ライフサイエンスコーパス: nigericin

1 idic organelles (bafilomycin, brefeldin, and nigericin).

2 s in the carboxylic acid polyether ionophore nigericin.

3 unctional in response to the NLRP3 activator nigericin.

4 ress Nlrp3 inflammasome activation by ATP or nigericin.

5 ll death triggered by lipopolysaccharide and nigericin.

6 ncreased by subsequent treatment with ATP or nigericin.

7 lls with a secretion stimulus such as ATP or nigericin.

8 lation with lipopolysaccharides (LPS) and/or nigericin.

9 Monensin (1 microM) and nigericin (1 microM), Na+H+ and K+H+ exchangers respecti

10 PKS as well of NigDH1, from module 1 of the nigericin (3) PKS.

11 requency, whereas a maximal concentration of nigericin (5 mum) collapsed the pH gradient and abolishe

12 Nigericin, a K(+)/H(+) antiporter, also increases NADPH

13 Caspase-1 activation by nigericin, a K+/H+ ionophore, similarly requires LPS pri

14 The release of IL-1beta in response to nigericin, a potassium ionophore, and maitotoxin, a pote

15 The ionophore nigericin also reduces cytosolic pH and induces PINK1/PA

16 d IL-18 normally after stimulation with ATP, nigericin, alum, silica, flagellin, or cytoplasmic DNA,

17 Nigericin, an alternate secretion stimulus, promotes rel

18 uorescence utilizing ionophore combinations (nigericin and CCCP) or digitonin.

19 -5(6)-carboxyfluorescein and calibrated with nigericin and elevated external [K+].

20 atment of drug-resistant MCF-7adr cells with nigericin and monensin, ionophores demonstrated to disru

21 Nigericin and NH(4)Cl released (45)Ca(2+) from preloaded

22 beta processing and secretion in response to nigericin and the Staphylococcus aureus toxin leukocidin

23 e thylakoid membrane, whereas the ionophores nigericin and valinomycin had little effect on membrane

24 roton gradient, and transport was blocked by nigericin and verapamil.

25 H+ could be manipulated by additions of HCN, nigericin, and DCCD (N,N'-dicyclohexylcarbodamide).

26 ve activating signals, anthrax lethal toxin, nigericin, and flagellin.

27 Nigericin, another potassium ionophore with activity aga

28 nt cell death, using the ionophoric compound nigericin as a potassium efflux-inducing stimulus.

29 ors including bacterial pore-forming toxins, nigericin, ATP, and particulate matter caused mitochondr

30 hlorophenylhydrazone, 2,4-dinitrophenol, and nigericin but not by the potassium ionophore valinomycin

31 ponse to ionomycin: low concentrations mimic nigericin by hyperpolarizing the mitochondria while slow

32 necessary correction (pHcor) to the high K+/nigericin-calibrated pHi was linearly dependent on pHi,

33 When the nigericin calibration data were corrected using this pHc

34 08 different from null estimates) than using nigericin calibrations alone (approximately 0.2 differen

35 Unlike high K+/nigericin calibrations, the error, pHcor, introduced by

36 stimuli; PMA, the calcium ionophore A23187, nigericin, Candida albicans and Group B Streptococcus.

37 t was readily collapsed upon the addition of nigericin, carbonyl cyanide p-(tri-fluoromethoxy) phenyl

38 Nigericin-catalyzed Pb(2+) transport is not inhibited by

39 rdiomyocytes (CMs) to LPS followed by ATP or nigericin caused release of mature IL-1beta.

40 Treatment with nigericin during influenza infection augmented IL-1beta

41 The selectivity of nigericin for Pb(2+) exceeds that of ionomycin or monens

42 43 (Cx43) and other proteins, we applied the nigericin/high K+ method to vary intracellular pH (pHi)

43 ions with m/z 755 and 585 helped to identify nigericin in a crude extract of Streptomyces sp. Eucal-2

44 function and is abolished in the presence of nigericin, indicating that the same pH gradient can driv

45 oth calcium and calmodulin were required for nigericin-induced IL-1beta secretion in THP-1 cells and

46 that targeting Nek7 rescued macrophages from nigericin-induced lethality.

47 S for 24 hours dramatically reduced ATP- and nigericin-induced NLRP3 inflammasome activation in naive

48 dent signaling pathways, strongly suppressed nigericin-induced NLRP3 inflammasome signaling via mecha

49 The K(+) ionophore nigericin is shown to be highly effective as an ionophor

50 Because nigericin is toxic, expensive, and complicated in its us

51 The H+-transporting ionophores nigericin/K+ and carbonyl cyanide 3-chlorophenylhydrazon

52 ure medium in the presence of ionomycin plus nigericin led to a very significant 3- or 2-fold increas

53 Low concentrations of nigericin (< 100 nM) that resulted in a mild dissipation

54 ling pathways triggered specifically by ATP, nigericin, maitotoxin, S. aureus or L. monocytogenes.

55 her selectivity and efficiency, suggest that nigericin may be more useful than monensin in the treatm

56 this compartment by the previous addition of nigericin, monensin, or NH4Cl.

57 owing: 1) the increase in [Ca2+]i induced by nigericin, monensin, or the weak base, NH4Cl, in the nom

58 nitiation of NLRP3 or Pyrin inflammasomes by nigericin (NG) or Clostridium difficile toxin B (TcdB),

59 e a similar pH dependence in the presence of nigericin/nonactin, decreasing by factors of 2.5 and 4,

60 monensin suppresses the effects of FCCP and nigericin on mitochondrial degradation.

61 al was further increased, by the addition of nigericin or by the imposition of a diffusion potential,

62 acidic lysosomal pH of TRP-ML1(-/-) cells by nigericin or chloroquine reversed the lysosomal storage

63 Using high K+/nigericin or in vitro calibrations, along with the respe

64 y pyrophosphate was collapsed by addition of nigericin or NH(4)Cl.

65 sing during respiration is also inhibited by nigericin or uncoupler, indicating that an acidic matrix

66 er, veratridine, or ionophores, monensin and nigericin) or inhibition of oxidative phosphorylation (a

67 s observed upon stimulation with ionophores, nigericin, or ionomycin.

68 channels, the exogenous bacterial ionophore nigericin, or the lysosomotropic agent Leu-Leu-O-methyl

69 urther elevated by addition of either NH4Cl, nigericin, or the vacuolar H+-ATPase inhibitor bafilomyc

70 , at least in part, from a high stability of nigericin-Pb(2+) complexes.

71 nflammasome activity and that treatment with nigericin rescues NLRP3 activation in elderly hosts.

72 ion facilitated by use of a K+-H+ exchanger (nigericin), respiration was inhibited by HCN, and ATP sy

73 ith the canonical NLRP3 inflammasome agonist nigericin results in release of bioactive IL-1beta in co

74 riggered by the NLRP3 inflammasome activator nigericin show reduced mitochondrial function and decrea

75 pe (WT) BMDC via NLRP3-dependent pyroptosis, nigericin-stimulated Casp1/11(-/-) BMDC exhibit markedly

76 Although nigericin-stimulated caspase-1 activation and activity a

77 as co-immunoprecipitated with caspase 1 from nigericin-stimulated THP-1 cell lysate.

78 nse to two canonical NLRP3 agonists (ATP and nigericin) that facilitate primary K(+) efflux by mechan

79 When this proton gradient was abolished with nigericin, the extramitochondrial pH optimum for protein

80 bstantial errors introduced by using high K+/nigericin to calibrate intracellular BCECF (1).

81 gether with the pH dependency, indicate that nigericin transports Pb(2+) via the species NigPbOH and

82 K(+) displaced INT only in nigericin-treated vesicles, and thus, INT binds to the l

83 n utilizing TLR4 ligation followed by ATP or nigericin treatment, inflammasome activation is enhanced

84 ly 26%; studies with cells, sodium loaded by nigericin treatment, suggested that this sodium increase

85 mplexes prior to extracellular export during nigericin treatment.

86 nucleophiles, which prevented both ATP- and nigericin-triggered pyroptosis of human THP-1 cells in a

87 of SDP on cells differs from that of nisin, nigericin, valinomycin and vancomycin-KCl, but resembles

88 lactate formed with veratridine, monensin or nigericin was as high or higher than with rotenone, but

89 y a combination of ionophores (ionomycin and nigericin) was associated with the hydrolysis of short a

90 In contrast, nigericin, which dissipates the DeltapH component of the

91 mn continuous infusion of internal standard (nigericin) with matrix-matched calibration method was ut

92 P or lactate and reversed by the addition of nigericin, with the addition of K(+)-valinomycin having