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1 sensitive to glutathione and its derivative S-nitrosoglutathione.
2 stant to the toxic effect of glutathione and S-nitrosoglutathione.
3 er molecule for nitric oxide, in the form of S-nitrosoglutathione.
4 by the physiologically relevant nitrosothiol S-nitrosoglutathione.
5 cts such as S-(hydroxymethyl)glutathione and S-nitrosoglutathione.
6 activity was potentiated by the presence of S-nitrosoglutathione.
7 lular proteins when the cells are exposed to S-nitrosoglutathione.
8 r GSH concentration is high and NOS can form S-nitrosoglutathione.
9 ely long-lived bioactive forms of NO such as S-nitrosoglutathione.
10 ase (GSNOR), which metabolizes the NO adduct S-nitrosoglutathione.
11 ivation and S-nitrosylation of RyR2 required S-nitrosoglutathione.
12 ier molecule for nitric oxide in the form of S-nitrosoglutathione.
15 by S-nitrosylation, preventing scavenging of S-nitrosoglutathione, a major cellular bio-reservoir of
20 t homogenates with the S-nitrosylating agent S-nitrosoglutathione and determined maximal SNO occupanc
21 cation of the killing of Escherichia coli by S-nitrosoglutathione and hydrogen peroxide and of Salmon
22 al reactions are obtained from photolysis of S-nitrosoglutathione and S-nitroso-N-acetyl-DL-penicilla
24 model, we observed that nitrosothiol donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine
25 was reversed by arginine, and the NO donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine
27 for the formation of S-nitrosothiols such as S-nitrosoglutathione and, as such, should be considered
28 times faster than that for its reaction with S-nitrosoglutathione, and consistent with Cys 34 being l
29 usside, S-nitroso-N-acetylpenicillamine, and S-nitrosoglutathione, and H2O2 at concentrations less th
30 hyl) aminodiazen-1-ium-1,2-diolate (NOC-18), S-nitrosoglutathione, and S-nitroso-N-acetylpenicillamin
31 is laboratory has shown that glutathione and S-nitrosoglutathione are directly toxic to mycobacteria.
32 s laboratory have shown that glutathione and S-nitrosoglutathione are directly toxic to mycobacteria.
34 nd GSSG, S-oxidised glutathione species, and S-nitrosoglutathione as oxidation products with the latt
36 Here we report that the NO donors NOC-12 and S-nitrosoglutathione both activate RyR1 by release of NO
37 glutathione, A4V SOD and G37R SOD catalyzed S-nitrosoglutathione breakdown three times more efficien
38 ehyde-3-phosphate dehydrogenase with GSSG or S-nitrosoglutathione, but these glutathionyl donors were
40 ensitivity of this strain to glutathione and S-nitrosoglutathione compared to that of the wild-type b
42 minimally active on CFTR; 3) a novel agent, S-nitrosoglutathione diethyl ester, bypasses the need fo
43 was added to the same mixture, the yield of S-nitrosoglutathione dramatically decreased as the activ
44 ischemia/reperfusion model and antimicrobial S-nitrosoglutathione-driven transnitrosylation of an ent
45 diethylamine NONOate, spermine NONOate, and S-nitrosoglutathione, exhibited concentration-dependent
53 ts of nitric oxide (NO) derivatives, such as S-nitrosoglutathione (GSNO) and peroxynitrite, were inve
55 nsor for the detection and quantification of S-nitrosoglutathione (GSNO) as a step toward the determi
56 We report that S-nitrosylation of NPR1 by S-nitrosoglutathione (GSNO) at cysteine-156 facilitates
57 onstrated previously that the degradation of S-nitrosoglutathione (GSNO) by cells absolutely required
59 trosylation occurs in IPC hearts and whether S-nitrosoglutathione (GSNO) elicits similar effects on S
61 hree compounds that exclude GSNOR substrate, S-nitrosoglutathione (GSNO) from its binding site in GSN
62 of Escherichia coli to the nitrosating agent S-nitrosoglutathione (GSNO) in both aerobic and anaerobi
63 ted to selection by exposure to the NO donor S-nitrosoglutathione (GSNO) in concentrations sufficient
64 that can denitrosylate proteins in vivo and S-nitrosoglutathione (GSNO) in vitro However, a periplas
65 at treatment with the physiological NO donor S-nitrosoglutathione (GSNO) increased the abundance of s
70 y, we found that application of the NO donor S-nitrosoglutathione (GSNO) or diethylammonium (Z)-1-1(N
71 d EA.hy926 endothelial cells were exposed to S-nitrosoglutathione (GSNO) or diethylenetriamine NONOat
72 apable of modest activation of proMMP-9, but S-nitrosoglutathione (GSNO) or the NONOates, DEA-NO, SPE
73 re we use a similar approach to confirm that S-nitrosoglutathione (GSNO) primarily impacts the metabo
75 avohemoglobin denitrosylase consumes NO, and S-nitrosoglutathione (GSNO) reductase metabolizes GSNO.
76 e regulators of S-nitrosylation, for example S-nitrosoglutathione (GSNO) reductase, provide for a sup
78 S-nitroso-L-cysteine-ethyl ester (SNCEE) and S-nitrosoglutathione (GSNO) that cause intracellular and
79 5) in this issue report on the capability of S-nitrosoglutathione (GSNO) to increase the expression,
81 tion of glutathione (GSH) in the presence of S-nitrosoglutathione (GSNO) was examined as a model reac
83 tion was S-nitroglutathione (GSNO2) and that S-nitrosoglutathione (GSNO) was not a detectable product
85 telet production, we exposed Meg-01 cells to S-nitrosoglutathione (GSNO) with or without thrombopoeit
87 is model, we determined the effectiveness of S-nitrosoglutathione (GSNO), a nitric oxide donor with r
90 er, the NOC-18 effect could be reproduced by S-nitrosoglutathione (GSNO), an endogenous nitrosonium d
91 we found that endogenous nitric oxide (NO), S-nitrosoglutathione (GSNO), and antioxidants blocked se
92 sion was attenuated by a nitric oxide donor, S-nitrosoglutathione (GSNO), and by a nonspecific oxidas
94 tudy, we show that S-nitrosocysteine (CSNO), S-nitrosoglutathione (GSNO), and S-nitroso-N-acetylpenic
95 isiae and mouse macrophages that metabolizes S-nitrosoglutathione (GSNO), and show that it is the glu
97 es and is inhibited by hydrogen peroxide and S-nitrosoglutathione (GSNO), donors of reactive oxygen a
99 )) of the E67L enzyme in reactions involving S-nitrosoglutathione (GSNO), S-hydroxymethylglutathione
101 thiazoline-6-sulfonic acid), when exposed to S-nitrosoglutathione (GSNO), S-nitrosocysteine, or S-nit
102 types were used to assess the involvement of S-nitrosoglutathione (GSNO), the primary NO source, in c
103 milar results were found with the tripeptide S-nitrosoglutathione (GSNO), thought to be a donor of NO
104 treated endothelial cells with an NO donor, S-nitrosoglutathione (GSNO), to determine its effect(s)
105 ive nitrogen intermediates (RNI) nitrite and S-nitrosoglutathione (GSNO), which are bactericidal in v
106 etermine a minimal mechanism for spontaneous S-nitrosoglutathione (GSNO)-mediated transnitrosation of
115 w that hmp expression is also upregulated by S-nitrosoglutathione (GSNO, widely used as an NO release
116 proaches, we here investigated the effect of S-nitrosoglutathione (GSNO; a physiological NO donor) in
118 nitric oxide (NO) and S-nitrosothiols (e.g., S-nitrosoglutathione, GSNO) and arises, at least in sign
120 ysteines is insensitive to the inhibition by S-nitrosoglutathione, hydrogen peroxide, or N-ethylmalei
121 we investigated the role of glutathione and S-nitrosoglutathione in animal and human macrophages in
122 , we examined the role of glutathione and/or S-nitrosoglutathione in controlling the growth of intrac
123 inistration of endogenous nitric oxide donor S-nitrosoglutathione in mice blocked the reduction of ex
125 usside (SNP), 3-morpholinosydnonimine-1, and S-nitrosoglutathione] in P19 stem cells within 4 hr.
127 steine and glutathione synthetases to NO and S-nitrosoglutathione indicates that GSH antagonizes the
130 oint to different mechanisms by which NO and S-nitrosoglutathione influence cardiac and skeletal musc
131 nitric oxide donors sodium nitroprusside and S-nitrosoglutathione inhibited degranulation, and this e
134 trate that the structural isostere of HMGSH, S-nitrosoglutathione, is an ideal hCBR1 substrate (Km =
135 splay excessive accumulation of the NO donor S-nitrosoglutathione, it rescued immunity in nox1 mutant
136 partially S-nitrosated by preincubation with S-nitrosoglutathione, its cardioprotective effect was ma
137 be due to a direct reaction of proteins with S-nitrosoglutathione or denitrosylation of S-nitrosylate
138 ivation, thus excluding the participation of S-nitrosoglutathione or more oxidizing NO.-derived speci
140 athione reductase is a negative regulator of S-nitrosoglutathione production) and nitric oxide-induce
141 of human thioredoxin-1 after treatment with S-nitrosoglutathione, providing a high-resolution view o
142 NO/SNO donors such as S-nitrosocysteine and S-nitrosoglutathione readily induced the S-nitrosylation
143 T mice and mice homozygous for a deletion of S-nitrosoglutathione reductase (GSNOR(-/-)), a denitrosy
146 redoxin (Trx) mediated transnitrosylation of S-nitrosoglutathione reductase (GSNOR) underpins the reg
150 erated mice with a targeted gene deletion of S-nitrosoglutathione reductase (GSNOR), and show that th
151 ls deficient in the SNO-metabolizing enzyme, S-nitrosoglutathione reductase (GSNOR), which exhibit en
154 ate assimilation suppresses the redox enzyme S-nitrosoglutathione Reductase 1 (GSNOR1) by S-nitrosyla
155 itrosylation are controlled predominantly by S-nitrosoglutathione reductase 1 (GSNOR1) which turns ov
157 gation, mice with a targeted deletion of the S-nitrosoglutathione reductase gene (GSNOR(-/-)) have re
158 glutathione reductase knockout mouse hearts (S-nitrosoglutathione reductase is a negative regulator o
160 odified cysteine data sets for wild-type and S-nitrosoglutathione reductase knockout mouse hearts (S-
161 accumulation, dendritic cell hyperplasia and S-nitrosoglutathione reductase stimulation being NO-depe
162 we show that MSCs isolated from mice lacking S-nitrosoglutathione reductase, a denitrosylase that reg
163 d cell expression of thioredoxin-1 (Trx1) or S-nitrosoglutathione reductase, both of which can functi
164 Salmonella virulence in mice, in contrast to S-nitrosoglutathione reductase, flavorubredoxin, or cyto
165 ase-deficient mice-1 [NOS1(-/-)]), and hyper S-nitrosoglutathione reductase-deficient (GSNOR(-/-)) mi
166 Consistent with this cellular phenotype, S-nitrosoglutathione reductase-deficient mice were small
168 S-nitrosylation of PPARgamma was elevated in S-nitrosoglutathione reductase-deficient MSCs, diminishi
170 s-1 (S-nitrosocysteine) and 12,800 M-1 s-1 (S-nitrosoglutathione), respectively, with a stoichiometr
171 ulfides, and could also be glutathiolated by S-nitrosoglutathione resulting in the incorporation of f
172 AF gels indicated that the NO donor compound S-nitrosoglutathione S-nitrosylates significantly more p
173 The results demonstrate that the NO donor S-nitrosoglutathione (S-NO-glutathione) inhibits the sti
174 pounds, S-nitroso-N-acetyl-dl-penicillamine, S-nitrosoglutathione, S-nitrosocaptopril, glucose-S-nitr
175 rolipoic acid, catalyze the denitrosation of S-nitrosoglutathione, S-nitrosocaspase 3, S-nitrosoalbum
176 hieved for low molecular weight RSNOs (i.e., S-nitrosoglutathione, S-nitrosocysteine) by tuning the i
177 acilitate photolysis of nitrosothiols (i.e., S-nitrosoglutathione, S-nitrosocysteine, and S-nitrosoal
178 hydroascorbate, DTNB, lipoic acid/lipoamide, S-nitrosoglutathione, selenodiglutathione, selenite, met
180 cytes were treated with either exogenous NO (S-nitrosoglutathione [SNO-GSH]) or a mixture of cytokine
183 ied actin was more readily glutathiolated by S-nitrosoglutathione than by oxidized GSH as determined
184 transpeptidase is to cleave glutathione and S-nitrosoglutathione to the dipeptide (Cys-Gly), which i
186 es were specified on 56 distinct proteins in S-nitrosoglutathione-treated (2-10 microM) rat cerebellu
188 tif that predicts stable transnitrosation by S-nitrosoglutathione under test conditions, suggesting t
190 cysteine (SNC) and, to a more modest extent, S-nitrosoglutathione were found to rapidly increase [(3)
191 l-containing tripeptide, exclusively yielded S-nitrosoglutathione when exposed to the NO donor, Et2NN
194 itrosative defense genes upon treatment with S-nitrosoglutathione, while the mucoid strain PAO578II s
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