ライフサイエンスコーパス: FCCP

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 mimic ACh chloride, and bafilomycin A(1) and FCCP completely blocked the ATP effect, which shows that

8 Cyanide and FCCP stimulation of 3-O-methylglucose uniport are associ

9 neously treating neurones with glutamate and FCCP, showed a response that was essentially all-or-none

10 ed by ryanodine, thapsigargin, lanthanum and FCCP could also be simulated.

11 olated parotid acinar cells to rottlerin and FCCP reduced cellular ATP levels and reduced stimuli-dep

12 the membrane potential with valinomycin and FCCP by using a potential-sensitive dye.

13 y attenuated the hyperpolarization caused by FCCP.

14 dependent on acidification of the cytosol by FCCP.

15 ighly specific for Fe2+ and was inhibited by FCCP, DCCD and vanadate, indicating an active process en

16 onse to impaired mitochondrial function (CN, FCCP or anoxia): DeltaPsim depolarized, followed rapidly

17 ocked ATP production in mitochondria, as did FCCP and rotenone.

18 However, FCCP inhibited chemotaxis at concentrations that paralle

19 yanide p-(trifluoromethoxy)phenyl hydrazone (FCCP) after the agonist exposure.

20 anide p-(trifluoromethoxy) phenyl hydrazone (FCCP).

21 yanide p-(trifluoromethoxy)phenyl-hydrazone (FCCP, a H+ ionophore).

22 cyanide p-trifluoromethoxyphenyl hydrazone (FCCP) caused an increase in [Ca2+]i which was largely in

23 ncoupler p-trifluoromethoxyphenyl hydrazone (FCCP).

24 The rate of decline of current in FCCP was faster for K(ir)2.3 than for K(ir)2.2.

25 Respiratory complex inhibitors, FCCP and oligomycin, and a producer of reactive oxygen s

26 The mitochondrial proton ionophore, FCCP, caused a large, prolonged increase in cytosolic Ca

27 ndrial uncouplers (5 microM CCCP or 5 microM FCCP), eliminated the ACh-induced [Ca2+]i decrease.

28 t of telencephalic mitochondria with MPP(+), FCCP, or rotenone, was evaluated by measuring DCF fluore

29 level comparable to that induced by 5-20 mum FCCP, was observed between 27 and 69 min of ischaemia.

30 3-20 mum), becoming undetectable at 5-20 mum FCCP.

31 ally averaged FTMRM in the presence of 5 mum FCCP, but no consistent change in this parameter during

32 Neither rottlerin nor FCCP reduced stimuli-dependent PKCdelta tyrosine phospho

33 (within 2 min) disrupted by the addition of FCCP (IC(50) = 20 nM), but not by the Fo-ATPase inhibito

34 occus aureus was affected by the addition of FCCP or oligomycin.

35 Whereas application of FCCP plus oligomycin 2s after neuronal depolarization in

36 Application of FCCP plus oligomycin elevated resting [Ca(2+)]c in SNL L

37 application of increasing concentrations of FCCP (0.3-20 mum), becoming undetectable at 5-20 mum FCC

38 e were insensitive to high concentrations of FCCP (100 microM) and thapsigargin (10 microM) indicatin

39 r pH with monensin suppresses the effects of FCCP and nigericin on mitochondrial degradation.

40 ction potentials elicited in the presence of FCCP triggered a sustained (>5 min) increase in [Ca2+]i

41 ndrial oxidation capacity in the presence of FCCP when compared to the chow-diet fed control mice.

42 lowered by the metabolic inhibitors azide or FCCP.

43 cortactin inhibited Mfn2 down-regulation- or FCCP-induced mitochondrial fragmentation.

44 yanide p-(trifluoromethoxy) phenylhydrazone (FCCP).

45 yanide 4-(trifluoromethoxy) phenylhydrazone (FCCP; 75 nm) m is maintained by electron transport worki

46 cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP) treatment.

47 cyanide-p-(trifluoromethoxy)phenylhydrazone (FCCP), a mitochondrial proton gradient uncoupler, to rel

48 cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP), N,N'-dicyclohexylcarbodiimide, phenamil, amilorid

49 cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP), which causes the mitochondrial membrane potential

50 cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP).

51 cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP).

52 cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP; 1 microm) had no significant effect on the membran

53 w doses of palmitic acid or the protonophore FCCP exacerbated Ca(2+)-induced sustained depolarization

54 ial membrane potential with the protonophore FCCP or blocking the mitochondrial Ca(2+) uniporter with

55 ochondrial uncoupling using the protonophore FCCP, and during I-R.

56 blocked with a low dose of the protonophore FCCP, or the mitochondrial KATP channel antagonist, tolb

57 ) influx and was blocked by the protonophore FCCP, thereby implicating mitochondria as the Ca(2+) sto

58 results were obtained with the protonophore FCCP, which is known to reduce the levels of intracellul

59 We found that FCCP-uncoupling in situ had a relatively small effect on

60 The FCCP effect on calcium storage may be related to mitocho

61 Oligomycin abolished the FCCP-induced rise in [Mg2+]i without altering the change

62 ane-N,N,N',N'-tetraacetic acid abolished the FCCP-stimulated rise in internal calcium, as well as the

63 of cell ATP depletion during ischemia in the FCCP-treated hearts to identically treated FCCP-free hea

64 entified as the structural correlate of the "FCCP-sensitive store, " is robust, reversible, graded wi

65 Exposure to cyanide and/or to FCCP (mitochondrial inhibitors) stimulates erythrocyte s

66 Glucose consumption in response to FCCP (1 microM) transiently increased, subsequently decr

67 Thus, the rise in [Mg2+]i in response to FCCP is consistent with the release of intracellular Mg2

68 The response to FCCP was independent of external Mg2+, confirming an int

69 In response to FCCP, [Mg2+]i rose towards a plateau coincident with the

70 In response to FCCP, an increase in KATP channel activity was seen only

71 ted to SGs that are assembled in response to FCCP-induced energy deprivation, but not arsenite-induce

72 For comparison, the respiratory toxins FCCP, a cyanide analog that uncouples mitochondrial ATP

73 , addition of either antioxidants or toxins (FCCP or CN(-)) that block mitochondrial Ca(2+) uptake at

74 e FCCP-treated hearts to identically treated FCCP-free hearts.

75 l cyanide 4-trifluoromethoxyphenylhydrazone (FCCP), consistent with the photo-response being detected

76 l cyanide p-trifluoromethoxyphenylhydrazone (FCCP) after excitotoxic glutamate treatment resulted in

77 l cyanide p-trifluoromethoxyphenylhydrazone (FCCP) inhibited K(ir)2.2 and K(ir)2.3 currents but was w

78 l cyanide p-trifluoromethoxyphenylhydrazone (FCCP), before making them ischemic.

79 l cyanide p-trifluoromethoxyphenylhydrazone (FCCP), the membrane potential hyperpolarized and membran

80 l cyanide-p-trifluoromethoxyphenylhydrazone (FCCP), we show that palmitate exposure induced comparabl

81 l cyanide p-trifluoromethoxyphenylhydrazone (FCCP).

82 l cyanide-p-trifluoromethoxyphenylhydrazone (FCCP, 50 nmol/L) and 2-deoxyglucose (2-DG, 10 mmol/L), t

83 ther hand, mitochondrial metabolic uncoupler FCCP, in the presence of oligomycin (to prevent ATP depl

84 of mitophagy by the mitochondrial uncoupler FCCP is independent of the effect of mitochondrial membr

85 d that (1) RN is stimulated by the uncoupler FCCP and high levels of substrates, demonstrating that b

86 ibited by hypoxia, cyanide and the uncoupler FCCP, but the greatest sensitivity was seen in TASK-1 an

87 Cs were treated with the chemical uncouplers FCCP and Valinomycin.

88 anced mitochondrial oxidation capacity under FCCP-induced maximal respiration, when compared to contr

89 ice had lower basal oxygen consumption under FCCP-induced maximal respiration, when compared to contr

90 Using FCCP (1microM) to eliminate mitochondrial Ca(2+) uptake

91 Conversely, using FCCP (carbonylcyanide p-trifluoromethoxyphenylhydrazone)

92 ing of mitochondrial membrane potential with FCCP or inhibition of mitochondrial Ca(2+) uptake by Ru3