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1 stress protein response with geldanamycin or pyrrolidine dithiocarbamate.
2 ally inhibited with the NF-kappaB antagonist pyrrolidine dithiocarbamate.
3 essed by the antioxidant NF-kappaB inhibitor pyrrolidine dithiocarbamate.
4 ted by the antioxidants N-acetylcysteine and pyrrolidine dithiocarbamate.
5 acetylcysteine, TEMPO, dihydrolipoic acid or pyrrolidine dithiocarbamate.
6 y antioxidants, N-acetyl-L-cysteine (NAC) or pyrrolidine dithiocarbamate.
7 )H oxidase inhibitors, N-acetylcysteine, and pyrrolidine dithiocarbamate].
8 on of nuclear factor kappa B (NF kappa B) by pyrrolidine dithiocarbamate (200 microM), dexamethasone
10 osyl-l-phenylalanine chloromethyl ketone and pyrrolidine dithiocarbamate, abrogate CD40-induced Smad7
11 nuclear factor kappaB (NF-kappaB) inhibitor pyrrolidine dithiocarbamate also inhibited NOS2 expressi
17 ysteine, a precursor of glutathione, but not pyrrolidine dithiocarbamate, an inhibitor of NF-kappaB a
18 ibited lactate dehydrogenase release, and by pyrrolidine dithiocarbamate, an inhibitor of NF-kappaB.
21 n-regulation was suggested by the ability of pyrrolidine dithiocarbamate, an inhibitor of the NFkappa
22 , palmitate-induced apoptosis was blocked by pyrrolidine dithiocarbamate and 4,5-dihydroxy-1,3-benzen
23 ultraviolet B and hydrogen peroxide whereas pyrrolidine dithiocarbamate and butyl hydroxyanisole are
25 on of these genes; and (iv) the antioxidants pyrrolidine dithiocarbamate and ebselen abolish transcri
26 o effectively suppressed by the antioxidants pyrrolidine dithiocarbamate and glutathione peroxidase.
27 addition of inhibitors to either NF kappa B (pyrrolidine dithiocarbamate and N-acetyl-l-cysteine) or
28 t were prevented by NF-kappaBeta inhibitors (pyrrolidine dithiocarbamate and SN-50), silencing of p65
29 pretreatment with two NF-kappaB inhibitors, pyrrolidine dithiocarbamate and the proteasome inhibitor
30 cetylcysteine, butylated hydroxyanisole, and pyrrolidine dithiocarbamate and was partially attenuated
31 as inhibited in the presence of antioxidant (pyrrolidine dithiocarbamate) and Ca2+ chelators (BAPTA-A
32 pounds including interferonbeta1, ribavirin, pyrrolidine dithiocarbamate, and fluoxetine were tested
33 cells with membrane-permeable antioxidants, pyrrolidine dithiocarbamate, and N-acetylcysteine abroga
35 cked by the antioxidant N-acetyl-L-cysteine, pyrrolidine dithiocarbamate, and the NADPH oxidase inhib
36 pplied for the extraction of Se(IV)-ammonium pyrrolidine dithiocarbamate (APDC) complex followed by S
37 ised in the presence of Sb(III) and ammonium pyrrolidine dithiocarbamate (APDC) using styrene as the
38 to the antioxidants N-acetyl L-cysteine and pyrrolidine dithiocarbamate, as well as to overexpressio
39 ly, the antioxidant and NF-kappa B inhibitor pyrrolidine dithiocarbamate blocked doxorubicin-induced
40 mentation was sensitive to cycloheximide and pyrrolidine dithiocarbamate, but not to dexamethasone or
41 -induced Cox-2 was sensitive to antioxidant (pyrrolidine dithiocarbamate), Ca(2+) chelator (BAPTA-AM)
42 -2 activities were sensitive to antioxidant (pyrrolidine dithiocarbamate), Ca(2+) chelator 1,2-bis(am
43 ited endotoxin-induced NF-kappaB activation, pyrrolidine dithiocarbamate did not affect p38 phosphory
44 on in HEp2 but not in DRHEp2 and antioxidant pyrrolidine dithiocarbamate eliminated docetaxel-induced
45 oM, respectively) compared to clioquinol and pyrrolidine dithiocarbamate (IC50 of 10 and 20 microM),
46 ioxidant inhibitor of NF-kappa B activation, pyrrolidine dithiocarbamate, in wild-type and NF-kappa B
51 issimilar antioxidants, N-acetyl cysteine or pyrrolidine dithiocarbamate, markedly attenuated both st
53 he constitutive activation of NF-kappaB with pyrrolidine dithiocarbamate or expression of IkappaBalph
54 eramide, and was attenuated by the inhibitor pyrrolidine dithiocarbamate or following transient trans
55 cell line MO7/p210 with the reducing agents pyrrolidine dithiocarbamate or N-acetylcysteine reduced
56 ted by NAC and DPI as well as an antioxidant pyrrolidine dithiocarbamate or reduced glutathione (GSH)
58 ted hydroxyanisole, N-acetyl-L-cysteine, and pyrrolidine dithiocarbamate, or by the H2O2-degrading en
59 mg/kg p.o. daily), or an antioxidant, either pyrrolidine dithiocarbamate (PDTC) (200 mg/kg s.c. daily
60 l or treatment of cells with the antioxidant pyrrolidine dithiocarbamate (PDTC) also reduces intracel
61 hich was reversed by the NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC) and by NF-kappaB sile
64 ough previous studies have demonstrated that pyrrolidine dithiocarbamate (PDTC) exerts protection aga
68 ied the effects of two NF-kappaB inhibitors (pyrrolidine dithiocarbamate (PDTC) or BAY11-7082 (BAY)),
69 utant IkappaBalpha or pharmacologically with pyrrolidine dithiocarbamate (PDTC) prevented cytokine, b
70 G2 cells to beta-naphthoflavone (beta-NF) or pyrrolidine dithiocarbamate (PDTC) resulted in the up-re
71 etatarsal bones in the presence of GH and/or pyrrolidine dithiocarbamate (PDTC), a known NF-kappaB in
72 tured rat metatarsal bones with IGF-I and/or pyrrolidine dithiocarbamate (PDTC), a known NF-kappaB in
73 lines (SH-EP1 and SK-N-AS) were treated with pyrrolidine dithiocarbamate (PDTC), a NFkappaB inhibitor
75 expression occurs in the presence of either pyrrolidine dithiocarbamate (PDTC), a selective inhibito
76 n this study, we investigated the ability of pyrrolidine dithiocarbamate (PDTC), an agent that inhibi
81 of ROS in leukemia cells by the antioxidants pyrrolidine dithiocarbamate (PDTC), N-acetylcysteine (NA
83 3 inhibitor, z-DEVD-CH2F, and an antioxidant pyrrolidine dithiocarbamate (PDTC), whereas cytochrome c
84 that the addition of an antioxidant, such as pyrrolidine dithiocarbamate (PDTC), would attenuate HO-1
86 econd group (n=6) injected with two doses of pyrrolidine dithiocarbamate (PDTC, 100 mg/kg, i.p.) 24 a
87 treated with IFN-gamma and supplemented with pyrrolidine dithiocarbamate (PDTC, an NF-kappaB inhibito
88 e (7-NI, specific nNOS inhibitor), 3) 7-NI + pyrrolidine dithiocarbamate (PDTC, NF-kappaB inhibitor),
90 teasome inhibitor MG-132 and the antioxidant pyrrolidine-dithiocarbamate (PDTC)-prevented poly IC + I
92 ells with three unrelated scavengers of ROS, pyrrolidine dithiocarbamate, pyruvate, or nordihydroguai
93 p38 and NF-kappaB activation by SB203580 and pyrrolidine dithiocarbamate, respectively, blocked endot
94 ependent VCAM-1 transcription with 50 microM pyrrolidine dithiocarbamate resulted in 87.7% inhibition
95 d that TNF activates NF-kappa B through both pyrrolidine dithiocarbamate-sensitive and -insensitive m
96 reporter gene led to cisplatin-inducible and pyrrolidine dithiocarbamate-sensitive luciferase activit
97 nhibitors of NF-kappaB (N-acetylcysteine and pyrrolidine dithiocarbamate) suggest that the stimulator
100 = 2-(diisopropylphosphino)ethanethiol; L1 = pyrrolidine dithiocarbamate) was determined by HPLC comp
102 -activated reporter gene could be blocked by pyrrolidine dithiocarbamate, which is known to inhibit N
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