ライフサイエンスコーパス: CCCP

1 th carbonyl cyanide m-chlorophenylhydrazone (CCCP).

2 by carbonyl cyanide m-chlorophenylhydrazone (CCCP).

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

4 ) and crus cerebri of the cerebral peduncle (ccCP).

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

6 ch were also completely inhibited by TTFA or CCCP.

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

8 ntimycin + oligomycin had the same effect as CCCP.

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

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

11 enes that require PRC for their induction by CCCP.

12 p62 seemed to affect autophagy induction by CCCP.

13 alone but not when added simultaneously with CCCP.

14 sites that can be simultaneously occupied by CCCP.

15 epolarization in response to a protonophore, CCCP.

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

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

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

19 h RAB-2 at the Golgi, and rab-2, rund-1, and cccp-1 mutants have similar defects in sorting soluble a

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

21 0 microM), cyclopiazonic acid (30 microM) or CCCP (10 microM) had no detectable effects.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 and M4 occupied the central subsector of the ccCP, and fibers from M3 resided medially.

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

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

66 At superior and mid-levels of the ccCP anteromedial lesions may disrupt projections from M

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

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

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

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

71 ansients and Ca2+ transients associated with CCCP application.

72 Our experiments demonstrate that CCCPs are powerful and versatile tools not only in QIP b

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

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

75 that occupied the medial three-fifths of the ccCP at superior and middle levels.

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

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

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

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

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

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

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

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

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

85 64Cu-incorporation into SOD was blocked with CCCP, copper accumulated in a Superose column fraction t

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

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

88 rations named ConCatenated Composite Pulses (CCCPs), developed as high-precision unitary operations i

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

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

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

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

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

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

95 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

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

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

98 n the crus cerebri of the cerebral peduncle (ccCP) in the rhesus monkey.

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

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

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

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

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

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

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

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

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

108 Nix promoted CCCP-induced mitochondrial depolarization and reactive o

109 CCCP-induced mitochondrial fragmentation leads to Mfn2 a

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

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

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

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

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

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

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

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

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

119 Finally, at inferior ccCP levels, all pathways overlapped.

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

121 In the ccCP, M3 fibers were located medially and M1 fibers cent

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 CCCP releases fewer quanta after stimulation than from u

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

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

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

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

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

164 CCCPs simultaneously compensate for two types of systema

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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