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1 idic organelles (bafilomycin, brefeldin, and nigericin).
2  or the release of acidic Ca(2+) stores with nigericin.
3  be reversed by increasing the DeltaPsi with nigericin.
4 lation with lipopolysaccharides (LPS) and/or nigericin.
5 unctional in response to the NLRP3 activator nigericin.
6 ress Nlrp3 inflammasome activation by ATP or nigericin.
7 ll death triggered by lipopolysaccharide and nigericin.
8 s in the carboxylic acid polyether ionophore nigericin.
9 ncreased by subsequent treatment with ATP or nigericin.
10 lls with a secretion stimulus such as ATP or nigericin.
11                      Monensin (1 microM) and nigericin (1 microM), Na+H+ and K+H+ exchangers respecti
12  PKS as well of NigDH1, from module 1 of the nigericin (3) PKS.
13 requency, whereas a maximal concentration of nigericin (5 mum) collapsed the pH gradient and abolishe
14                                              Nigericin, a K(+)/H(+) antiporter, also increases NADPH
15                      Caspase-1 activation by nigericin, a K+/H+ ionophore, similarly requires LPS pri
16       The release of IL-1beta in response to nigericin, a potassium ionophore, and maitotoxin, a pote
17 hese findings resolve the mechanism by which nigericin activates NLRP1 in nonhematopoietic cell types
18        Recent findings, however, showed that nigericin also activates the NLRP1 inflammasome in human
19                                The ionophore nigericin also reduces cytosolic pH and induces PINK1/PA
20 d IL-18 normally after stimulation with ATP, nigericin, alum, silica, flagellin, or cytoplasmic DNA,
21                                              Nigericin, an alternate secretion stimulus, promotes rel
22                                              Nigericin, an ionophore derived from Streptomyces hygros
23 uorescence utilizing ionophore combinations (nigericin and CCCP) or digitonin.
24 -5(6)-carboxyfluorescein and calibrated with nigericin and elevated external [K+].
25 ype NLRP3 activation by the agonist molecule nigericin and in a model of CAPS-mediated NLRP3 inflamma
26 atment of drug-resistant MCF-7adr cells with nigericin and monensin, ionophores demonstrated to disru
27                                              Nigericin and NH(4)Cl released (45)Ca(2+) from preloaded
28 beta processing and secretion in response to nigericin and the Staphylococcus aureus toxin leukocidin
29 e thylakoid membrane, whereas the ionophores nigericin and valinomycin had little effect on membrane
30 roton gradient, and transport was blocked by nigericin and verapamil.
31 H+ could be manipulated by additions of HCN, nigericin, and DCCD (N,N'-dicyclohexylcarbodamide).
32 ve activating signals, anthrax lethal toxin, nigericin, and flagellin.
33                                              Nigericin, another potassium ionophore with activity aga
34 nt cell death, using the ionophoric compound nigericin as a potassium efflux-inducing stimulus.
35 ors including bacterial pore-forming toxins, nigericin, ATP, and particulate matter caused mitochondr
36 hlorophenylhydrazone, 2,4-dinitrophenol, and nigericin but not by the potassium ionophore valinomycin
37 ponse to ionomycin: low concentrations mimic nigericin by hyperpolarizing the mitochondria while slow
38  necessary correction (pHcor) to the high K+/nigericin-calibrated pHi was linearly dependent on pHi,
39                                     When the nigericin calibration data were corrected using this pHc
40 08 different from null estimates) than using nigericin calibrations alone (approximately 0.2 differen
41                               Unlike high K+/nigericin calibrations, the error, pHcor, introduced by
42  stimuli; PMA, the calcium ionophore A23187, nigericin, Candida albicans and Group B Streptococcus.
43 t was readily collapsed upon the addition of nigericin, carbonyl cyanide p-(tri-fluoromethoxy) phenyl
44                                              Nigericin-catalyzed Pb(2+) transport is not inhibited by
45 rdiomyocytes (CMs) to LPS followed by ATP or nigericin caused release of mature IL-1beta.
46                               We report that nigericin-driven keratinocyte pyroptosis occurs through
47 s study, we resolve the mechanistic basis of nigericin-driven NLRP1 inflammasome activation.
48                               Treatment with nigericin during influenza infection augmented IL-1beta
49                           The selectivity of nigericin for Pb(2+) exceeds that of ionomycin or monens
50 43 (Cx43) and other proteins, we applied the nigericin/high K+ method to vary intracellular pH (pHi)
51 ions with m/z 755 and 585 helped to identify nigericin in a crude extract of Streptomyces sp. Eucal-2
52 inhibited caspase-1 activity caused by LPS + nigericin in BMDMs independent of PLD1 activity.
53 function and is abolished in the presence of nigericin, indicating that the same pH gradient can driv
54                                      ATP and nigericin induce MST1/2 cleavage and apoptosis, while th
55 i localised thioesterase enzymes caused by a nigericin induced breakdown in Golgi organisation and fu
56 ivation and, in doing so, inhibited LPS- and nigericin-induced assembly of the NLRP3 inflammasome dur
57 oth calcium and calmodulin were required for nigericin-induced IL-1beta secretion in THP-1 cells and
58 that targeting Nek7 rescued macrophages from nigericin-induced lethality.
59 S for 24 hours dramatically reduced ATP- and nigericin-induced NLRP3 inflammasome activation in naive
60 dent signaling pathways, strongly suppressed nigericin-induced NLRP3 inflammasome signaling via mecha
61                                 As a result, nigericin-induced pyroptosis in human keratinocytes is b
62                           The K(+) ionophore nigericin is shown to be highly effective as an ionophor
63                                      Because nigericin is toxic, expensive, and complicated in its us
64               The H+-transporting ionophores nigericin/K+ and carbonyl cyanide 3-chlorophenylhydrazon
65 ure medium in the presence of ionomycin plus nigericin led to a very significant 3- or 2-fold increas
66                        Low concentrations of nigericin (< 100 nM) that resulted in a mild dissipation
67 ling pathways triggered specifically by ATP, nigericin, maitotoxin, S. aureus or L. monocytogenes.
68 her selectivity and efficiency, suggest that nigericin may be more useful than monensin in the treatm
69                                              Nigericin mediated intracellular pH (3.0, 5.0, and 7.0)
70 this compartment by the previous addition of nigericin, monensin, or NH4Cl.
71 owing: 1) the increase in [Ca2+]i induced by nigericin, monensin, or the weak base, NH4Cl, in the nom
72 nitiation of NLRP3 or Pyrin inflammasomes by nigericin (NG) or Clostridium difficile toxin B (TcdB),
73 e a similar pH dependence in the presence of nigericin/nonactin, decreasing by factors of 2.5 and 4,
74  monensin suppresses the effects of FCCP and nigericin on mitochondrial degradation.
75 OS generation and calcium increase caused by nigericin or ATP, and subsequent ASC oligomerization cau
76 s decreased following activation of NLRP3 by nigericin or ATP, with no effect on pyroptosis.
77 al was further increased, by the addition of nigericin or by the imposition of a diffusion potential,
78 acidic lysosomal pH of TRP-ML1(-/-) cells by nigericin or chloroquine reversed the lysosomal storage
79                                Using high K+/nigericin or in vitro calibrations, along with the respe
80 y pyrophosphate was collapsed by addition of nigericin or NH(4)Cl.
81 sing during respiration is also inhibited by nigericin or uncoupler, indicating that an acidic matrix
82 er, veratridine, or ionophores, monensin and nigericin) or inhibition of oxidative phosphorylation (a
83 s observed upon stimulation with ionophores, nigericin, or ionomycin.
84  channels, the exogenous bacterial ionophore nigericin, or the lysosomotropic agent Leu-Leu-O-methyl
85 urther elevated by addition of either NH4Cl, nigericin, or the vacuolar H+-ATPase inhibitor bafilomyc
86 , at least in part, from a high stability of nigericin-Pb(2+) complexes.
87 onists such as adenosine triphosphate (ATP), nigericin, poly(dA:dT), and flagellin induced normal IL-
88     In multiple nonhematopoietic cell types, nigericin rapidly and specifically inhibits the elongati
89  when stimulated at 32 degrees C with ATP or nigericin, release less IL-1beta associated with reduced
90 nflammasome activity and that treatment with nigericin rescues NLRP3 activation in elderly hosts.
91 ion facilitated by use of a K+-H+ exchanger (nigericin), respiration was inhibited by HCN, and ATP sy
92 ith the canonical NLRP3 inflammasome agonist nigericin results in release of bioactive IL-1beta in co
93                     Thus, our work defines a nigericin sensitive S-acylation cycle that gates access
94 riggered by the NLRP3 inflammasome activator nigericin show reduced mitochondrial function and decrea
95 pe (WT) BMDC via NLRP3-dependent pyroptosis, nigericin-stimulated Casp1/11(-/-) BMDC exhibit markedly
96                                     Although nigericin-stimulated caspase-1 activation and activity a
97 as co-immunoprecipitated with caspase 1 from nigericin-stimulated THP-1 cell lysate.
98  to be associated with NETs following PMA or Nigericin stimulation.
99  human myeloid cells exposed to TNF-alpha or nigericin, suppression of PEX11beta and catalase protein
100 nse to two canonical NLRP3 agonists (ATP and nigericin) that facilitate primary K(+) efflux by mechan
101 When this proton gradient was abolished with nigericin, the extramitochondrial pH optimum for protein
102 bstantial errors introduced by using high K+/nigericin to calibrate intracellular BCECF (1).
103 gether with the pH dependency, indicate that nigericin transports Pb(2+) via the species NigPbOH and
104                   K(+) displaced INT only in nigericin-treated vesicles, and thus, INT binds to the l
105 n utilizing TLR4 ligation followed by ATP or nigericin treatment, inflammasome activation is enhanced
106 ly 26%; studies with cells, sodium loaded by nigericin treatment, suggested that this sodium increase
107 mplexes prior to extracellular export during nigericin treatment.
108  nucleophiles, which prevented both ATP- and nigericin-triggered pyroptosis of human THP-1 cells in a
109 ome can be activated by stimuli that include nigericin, uric acid crystals, amyloid-beta fibrils and
110  of SDP on cells differs from that of nisin, nigericin, valinomycin and vancomycin-KCl, but resembles
111 lactate formed with veratridine, monensin or nigericin was as high or higher than with rotenone, but
112 y a combination of ionophores (ionomycin and nigericin) was associated with the hydrolysis of short a
113               Furthermore, pretreatment with nigericin, which acts as an H(+)/K(+) antiporter and dis
114                                 In contrast, nigericin, which dissipates the DeltapH component of the
115 mn continuous infusion of internal standard (nigericin) with matrix-matched calibration method was ut
116 P or lactate and reversed by the addition of nigericin, with the addition of K(+)-valinomycin having

 
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