP and is thus secondary to the primary, electrogenic

29 o LjSUT4-expressing oocytes was inhibited by CCCP and sucrose induced membrane depolarization in LjSU

30 ins were also more susceptible to killing by CCCP or by a bactericidal/permeability-increasing protei

31 y melittin, LL37, and alamethicin but not by CCCP or daptomycin, agents known to cause ion leakage.

32 sites that can be simultaneously occupied by CCCP.

33 Generation of ROS by CCCP was responsible for TRAIL-induced Bax and caspase a

34 ther increased when cells were stimulated by CCCP and MSB.

35 Na+ efflux, which was further stimulated by CCCP.

36 ition of the InsP3-induced Ca2+ transient by CCCP thus minimizing the possibility that CCCP lowered A

37 by carbonyl cyanide m-chlorophenylhydrazine (CCCP) requires active glucose metabolism.

38 er carbonyl cyanide 3-chlorophenylhydrazone (CCCP), expression of a dominant negative allele of nucle

39 e, carbonyl cyanide m-chlorophenylhydrazone (CCCP) almost completely blocked NBD-phospholipid flip wh

40 er carbonyl cyanide m-chlorophenylhydrazone (CCCP) and mtDNA instability.

41 er carbonyl cyanide m-chlorophenylhydrazone (CCCP) inhibited Hyd-2-dependent H2 evolution from glycer

42 ith carbonylcyanide m-chlorophenylhydrazone (CCCP) or antimycin A1 caused cytosolic [Ca(2+)] to rise

43 at was abolished in m-chlorophenylhydrazone (CCCP) or on omitting intracellular Na(+).

44 th carbonyl cyanide m-chlorophenylhydrazone (CCCP) or Ruthenium Red, which abolished the initial rapi

45 r, carbonyl cyanide m-chlorophenylhydrazone (CCCP) that Parkin translocation resulted in mitochondria

46 en carbonyl cyanide m-chlorophenylhydrazone (CCCP) was applied in the presence of the Ca(2+)-releasin

47 th carbonyl cyanide m-chlorophenylhydrazone (CCCP), a mitochondrial uncoupler, found that more than h

48 nd carbonyl cyanide m-chlorophenylhydrazone (CCCP), an uncoupler of oxidative phosphorylation, comple

49 l, carbonyl cyanide m-chlorophenylhydrazone (CCCP), and different pH and sodium conditions indicated

50 e, carbonyl cyanide m-chlorophenylhydrazone (CCCP), and ethidium, which bind to bacterial MarRs.

51 nd carbonyl cyanide m-chlorophenylhydrazone (CCCP), antimicrobial agents that dissipate the DeltapH a

52 ng carbonyl cyanide m-chlorophenylhydrazone (CCCP), antimycin, valinomycin and azide.

53 on carbonyl cyanide m-chlorophenylhydrazone (CCCP), dinitrophenol (DNP), or CN(-), resulted in massiv

54 th carbonyl cyanide m-chlorophenylhydrazone (CCCP), Flag-gp78 induced a threefold loss of depolarized

55 ore carbonylcyanide m-chlorophenylhydrazone (CCCP), indicating that TonB and an intact proton motive

56 n, carbonyl cyanide m-chlorophenylhydrazone (CCCP), induced a reduction in DeltaPsim and generation o

57 th carbonyl cyanide m-chlorophenylhydrazone (CCCP), led to reduced posttransfusion recovery in mice,

58 ), carbonyl cyanide m-chlorophenylhydrazone (CCCP), Mn(III)tetrakis (4-benzoic acid) porphyrin (MnTBA

59 r, carbonyl cyanide m-chlorophenylhydrazone (CCCP), requires Parkin, but it is not clear why Parkin i

60 re carbonyl cyanide m-chlorophenylhydrazone (CCCP), which dissipates the proton motive force.

61 by carbonyl cyanide m-chlorophenylhydrazone (CCCP).

62 f the protonophore, m-chlorophenylhydrazone (CCCP).

63 th carbonyl cyanide m-chlorophenylhydrazone (CCCP).

64 ore carbonylcyanide-m-chlorophenylhydrazone (CCCP, 10 microM) and the calcium ionophore A23187 (10 mi

65 to carbonyl cyanide m-chlorophenylhydrazone (CCCP, 2 M), oligomycin (8 g x ml(-1)) or CCCP and oligom

66 th carbonyl cyanide m-chlorophenylhydrazone (CCCP, 5 microM) causes release of mitochondrial Ca2+ and

67 at was abolished i nm-chlorophenylhydrazone (CCCP) or on omitting intracellular Na+.

68 ore carbonylcyanide p-chlorophenylhydrazone (CCCP), and more modestly, by Na+, and K+, but not by cho

69 In contrast, CCCP failed to inhibit H2-coupled fumarate reduction.

70 by FM1-43 in preparations exposed to either CCCP or oligomycin.

71 clinical and laboratory derived) with either CCCP (a proton ionophore which collapses the proton moti

72 ss of DeltaPsim and ROS generation following CCCP treatment, but did prevent cell death following TRA

73 parkin were required for mitophagy following CCCP-induced mitochondrial damage.

74 The apparent affinity for CCCP decreased in a linear manner with increasing concen

75 Furthermore, CCCP, a protonophore that disrupts the proton gradient n

76 , carbonyl cyanide m-chlorophenyl hydrazine (CCCP).

77 e carbonyl cyanide m-chlorophenil hydrazone (CCCP) causes decreased growth in yeast lacking SDO1.

78 f carbonyl cyanide m-chlorophenyl hydrazone (CCCP), an inhibitor of mitochondrial Ca2+ uptake, was in

79 , carbonyl cyanide m-chlorophenyl hydrazone (CCCP)-induced mitochondrial depolarization decreased mit

80 f carbonyl cyanide m-chlorophenyl hydrazone (CCCP, 1-2 microM) to dissipate the proton electrochemica

81 Carbonyl cyanide m-chlorophenyl hydrazone (CCCP; 5 microM), which dissipates the mitochondrial prot

82 d carbonyl cyanide m-chlorophenyl hydrazone (CCCP; a mitochondrial uncoupler) alter [Ca2+]i and force

83 , carbonyl cyanide m-chlorophenyl-hydrazone (CCCP), and by Ruthenium Red, a mitochondrial Ca(2+)-unip

84 In CCCP, the magnitudes of evoked Ca2+ transients are incre

85 ) knockdown of the autophagy protein Atg5 in CCCP-treated cells.

86 tify Parkin-dependent selective mitophagy in CCCP-treated HeLa cells.

87 In the presence of proton ionophores (CCCP, inhibitor of proton motive force), we found that i

88 cation of mitochondrial uncouplers (5 microM CCCP or 5 microM FCCP), eliminated the ACh-induced [Ca2+

89 In contrast, micromolar CCCP, or rotenone, an electron transport chain blocker,

90 ochondrial depolarization, because nanomolar CCCP, a protonophore, similarly depolarized mitochondria

91 In the absence of CCCP, NatAB-mediated Na+ efflux was stimulated by K+.

92 Addition of CCCP at the nadir of the decrease restored intracellular

93 mM Cao2+) external solutions, application of CCCP (1-2 microM) evoked an inward current and prolonged

94 At the lower temperatures, application of CCCP continued to depolarize mitochondria but produced a

95 The effect of CCCP on tau was greater in cells where the amplitude of

96 large and, in different cells, the effect of CCCP on tau was positively correlated with the amplitude

97 overexpression of BTN1 mirrors the effect of CCCP, with both resulting in increased vacuolar pH due t

98 and mitofusin 2, were detected within 3 h of CCCP treatment.

99 d TRAIL-induced apoptosis in the presence of CCCP and decreased initiator procaspase-8 processing, in

100 The presence of CCCP and salicylate suppressed ST1710-ST1 interaction, i

101 L synthesis was decreased in the presence of CCCP, an inhibitor of oxidative phosphorylation that red

102 in and vancomycin-KCl, but resembles that of CCCP, DNP and azide.

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

104 rapidly in preparations treated with CCCP or CCCP and oligomycin together because mitochondrial Ca2+

105 rapidly in preparations treated with CCCP or CCCP and oligomycin together than in those treated with

106 carbonyl cyanide m-chlorophenylhydrazone or CCCP, and ruthenium red) blocked PTP and the persistence

107 0 microM), cyclopiazonic acid (30 microM) or CCCP (10 microM) had no detectable effects.

108 reparations treated with CCCP, oligomycin or CCCP and oligomycin together could result from a progres

109 ch were also completely inhibited by TTFA or CCCP.

110 tDNA) or treatment with mitochondrial poison CCCP initiates mitochondrial stress signaling, which ope

111 e absence of Sarm1, the mitochondrial poison CCCP still induces depolarization of mitochondria, ATP d

112 Nix promoted CCCP-induced mitochondrial depolarization and reactive o

113 Treatment with the protonophore CCCP indicated that only a small percentage of sperm cou

114 ochondrial Ca(2+) uptake by the protonophore CCCP reduced the frequency of GnRH-induced [Ca(2+)](cyt)

115 ments using both A23187 and the protonophore CCCP revealed that free calcium is absolutely required f

116 warmed to 24 degrees C, and the protonophore CCCP was added (20 microM) followed 2 min later by valin

117 dent on Na(+), resistant to the protonophore CCCP, and sensitive to the sodium ionophore ETH-157, sho

118 prevented by treatment with the protonophore CCCP, with no accompanying decrease in cellular ATP leve

119 epolarization in response to a protonophore, CCCP.

120 The protonophore, CCCP markedly inhibited 64Cu incorporation into SOD in b

121 Since protonophores CCCP (carbonyl cyanide m-chlorophenylhydrazone) and DTHB

122 esicle membrane endocytosis occurred at some CCCP- or oligomycin-treated nerve terminals after 120 or

123 by CCCP thus minimizing the possibility that CCCP lowered ATP levels by reversing the mitochondrial A

124 f DNA, indicative of competition between the CCCP and DNA for binding to VceR.

125 ion by the Akt inhibitor MK-2206 blocked the CCCP induction of PRC, c-MYC, and representative PRC str

126 The rate of the CCCP-induced conformational change in VceR was determine

127 sion of pspA could be induced by exposure to CCCP, a protonophore that disrupts PMF.

128 d P. putida biofilms remained insensitive to CCCP addition.

129 mutant has shown it to be more sensitive to CCCP, PMA, PCP, nalidixic acid and DOC than the parent s

130 n RKO cells did not protect cells from TRAIL/CCCP-induced apoptosis, indicating that apoptosis occurr

131 re found to be completely prevented by TTFA, CCCP, or Mn(III)tetrakis (4-benzoic acid) porphyrin, a s

132 membrane suspensions by the energy-uncoupler CCCP or by lysis of the cells.

133 pendent and was unaffected by the uncouplers CCCP (carbonyl cyanide m-chlorophenylhydrazone) and DNP

134 cholerae were also induced to dissolve upon CCCP addition to an extent similar to that in S. oneiden

135 or in the presence of 2-deoxy-D-glucose upon CCCP treatment.

136 t the equilibrium between free VceR and VceR-CCCP plays a critical role in controlling expression of

137 olarizing voltage trains were increased when CCCP was added, showing that mitochondria lower the loca

138 onsumption rates in both cell lines, whereas CCCP (carbonyl cyanide m-chlorophenylhydrazone) stimulat

139 While CCCP reduced the magnitude of the InsP3-evoked Ca2+ sign

140 ansients and Ca2+ transients associated with CCCP application.

141 64Cu-incorporation into SOD was blocked with CCCP, copper accumulated in a Superose column fraction t

142 y the reconstituted enzyme, in contrast with CCCP, which both abolished the proton gradient and stimu

143 or mitochondrial ATP production (e.g., with CCCP) reduced mitochondrial Ca(2+) uptake and membrane p

144 l-cyclodextrin and metabolic inhibition with CCCP or 4 degrees C showed no effect.

145 Inhibition of mitochondria with CCCP, KCN, or rotenone blocked intracellular ATP product

146 alone but not when added simultaneously with CCCP.

147 egion and is dissociated from this site with CCCP, a pump substrate.

148 Treatment of tissues with CCCP, which interferes with the uptake of calcium ions b

149 ur more rapidly in preparations treated with CCCP or CCCP and oligomycin together because mitochondri

150 ed more rapidly in preparations treated with CCCP or CCCP and oligomycin together than in those treat

151 quantal release in preparations treated with CCCP, oligomycin or CCCP and oligomycin together could r