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1                                              FCCP and DNP also depolarized type I cell mitochondria.
2                                              FCCP and Valinomycin treatment mildly decreased ATP and
3                                              FCCP does not stimulate GLUT1-mediated 3-O-methylglucose
4                                              FCCP stimulation of 3-O-methylglucose uniport in reseale
5                                              FCCP treatment of previously unstimulated neurones barel
6                                              FCCP, MPP(+) and rotenone caused a rapid but stable decr
7                                              FCCP-induced mitochondrial fragmentation was exacerbated
8 iscovery that mitochondrial uncoupling agent FCCP acts as a covalent-reversible cysteine-reactive ele
9 mimic ACh chloride, and bafilomycin A(1) and FCCP completely blocked the ATP effect, which shows that
10                                  Cyanide and FCCP stimulation of 3-O-methylglucose uniport are associ
11 neously treating neurones with glutamate and FCCP, showed a response that was essentially all-or-none
12 ed by ryanodine, thapsigargin, lanthanum and FCCP could also be simulated.
13 olated parotid acinar cells to rottlerin and FCCP reduced cellular ATP levels and reduced stimuli-dep
14  the membrane potential with valinomycin and FCCP by using a potential-sensitive dye.
15 y attenuated the hyperpolarization caused by FCCP.
16 dependent on acidification of the cytosol by FCCP.
17 ighly specific for Fe2+ and was inhibited by FCCP, DCCD and vanadate, indicating an active process en
18 d preimplantation embryos were unaffected by FCCP treatment.
19 onse to impaired mitochondrial function (CN, FCCP or anoxia): DeltaPsim depolarized, followed rapidly
20 ocked ATP production in mitochondria, as did FCCP and rotenone.
21 e direct measurement of I(H) induced by DNP, FCCP and other common protonophores and find that it is
22 y, we showed that administration of low dose FCCP or of FTY720 (both of which cause mild, ~ 10%, mito
23                                     However, FCCP inhibited chemotaxis at concentrations that paralle
24 yanide p-(trifluoromethoxy)phenyl hydrazone (FCCP) after the agonist exposure.
25 anide p-(trifluoromethoxy) phenyl hydrazone (FCCP).
26 yanide p-(trifluoromethoxy)phenyl-hydrazone (FCCP); the mitochondrial calcium uniporter inhibitor KB-
27 yanide p-(trifluoromethoxy)phenyl-hydrazone (FCCP, a H+ ionophore).
28  cyanide p-trifluoromethoxyphenyl hydrazone (FCCP) caused an increase in [Ca2+]i which was largely in
29 ncoupler p-trifluoromethoxyphenyl hydrazone (FCCP).
30            The rate of decline of current in FCCP was faster for K(ir)2.3 than for K(ir)2.2.
31              Respiratory complex inhibitors, FCCP and oligomycin, and a producer of reactive oxygen s
32          The mitochondrial proton ionophore, FCCP, caused a large, prolonged increase in cytosolic Ca
33 ndrial uncouplers (5 microM CCCP or 5 microM FCCP), eliminated the ACh-induced [Ca2+]i decrease.
34 t of telencephalic mitochondria with MPP(+), FCCP, or rotenone, was evaluated by measuring DCF fluore
35 level comparable to that induced by 5-20 mum FCCP, was observed between 27 and 69 min of ischaemia.
36 3-20 mum), becoming undetectable at 5-20 mum FCCP.
37 ally averaged FTMRM in the presence of 5 mum FCCP, but no consistent change in this parameter during
38                        Neither rottlerin nor FCCP reduced stimuli-dependent PKCdelta tyrosine phospho
39  (within 2 min) disrupted by the addition of FCCP (IC(50) = 20 nM), but not by the Fo-ATPase inhibito
40 occus aureus was affected by the addition of FCCP or oligomycin.
41                       Whereas application of FCCP plus oligomycin 2s after neuronal depolarization in
42                               Application of FCCP plus oligomycin elevated resting [Ca(2+)]c in SNL L
43  application of increasing concentrations of FCCP (0.3-20 mum), becoming undetectable at 5-20 mum FCC
44 e were insensitive to high concentrations of FCCP (100 microM) and thapsigargin (10 microM) indicatin
45 r pH with monensin suppresses the effects of FCCP and nigericin on mitochondrial degradation.
46 ction potentials elicited in the presence of FCCP triggered a sustained (>5 min) increase in [Ca2+]i
47 ndrial oxidation capacity in the presence of FCCP when compared to the chow-diet fed control mice.
48 lowered by the metabolic inhibitors azide or FCCP.
49 cortactin inhibited Mfn2 down-regulation- or FCCP-induced mitochondrial fragmentation.
50 yanide-4-(trifluoromethoxy) phenylhydrazone (FCCP)(10,11).
51 yanide p-(trifluoromethoxy) phenylhydrazone (FCCP).
52 yanide 4-(trifluoromethoxy) phenylhydrazone (FCCP; 75 nm) m is maintained by electron transport worki
53 cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP) treatment.
54 cyanide-p-(trifluoromethoxy)phenylhydrazone (FCCP), a mitochondrial proton gradient uncoupler, to rel
55 cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP), N,N'-dicyclohexylcarbodiimide, phenamil, amilorid
56 cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP), which causes the mitochondrial membrane potential
57 cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP).
58 cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP).
59 cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP; 1 microm) had no significant effect on the membran
60 es of clusters: face-center-cubic-preferred (FCCP) clusters, indifferent clusters, and body-center-cu
61 w doses of palmitic acid or the protonophore FCCP exacerbated Ca(2+)-induced sustained depolarization
62 ial membrane potential with the protonophore FCCP or blocking the mitochondrial Ca(2+) uniporter with
63 ochondrial uncoupling using the protonophore FCCP, and during I-R.
64  blocked with a low dose of the protonophore FCCP, or the mitochondrial KATP channel antagonist, tolb
65 ) influx and was blocked by the protonophore FCCP, thereby implicating mitochondria as the Ca(2+) sto
66  results were obtained with the protonophore FCCP, which is known to reduce the levels of intracellul
67 membrane potential depolarization (rotenone, FCCP) and hyperpolarization (oligomycin).
68                                We found that FCCP-uncoupling in situ had a relatively small effect on
69                                          The FCCP effect on calcium storage may be related to mitocho
70                     Oligomycin abolished the FCCP-induced rise in [Mg2+]i without altering the change
71 ane-N,N,N',N'-tetraacetic acid abolished the FCCP-stimulated rise in internal calcium, as well as the
72 of cell ATP depletion during ischemia in the FCCP-treated hearts to identically treated FCCP-free hea
73 clusters playing the role of the matrix, the FCCP clusters serving as hard fillers to enhance the str
74 entified as the structural correlate of the "FCCP-sensitive store, " is robust, reversible, graded wi
75                Exposure to cyanide and/or to FCCP (mitochondrial inhibitors) stimulates erythrocyte s
76           Glucose consumption in response to FCCP (1 microM) transiently increased, subsequently decr
77     Thus, the rise in [Mg2+]i in response to FCCP is consistent with the release of intracellular Mg2
78                              The response to FCCP was independent of external Mg2+, confirming an int
79                               In response to FCCP, [Mg2+]i rose towards a plateau coincident with the
80                               In response to FCCP, an increase in KATP channel activity was seen only
81 ted to SGs that are assembled in response to FCCP-induced energy deprivation, but not arsenite-induce
82       For comparison, the respiratory toxins FCCP, a cyanide analog that uncouples mitochondrial ATP
83 , addition of either antioxidants or toxins (FCCP or CN(-)) that block mitochondrial Ca(2+) uptake at
84 e FCCP-treated hearts to identically treated FCCP-free hearts.
85 l cyanide 4-trifluoromethoxyphenylhydrazone (FCCP), consistent with the photo-response being detected
86 l cyanide p-trifluoromethoxyphenylhydrazone (FCCP) after excitotoxic glutamate treatment resulted in
87 l cyanide p-trifluoromethoxyphenylhydrazone (FCCP) inhibited K(ir)2.2 and K(ir)2.3 currents but was w
88 l cyanide-p-trifluoromethoxyphenylhydrazone (FCCP) uncouples mitochondrial oxygen consumption to its
89 l cyanide p-trifluoromethoxyphenylhydrazone (FCCP), before making them ischemic.
90 l cyanide p-trifluoromethoxyphenylhydrazone (FCCP), the membrane potential hyperpolarized and membran
91 l cyanide-p-trifluoromethoxyphenylhydrazone (FCCP), we show that palmitate exposure induced comparabl
92 l cyanide-p-trifluoromethoxyphenylhydrazone (FCCP), which strongly stratifies the phenotype of polari
93 l cyanide p-trifluoromethoxyphenylhydrazone (FCCP).
94 l cyanide-p-trifluoromethoxyphenylhydrazone (FCCP, 50 nmol/L) and 2-deoxyglucose (2-DG, 10 mmol/L), t
95 ther hand, mitochondrial metabolic uncoupler FCCP, in the presence of oligomycin (to prevent ATP depl
96  of mitophagy by the mitochondrial uncoupler FCCP is independent of the effect of mitochondrial membr
97 OLs treated with the mitochondrial uncoupler FCCP.
98 d that (1) RN is stimulated by the uncoupler FCCP and high levels of substrates, demonstrating that b
99  the trifluoromethoxy group in the uncoupler FCCP with a C8-hydrocarbon chain resulted in potent unco
100 tionally low concentrations of the uncoupler FCCP without the need for exogenous pools of dye (unlike
101 ibited by hypoxia, cyanide and the uncoupler FCCP, but the greatest sensitivity was seen in TASK-1 an
102 roduction, a mitochondrial proton uncoupler, FCCP, and a glucose metabolic inhibitor, 2-DG, activated
103 Cs were treated with the chemical uncouplers FCCP and Valinomycin.
104 anced mitochondrial oxidation capacity under FCCP-induced maximal respiration, when compared to contr
105 ice had lower basal oxygen consumption under FCCP-induced maximal respiration, when compared to contr
106                                        Using FCCP (1microM) to eliminate mitochondrial Ca(2+) uptake
107                            Conversely, using FCCP (carbonylcyanide p-trifluoromethoxyphenylhydrazone)
108 Treatment with oligomycin increased, whereas FCCP decreased, DeltaPsi(m) heterogeneity along the IMM.
109 ing of mitochondrial membrane potential with FCCP or inhibition of mitochondrial Ca(2+) uptake by Ru3
110                               Treatment with FCCP, a mitochondrial uncoupler, reduced ROS levels and

 
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