ライフサイエンスコーパス: valinomycin

1 oxidase-dependent uptake of potassium (plus valinomycin).

2 nt with the electrogenic potassium ionophore valinomycin.

3 nated with the potassium-selective ionophore valinomycin.

4 on on mitochondria and apoptotic response to valinomycin.

5 reated with the chemical uncouplers FCCP and Valinomycin.

6 CFTR agonist genistein or the K(+) ionophore valinomycin.

7 increases when cells are hyperpolarized with valinomycin.

8 trol cells and cells treated for 30 min with valinomycin.

9 ed conditions of high medium K+ and 1 microM valinomycin.

10 similar to that with the potassium ionophore valinomycin.

11 was prevented by bafilomycin but restored by valinomycin.

12 el openers, without preventing the action of valinomycin.

13 ffer containing mannitol, NaSCN, and/or KSCN/valinomycin.

14 n of matrix volume, whereas the K+ ionophore valinomycin (0.2 nM), produced a 10-20 % increase in mat

15 A valuable analog of the K(+)-ionophore valinomycin (1), bearing a pentafluorophenyl ester moiet

16 ed in the presence of a low concentration of valinomycin (10 nM) to prevent buildup of a membrane pot

17 xtracellular [K+] ([K+]e) in the presence of valinomycin (5 microM), altered the waveform of the Ni2+

18 as added (20 microM) followed 2 min later by valinomycin (60 microM).

19 %, respectively, on the addition of 1 microM valinomycin (a K+ ionophore) in both bathing fluids or i

20 SRBCs) that were resistant to dehydration by valinomycin, a K(+) ionophore.

21 Furthermore, application of valinomycin, a K+ ionophore, to mimic the effect of mass

22 r-dependent glutamate uptake is sensitive to valinomycin, a K+/H+ translocator, whereas the ATP-depen

23 t to lysis were measured from the instant of valinomycin addition by sampling suspension aliquots int

24 tenths of a pH unit over a few minutes after valinomycin addition, but proton uptake was not signific

25 Treatment with tunicamycin or valinomycin also induced hepatic lipid accumulation.

26 hannel openers as well as the K(+) ionophore valinomycin also inhibited MPT opening and that this inh

27 inner walls filled with a solution of 10 mM valinomycin and 10 mM ETH 500 in dichloroethane.

28 functional contexts: in the cyclic peptides valinomycin and antamanide; in several enzymes that are

29 e m-chlorophenylhydrazone (CCCP), antimycin, valinomycin and azide.

30 able to modulate the membrane potential with valinomycin and FCCP by using a potential-sensitive dye.

31 duced using the K+ ion channel-opening agent valinomycin and has been used in this study to determine

32 ocesses blocking hyperpolarization by adding valinomycin and increasing K(+) concentrations inhibited

33 an electrogenic mechanism (determined using valinomycin and monensin coupled transport assays and an

34 cells differs from that of nisin, nigericin, valinomycin and vancomycin-KCl, but resembles that of CC

35 cantly increased by 30 min of treatment with valinomycin and was still apparent after 3.5 h of incuba

36 +)-NQR was accelerated by CCCP, inhibited by valinomycin, and completely arrested by ETH-157.

37 odels), those triggered by heat shock and by valinomycin, are calpain independent, as is calcium-trig

38 theoretical predictions were confirmed using valinomycin as a K(+)-selective ionophore, which forms a

39 as well as the effects of exposure to a drug valinomycin at sub-nanomolar concentrations.

40 rves (initial current, slope, break time) of valinomycin-based, potassium-selective membranes loaded

41 In this paper, the five ionophores valinomycin, BME-44, ETH 2120, tert-butylcalix[4]arene t

42 eparable mitochondrial damage agents such as valinomycin can undergo PINK1-Parkin-dependent apoptosis

43 Valinomycin, carbonyl cyanide 4-(trifluoromethoxy)phenyl

44 he presence of substrates/ADP or uncouplers (valinomycin/carbonyl cyanide p-(trifluoromethoxy)phenylh

45 Acidification is rescued by the presence of valinomycin, consistent with a selective loss of chlorid

46 vesicular acidification, which is rescued by valinomycin, consistent with the loss of chloride conduc

47 reconstituted vesicles was assessed using a valinomycin dependent chloride efflux assay, demonstrati

48 ons of extracellular K(+) in the presence of valinomycin did not inhibit the ability of Pgp to reduce

49 To test these models, valinomycin-doped K(+)-selective membranes were studied

50 Valinomycin enforces these constraints by using a combin

51 -selective electrodes based on the ionophore valinomycin exhibit electrode-to-electrode standard devi

52 MCF-7 cells were treated with valinomycin for 30 min, inducing loss of mitochondrial m

53 with selectivity ratios approaching that of valinomycin for K+ over Na+ when conditions are optimal.

54 mbrane, whereas the ionophores nigericin and valinomycin had little effect on membrane insertion.

55 tion of nigericin, with the addition of K(+)-valinomycin having little effect.

56 hydroxyl moiety of analog 2 (available from valinomycin hydroxylation) and the isocyanate group of p

57 lable for the ion-complexation properties of valinomycin in solvents of varying polarity.

58 ) upon induction of a diffusion potential by valinomycin in the presence of ascorbate.

59 ffect that was diminished by the addition of valinomycin in the presence of K(+).

60 ffect that was diminished by the addition of valinomycin in the presence of K+.

61 prepared at pH 7.4; and was not inhibited by valinomycin in the presence of potassium ions.

62 eak were affected by Cl(-)-free solutions or valinomycin, indicating that MSG membrane potential was

63 Valinomycin-induced hyperpolarization of plasma membrane

64 Moreover, this valinomycin-induced RVD in CF mice was inhibited by 5-ni

65 luorescence technique based upon the loss of valinomycin-inducible membrane potential to characterize

66 sensor was based on a polymeric membrane and valinomycin ionophore.

67 The proapoptotic response elicited by valinomycin is associated with the degradation of Mcl-1.

68 /Na(+) diffusion potentials upon addition of valinomycin, MDR-TCBD PLs do not.

69 orm protects the mitochondria against GrB or valinomycin-mediated depolarization.

70 n mitochondrial Ca2+, while the K+ ionophore valinomycin mimicked the effects of the potassium channe

71 Yet, valinomycin molecules achieve selectivity by providing o

72 Potassium channels and valinomycin molecules share the exquisite ability to sel

73 drate when permeabilized to K(+) with either valinomycin or elevated internal Ca(2+).

74 al was collapsed upon the addition of either valinomycin or HQNO.

75 tion that reduces the pH gradient but not by valinomycin or oligomycin, both of which reduce the memb

76 tracellular [K(+)] in the presence of either valinomycin or the K(+) channel opener 1-EBIO.

77 Furthermore, exposure to the K+ ionophore valinomycin or the K+-channel opener cromakalim induced

78 r such as NH4OAc, malonamide, and KSCN (plus valinomycin) or even for cytochrome c oxidase-dependent

79 -butylcalix[4]arene, the potassium ionophore valinomycin, or the iodide carrier [9]mercuracarborand-3

80 with rapamycin, tunicamycin (ER stress), or valinomycin (oxidative stress).

81 treatment of MCF-7 cells with 1 micromol of valinomycin per liter resulted in absence of red fluores

82 ibration curve for the coulometric cell with valinomycin potassium-selective membrane was obtained in

83 eabilized to K+ with a high concentration of valinomycin, rendering PCl the main rate-limiting factor

84 Interestingly, relative valinomycin resistance and growth of the 9.3/hu MDR 1 st

85 Valinomycin resistance of intact cells and Western blot

86 The nonshrinking, valinomycin-resistant (val-res) fractions, first detecte

87 The last subset contained low-density valinomycin-resistant RBCs, previously shown to have hig

88 ministration of the K(+)-selective ionophore valinomycin restored RVD in CF mouse BDCCs, suggesting t

89 estigations undertaken here demonstrate that valinomycin selectivity is due to cavity size constraint

90 hyperpolarization induced with cromakalim or valinomycin significantly reduced both 5-HT and TG respo

91 response with all of the tested ionophores (valinomycin, sodium ionophore X, and nonactin).

92 anced by increasing the K+ permeability with valinomycin, suggesting that net positive charge is tran

93 nigericin but not by the potassium ionophore valinomycin, suggesting that the transport is driven by

94 of the proton current with the K+-ionophore valinomycin supports that the influx is because of volta

95 selective electrodes based on the ionophores valinomycin, tert-butylcalix[4]arene tetraethyl ester, a

96 Upon addition of valinomycin, the induced diffusion potential caused a pa

97 ntial treatment with the potassium ionophore valinomycin, the protonophore carbonyl cyanide 3-chlorop

98 carbonyl cyanide m-chlorophenylhydrazone or valinomycin, the rates in the DEM system are similar to

99 ine and bacitracin, but not to fosfomycin or valinomycin; these drugs, like beta-lactams, inhibit pep

100 nine are easily established upon addition of valinomycin to either control or MDR-TCBD PLs.

101 e explanations for val-res cells, failure of valinomycin to K(+)-permeabilize the cells, low co-ion p

102 native or mutant form blunts the ability of valinomycin to reduce CQ accumulation in transformed ves

103 by monitoring external pH after addition of valinomycin to vesicles with 100-fold-diluted external [

104 te production were determined on control and valinomycin-treated cells.

105 eatosis, as did treatment of tunicamycin- or valinomycin-treated fish.

106 membrane potential, and promoted swelling of valinomycin-treated mitochondria in potassium acetate me

107 FCCP and Valinomycin treatment mildly decreased ATP and reactive

108 mbrane potential hyperpolarization caused by valinomycin treatment.

109 Does valinomycin use additional coordinating ligands from the

110 polyvinyl chloride (PVC) membrane containing valinomycin (VAL) was employed as a biosensor (referred

111 For a demonstration, valinomycin was used as K(+) ionophore, and a good Nerns

112 ed transport assays, with either monensin or valinomycin, we have elucidated the fundamental transpor

113 e effects of K(ATP) channel openers, PKG, or valinomycin were mediated by a PKCepsilon.

114 -ion-like membrane defects and the ionophore valinomycin, which exhibit little membrane deformation,

115 In addition, valinomycin, which specifically collapses the DeltaPsi,

116 site of KcsA, its semisynthetic analog, and valinomycin yields the free energy change in exchanging