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 poxia from 24.9 +/- 2.6% ID to 0.4 +/- 6.2%, CCCP from 22.8 +/- 2.5% ID to -3.5 +/- 3.1%, and doxorub

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

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

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

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

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

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

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

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

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

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

22 ntimycin + oligomycin had the same effect as CCCP.

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

24 BK1) phosphorylation is increased after both CCCP and 991 treatments, suggesting TBK1 activation to b

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

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

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

28 ffect mitochondrial shape changes induced by CCCP treatment, suggesting that LACTB action is apoptosi

29 enes that require PRC for their induction by CCCP.

30 p62 seemed to affect autophagy induction by CCCP.

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

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

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

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

35 sites that can be simultaneously occupied by CCCP.

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

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

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

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

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

41 nd carbonyl cyanide 3-chlorophenylhydrazone (CCCP) and used to measure the effect of four environment

42 or carbonyl cyanide 3-chlorophenylhydrazone (CCCP) promotes MFF SUMOylation and mitochondrial fragmen

43 by carbonyl cyanide 3-chlorophenylhydrazone (CCCP), a disruptor of mitochondrial membrane potential.

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

45 r, carbonyl cyanide 3-chlorophenylhydrazone (CCCP), resulted in accumulation of P-STAT3(Ser727) in mi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 by carbonyl cyanide m-chlorophenylhydrazone (CCCP).

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

70 th carbonyl cyanide m-chlorophenylhydrazone (CCCP).

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

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

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

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

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

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

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

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

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

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

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

82 The effect concentrations for CCCP were lower by a factor of 30 compared with the trad

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

84 However, CCCP-induced fragmentation is impaired in MFF-knockout m

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

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

87 e carbonyl cyanide m-chlorophenyl hydrazone (CCCP) prevented dibucaine-induced IMD de-partitioning.

88 h carbonyl cyanide m-chlorophenyl hydrazone (CCCP) treatment and adenosine monophosphate activated pr

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

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

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

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

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

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

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

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

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

98 ADA-inducing treatments include CCCP, antimycin, rotenone, oligomycin, and hypoxia.

99 , which inhibits GSK-3a/b and CDKs inhibited CCCP mediated mitochondrial depolarisation and augments

100 , we showed that knocking-down IRGM inhibits CCCP induced mitophagy in SH-SY5Y cells.

101 hondrial perturbation by hypoxia, ionophore (CCCP) or doxorubicin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 Short-term menadione, antimycin A, or CCCP cell treatment led to the inhibition of protein syn

120 by treatment with menadione, antimycin A, or CCCP.

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

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

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

124 0 microM), cyclopiazonic acid (30 microM) or CCCP (10 microM) had no detectable effects.

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

126 se to stress induced by hydrogen peroxide or CCCP, parkin degradation also requires its association w

127 ch were also completely inhibited by TTFA or CCCP.

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

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

130 ility transition pore inhibitors) to prevent CCCP mediated mitochondrial depolarisation and found tha

131 sent the Consistent Contig Covering Problem (CCCP) of recovering unambiguous cancer contigs from the

132 Nix promoted CCCP-induced mitochondrial depolarization and reactive o

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

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

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

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

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

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

139 epolarization in response to a protonophore, CCCP.

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

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

142 ibe a novel algorithm CCR capable of solving CCCP in polynomial time.

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

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

145 Zn-STIMO with this probe shows that CCCP-induced mitophagy in HeLa cells is associated with

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

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

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

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

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

151 n signaling pathway is active in response to CCCP treatment, we observed no change in markers of mito

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

153 the IMD de-partitioning in a way similar to CCCP.

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

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

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

157 de), its derivative RM4848 and the uncoupler CCCP were applied to a virus-releasing cell line to obta

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

159 Upon CCCP treatment, but not 991, ubiquitin phosphorylation,

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

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

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

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

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

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

166 ansients and Ca2+ transients associated with CCCP application.

167 64Cu-incorporation into SOD was blocked with CCCP, copper accumulated in a Superose column fraction t

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

169 Induction of mitochondrial damage with CCCP, as a model of selective autophagy, also reveals a

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

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

172 contrast to ER, disabling mitochondria with CCCP or blocking mitochondria Ca(2+) uniporters (MCUs) e

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

174 alone but not when added simultaneously with CCCP.

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

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

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

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

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