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1 d is abolished by the flavoenzyme inhibitor, diphenyleneiodonium.
2 nhibition of NADPH oxidases with apocynin or diphenyleneiodonium.
3 ed completely when rats were pretreated with diphenyleneiodonium (1 mg/kg), an inhibitor of NADPH OX.
12 oscillations were abolished by 10 micromol/L diphenyleneiodonium, an inhibitor of NAD(P)H oxidase (n=
14 de dismutase, the NAD(P)H oxidase inhibitors diphenyleneiodonium and apocynin, or the protein kinase
17 a(2+) release was blocked by catalase and by diphenyleneiodonium and was not observed in cells lackin
18 was inhibited by the NADPH oxidase inhibitor diphenyleneiodonium and was significantly attenuated in
19 P)H oxidase (10 micromol/L to 200 micromol/L diphenyleneiodonium) and xanthine oxidase (1 mmol/L allo
22 Moreover, both an NADPH oxidase inhibitor, diphenyleneiodonium, and NAPDH oxidase genetic deficienc
23 agonist, ABT-627, the flavoprotein inhibitor diphenyleneiodonium, and the NADPH oxidase inhibitor apo
24 inistration of the NAD(P)H oxidase inhibitor diphenyleneiodonium, apocynin, the protein kinase C (PKC
25 of apparent toxic side effects suggest that diphenyleneiodonium at ultra-low dose may be a promising
27 tivation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-
28 6a2 and lacs2 mutants were hypersensitive to diphenyleneiodonium but could be reverted to wild-type P
29 synthesis, an effect that was antagonized by diphenyleneiodonium but not by other inhibitors of cellu
30 which was inhibited by superoxide dismutase, diphenyleneiodonium, chelerythrine, or removal of extrac
31 I activates the NADH/NADPH oxidase; however, diphenyleneiodonium chloride (10 micromol/L), an inhibit
32 EK inhibitor), SP600125 (JNK inhibitor), and diphenyleneiodonium chloride (an NADPH oxidase inhibitor
34 abrogated by the respiratory burst inhibitor diphenyleneiodonium chloride (DPI), but infection of MDM
36 jections (approximately C(4)) of apocynin or diphenyleneiodonium chloride (DPI), two structurally and
37 reated with catalase (H(2)O(2) scavenger) or diphenyleneiodonium chloride (NADPH oxidase inhibitor) e
38 AT, NADPH oxidase inhibitors (apocynin and diphenyleneiodonium chloride [DPI]), and an inhibitor to
41 d increase in IGF-1R mRNA was inhibitable by diphenyleneiodonium chloride but not by other inhibitors
42 substantially decreased by the RED inhibitor diphenyleneiodonium chloride or by the P450 inhibitor me
43 d coincubation studies with the GPR3 agonist diphenyleneiodonium chloride revealed allosteric modulat
44 ble of driving the production of superoxide, diphenyleneiodonium chloride was an efficient inhibitor
46 -overexpressing MCF-7 cells was inhibited by diphenyleneiodonium chloride, a general NADPH reductase
47 directly associated with ROS generation; (c) diphenyleneiodonium chloride, a ROS blocker, or BAX-inhi
48 lus (iron loading plus PMA) and inhibited by diphenyleneiodonium chloride, an inhibitor of NADPH oxid
50 e, the NADPH oxidase inhibitors apocynin and diphenyleneiodonium chloride, the superoxide scavenger t
54 , zileuton) but not a flavoenzyme inhibitor (diphenyleneiodonium) completely abrogated Ag-induced dic
56 responsible for ROS generation, as seen by a diphenyleneiodonium-dependent suppression of basal and a
57 r absence of BP autoantibodies, brefeldin A, diphenyleneiodonium, DNase or blocking F(ab')2 fragments
59 as-positive stems by NADPH oxidase inhibitor diphenyleneiodonium (DPI) indicates that NADPH oxidases
61 sue damage, we treated colonic explants with diphenyleneiodonium (DPI), a flavoenzyme inhibitor, or N
63 etylcysteine (NAC), a thiol antioxidant, and diphenyleneiodonium (DPI), a potent NADH/NADPH oxidase i
64 ing potent inhibition of the GTN response by diphenyleneiodonium (DPI), a widely used inhibitor of fl
65 ration on downstream insulin signaling using diphenyleneiodonium (DPI), an inhibitor of cellular NADP
66 treatment with the NADPH oxidase inhibitors, diphenyleneiodonium (DPI), and 4-(2-aminoethyl)-benzenes
67 oxidative phosphorylation (OXPHOS) inhibitor diphenyleneiodonium (DPI), and a fatty acid oxidation (F
69 ced by treatment with NOX inhibitors such as diphenyleneiodonium (DPI), apocynin (APO) and VAS2870.
70 oncentrations of the flavoprotein inhibitor, diphenyleneiodonium (DPI), reduced nicotinamide adenine
71 lly inhibited by the NADPH oxidase inhibitor diphenyleneiodonium (DPI, 10 microm), by the farnesyltra
72 was abrogated by the NADPH oxidase inhibitor diphenyleneiodonium (DPI; 10 microM) and in AMs derived
74 flavoproteins and heme-containing proteins, diphenyleneiodonium, effectively inhibited phenazine red
76 nucleotide phosphate oxidase activation with diphenyleneiodonium following hypoxia but before reoxyge
77 h such mutants, the NADPH oxidase inhibitor, diphenyleneiodonium, had no effect on VPA-induced transc
79 ine dinucleotide phosphate oxidase inhibitor diphenyleneiodonium in both endotoxin (lipopolysaccharid
81 in, a dominant negative Ras, and myxothiazol/diphenyleneiodonium, indicating a mitochondrial origin f
85 ic complex, since the flavoprotein inhibitor diphenyleneiodonium not only blocked a productive respir
88 al cell coculture; this was not inhibited by diphenyleneiodonium or by SOD plus catalase, but was inh
90 ro treatment with the flavoprotein inhibitor diphenyleneiodonium or the angiotensin II type I recepto
91 ia was attenuated by myxothiazol, but not by diphenyleneiodonium or the nitric-oxide synthase inhibit
92 y the NADPH oxidase inhibitors, apocynin and diphenyleneiodonium, or the antioxidant, N-acetyl-L-cyst
95 of enzyme components (p47(phox) or rac1) or diphenyleneiodonium, prevented the pressure-induced gene
98 thelial cells possess a distinct cytoplasmic diphenyleneiodonium-sensitive NAD(P)H:paraquat oxidoredu
99 gulation of Nox4 enhanced both rotenone- and diphenyleneiodonium-sensitive O(2)(-) production in mito
100 Our data revealed that post-treatment with diphenyleneiodonium significantly attenuated progressive
101 primary cultured aortic VSMCs, catalase and diphenyleneiodonium significantly suppressed AVP- and an
102 rombin pretreatment could also be blocked by diphenyleneiodonium, suggesting that the NAD(P)H oxidase
104 tion of iNOS with the flavoprotein inhibitor diphenyleneiodonium totally blocked these O-2 signals.
106 n of Nox2 by coadministration of apocynin or diphenyleneiodonium was associated with reduced fibrogen
107 her nitrite or nitrate was the active anion, diphenyleneiodonium was used to inhibit oxidation/reduct
108 n is inhibited by the flavoprotein inhibitor diphenyleneiodonium, whereas inhibitors of electron tran
109 rfused rat lungs, rotenone, myxothiazol, and diphenyleneiodonium, which inhibit mitochondria in the p