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1 tions of inhibition of GSH synthesis with dl-buthionine sulfoximine.
2  mM), and it is inactivated by cystamine and buthionine sulfoximine.
3  the enhancing effects of GSH depletion with buthionine sulfoximine.
4 e gamma-glutamylcysteine synthesis inhibitor buthionine sulfoximine.
5 ort in transgenic plants were abrogated by l-buthionine sulfoximine.
6 and direct inhibition of GSH biosynthesis by buthionine sulfoximine.
7 ll as by treatment with homocysteic acid and buthionine sulfoximine.
8 nt mice, despite further depletion of GSH by buthionine sulfoximine.
9 e (0 to 0.2 mM) with or without GSH ester or buthionine sulfoximine.
10 p to 60% by subcutaneous administration of L-buthionine sulfoximine.
11 to ethacrynic acid (an inhibitor of GST-Pi), buthionine sulfoximine (a glutathione synthesis inhibito
12                  Treating tolerant mice with buthionine sulfoximine, a gamma-GCS inhibitor, eliminate
13 as a requirement for cellular sensitivity to buthionine sulfoximine, a glutathione synthesis inhibito
14 NF-alpha neutralizing antibody (Ab) and by L-buthionine-sulfoximine, a GSH-depleting agent.
15 cid, and the glutathione synthesis inhibitor buthionine sulfoximine all cause oxidative injury to imm
16 ibitor of gamma-glutamylcysteine synthetase, buthionine sulfoximine, also decreased intracellular glu
17 maintenance of NFI activity in vivo, we used buthionine sulfoximine, an agent that inhibits GSH synth
18 mmatory cytokine production was inhibited by buthionine sulfoximine, an inhibitor of GCL.
19  in I(Ca,L), dogs were treated for 48 h with buthionine sulfoximine, an inhibitor of glutathione synt
20                Treatment of MCF-7 lines with buthionine sulfoximine, an inhibitor of glutathione synt
21                               Treatment with buthionine sulfoximine, an inhibitor of GSH synthesis, a
22 fluent HLE-B3 cells pretreated with 10 mM DL-buthionine sulfoximine and 0.5 mM acivicin were used in
23               Hepatocytes were cultured with buthionine sulfoximine and 1,3-bis(chloroethyl)-1-nitros
24 tants were increased up to 80% with combined buthionine sulfoximine and arsenic treatments, suggestin
25                                         Both buthionine sulfoximine and BCNU inhibited the induction
26                           As with other GCL, buthionine sulfoximine and cystamine inactivate the Arab
27    Although the glutathione-depleting agents buthionine sulfoximine and diethylmaleate were more pote
28 r treatment with the GSH synthesis inhibitor buthionine sulfoximine, and aminonicotinamide (6-ANAM),
29  hydroxymethylcytosine in cells treated with buthionine sulfoximine, and in mice depleted for the maj
30                             Aminotriazole, L-buthionine sulfoximine, and sodium azide partly abrogate
31 ellular hydrogen peroxide concentrations and buthionine sulfoximine- and auranofin-induced inhibition
32 ma-glutamylcysteine synthetase (gammaGCS) by buthionine sulfoximine augmented the increase in islet p
33 ated by enhanced toxicity in the presence of buthionine sulfoximine (BSO) and attenuation of toxicity
34    Inhibition of GSH and Trx metabolism with buthionine sulfoximine (BSO) and auranofin (AUR), respec
35    MTST was used to investigate effects of l-buthionine sulfoximine (BSO) and pyrrolidine dithiocarba
36 vious studies have identified nifurtimox and buthionine sulfoximine (BSO) as effective agents in chil
37 e events, whereas glutathione depletion with buthionine sulfoximine (BSO) augmented them.
38  CYP2E1-expressing cells by treatment with l-buthionine sulfoximine (BSO) causes decreased cell viabi
39 6 hours with 0.2 mmol/L diamide and 1 mmol/L buthionine sulfoximine (BSO) decreased GSH levels and in
40 alogues with glutathione synthesis inhibitor buthionine sulfoximine (BSO) leads to synergistic cell g
41 the present study, we examined the effect of buthionine sulfoximine (BSO) on mutation frequency and t
42 ith the irreversible inhibitor of gammaGCS L-buthionine sulfoximine (BSO) reduced intracellular GSH l
43                          Depletion of GSH by buthionine sulfoximine (BSO) restores the sensitivity of
44           Reduction of glutathione levels by buthionine sulfoximine (BSO) significantly enhanced the
45 through day 7, the cells were treated with L-buthionine sulfoximine (BSO) to deplete glutathione stor
46 was further increased after treatment with L-buthionine sulfoximine (BSO) to lower GSH levels.
47     Cell death caused by depletion of GSH by buthionine sulfoximine (BSO) was increased in mE10 and m
48  with As(2)O(3) alone or in combination with buthionine sulfoximine (BSO) was studied in NB4, U937, N
49 NT and on RGC-5 cells treated with glutamate/buthionine sulfoximine (BSO) were determined by RGC dens
50 icin-resistant cells and tumor xenografts to buthionine sulfoximine (BSO), a drug that interferes wit
51 hiols by treating uninfected astrocytes with buthionine sulfoximine (BSO), a glutathione synthesis in
52                      Treatment of cells with buthionine sulfoximine (BSO), an enzyme-activated inhibi
53                                              Buthionine sulfoximine (BSO), an inhibitor of glutathion
54 ate (DEM), a glutathione-depleting agent, or buthionine sulfoximine (BSO), an inhibitor of glutathion
55                                              Buthionine sulfoximine (BSO), an inhibitor of glutathion
56 els in surviving T cells and is abrogated by buthionine sulfoximine (BSO), an inhibitor of GSH synthe
57  inhibited when GSH synthesis was blocked by buthionine sulfoximine (BSO), an inhibitor of the enzyme
58 ats received tap water (vehicle) and 30 mM L-buthionine sulfoximine (BSO), an oxidant, with and witho
59 ms examined to date are rapidly inhibited by buthionine sulfoximine (BSO), most reports indicate that
60 eating cells with diethyl maleate (DEM), D,L-buthionine sulfoximine (BSO), or tert-butylhydroquinone
61 onic depletion by 18 hours pretreatment with buthionine sulfoximine (BSO), which depletes GSH by bloc
62 otected the E47 cells against AA toxicity or buthionine sulfoximine (BSO)-dependent toxicity.
63 nd were exposed to either L-glutamic acid or buthionine sulfoximine (BSO).
64 restored GSH synthesis in a Glu (10 mM) plus buthionine-sulfoximine (BSO) (0.2 mM)-treated group, ind
65 athways regulating redox homeostasis using l-buthionine-sulfoximine (BSO, glutathione synthesis inhib
66 e synthase inhibitor buthionine sulfoximine (buthionine sulfoximine [BSO], 30 mmol/L) in drinking wat
67 ere given the glutathione synthase inhibitor buthionine sulfoximine (buthionine sulfoximine [BSO], 30
68          Conversely, the GSH-depleting agent buthionine sulfoximine completely abolished the protecti
69 ng-term process elaboration was blocked by L-buthionine sulfoximine, consistent with mediation by an
70 uperoxide generators menadione, paraquat, or buthionine sulfoximine down-regulates c-FLIP long (c-FLI
71 ess by inhibiting glutathione synthesis with buthionine-sulfoximine dramatically increased red blood
72 ,4,3',4'-tetrachlorobiphenyl, dexamethasone, buthionine sulfoximine, ethacrynic acid, or N-acetylcyst
73              Pretreatment of HeLa cells with buthionine sulfoximine greatly potentiated the inactivat
74 SH synthesis was inhibited by treatment with buthionine sulfoximine, GSH levels rapidly declined in E
75         Moreover, glutathione depletion with buthionine sulfoximine had no effect on MX transport or
76 ro-injections of the GSH synthesis inhibitor buthionine sulfoximine in the nucleus accumbens impaired
77             We show that nontoxic doses of l-buthionine sulfoximine increase the selectivity of organ
78 l ester decreased, whereas the Gcl inhibitor buthionine sulfoximine increased DomA toxicity.
79                          Pretreatment with L-buthionine sulfoximine increased SFN-induced ARE express
80  glutathione by treatment of Hepa cells with buthionine sulfoximine increased the inducer potencies o
81        Depletion of intracellular GSH by D,L-buthionine sulfoximine increased the intracellular accum
82  H9c2 cardiomyocytes, Rac1 activation with l-buthionine sulfoximine increased; Rac1 inhibition with N
83  of glutathione using N-acetylcysteine and L-buthionine-sulfoximine indicate that changes in glutathi
84 esistant to glutamate-, homocysteine-, and l-buthionine sulfoximine-induced toxicity.
85  the glutathione (GSH)-depleting compound, L-buthionine sulfoximine (L-BSO), exhibited enhanced sensi
86 n of TrxR activity by ATG and glutathione by buthionine sulfoximine led to overoxidation of Trx1 and
87                 Depleting the GSH pool using buthionine sulfoximine limits fly survival, thus confirm
88                           MK571, PSC833, and buthionine sulfoximine markedly increased cellular arsen
89 ly, intracellular glutathione depletion with buthionine sulfoximine or energy depletion using 2-deoxy
90     Inhibition of glutathione synthesis with buthionine sulfoximine or inhibition of glutathione redu
91 e), an inhibitor of glutathione synthesis (L-buthionine-sulfoximine) or glutathione reductase (1,3-bi
92 y by the inhibitor of glutathione synthesis, buthionine sulfoximine, or by the precursor of cysteine,
93          Treatment of HeLa cells with 2 mm l-buthionine sulfoximine promoted the formation of ox-HSF1
94 epletion of glutathione by pretreatment with buthionine sulfoximine rendered cells more susceptible t
95 verted or aggravated by N-acetylcysteine and buthionine sulfoximine, respectively.
96 rols by the glutathione synthetase inhibitor buthionine sulfoximine resulted in more rapid injury by
97 intracellular antioxidant, glutathione, with buthionine sulfoximine significantly increased B[a]P-med
98 ving continuous GSH infusion, treatment with buthionine sulfoximine starting day - 2 decreased sinuso
99 enous GSH and intracellular GSH depletion by buthionine sulfoximine, suggesting that GSH transport is
100        Accordingly, glutathione depletion by buthionine sulfoximine together with restoration of p53
101 tBHQ protected cells from both glutamate and buthionine sulfoximine toxicity.
102 uptake kinetics were studied in acivicin and buthionine sulfoximine-treated HLE-B3 cells in NaCl medi
103 blood cell sickling in the sickle kidney: in buthionine-sulfoximine-treated sickle mice, red blood ce
104                                              Buthionine sulfoximine treatment resulted in a 24% reduc
105 tressed by depleting the glutathione pool by buthionine sulfoximine treatment.
106 was markedly enhanced after GSH depletion by buthionine sulfoximine treatment.
107  two experimental drugs, i.e., auranofin and buthionine sulfoximine, was able to reduce the viral res
108 moter transactivation; whereas TNFalpha or l-buthionine sulfoximine, which depletes GSH, further enha
109 thione (to less than 15% of basal levels) by buthionine sulfoximine, which does not directly modify K

 
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