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1 th intracellular reactive oxygen species and S-nitrosothiol.
2 -dependent conformational change, to form an S-nitrosothiol.
3 iate reduces an electron acceptor to produce S-nitrosothiol.
4  ion-catalyzed decomposition than the parent S-nitrosothiol.
5 ysteine thiol (or thiolate anion) to form an S-nitrosothiol.
6 o form thionitrous acid (HSNO), the smallest S-nitrosothiol.
7 ction that converts a protein Cys thiol to a S-nitrosothiol.
8 sms encompassing the cellular homeostasis of S-nitrosothiols.
9 his release occurs due to NO liberation from S-nitrosothiols.
10 enerate high levels of intracellular protein S-nitrosothiols.
11 ical effects of nitric oxide are mediated by S-nitrosothiols.
12 ay be involved in the regulation of cellular S-nitrosothiols.
13 obes and the instability of cellular protein S-nitrosothiols.
14 esult in decreased rates of decomposition of S-nitrosothiols.
15 f intracellular glutathione and formation of S-nitrosothiols.
16 ed that NO reacts with ---SH groups, forming S-nitrosothiols.
17 volvement of superoxide in the metabolism of S-nitrosothiols.
18 associated with low concentrations of airway S-nitrosothiols.
19 ted in release of nitric oxide (NO) from the S-nitrosothiols.
20 in is promoted by the erythrocytic export of S-nitrosothiols.
21 ric methods for the reliable quantitation of S-nitrosothiols.
22 ur species and related modifications such as S-nitrosothiols.
23 yl anion, the nitric oxide free radical, and S-nitrosothiols.
24 s from reaction of copper(II) thiolates with S-nitrosothiols.
25 roducts, with a decrease in the formation of S-nitrosothiols.
26 the presence of nitrite to form N(2)O(3) and S-nitrosothiols.
27 y can be achieved through rational design of S-nitrosothiols.
28 trite versus chemical intermediates, such as S-nitrosothiols.
29 significantly higher concentrations of total S-nitrosothiols (11.1+/-2.9 nmol/mL) than normal pregnan
30 osation, did not change total red blood cell S-nitrosothiol abundance but did shift S-nitrosothiol di
31 , manually curated data set of proteins with S-nitrosothiols, accounting for a variety of biochemical
32 ition of NO provides the fully characterized S-nitrosothiol adduct [Cu(I)](kappa(1)-N(O)SR), which re
33  we demonstrate the interconversion of metal-S-nitrosothiol adduct M(RSNO) and metal nitrosyl thiolat
34                                              S-Nitrosothiol and iron-nitrosyl-protein adducts did not
35          We tested the hypothesis that total S-nitrosothiol and S-nitrosoalbumin concentrations are i
36   Further reaction of HNO with the remaining S-nitrosothiol and thiol results in the generation of ot
37 se this is a NO-containing factor such as an S-nitrosothiol and/or a dinitrosyl-iron (II) cysteine co
38 iol groups of proteins to give corresponding S-nitrosothiols and 5-thio-2-nitrobenzoate dianion.
39 esulted in a time-dependent decomposition of S-nitrosothiols and accumulation of nitrite/nitrate in r
40             Dietary nitrate increased plasma S-nitrosothiols and nitrite, enhanced revascularization,
41                                Nitric oxide, S-nitrosothiols and peroxynitrite are reported to variou
42                                          For S-nitrosothiols and peroxynitrite to interfere with the
43 n could facilitate nitric oxide release from S-nitrosothiols and represents a potential physiological
44                      The role of circulating S-nitrosothiols and SNO-Hb in the regulation of basal va
45  through exposure to cell membrane-permeable S-nitrosothiols and that sGC is S-nitrosylated and desen
46 tes to be more susceptible to NO (especially S-nitrosothiols) and subsequent necrotic cell death.
47 n to stain for NADPH diaphorase were rich in S-nitrosothiols, and (7) procedures that accelerate deco
48 trate (NO(3) (-)), nitrosyl-metal complexes, S-nitrosothiols, and 3-nitrotyrosine.
49 e to the anaerobic regulon protected against S-nitrosothiols, and anaerobic growth of E. coli lacking
50 ycerin (GTN) and nitric oxide donors such as S-nitrosothiols are clinically vasoactive through stimul
51                                              S-Nitrosothiols are known as reagents for NO storage and
52                                      Because S-nitrosothiols are known to modify enzymes containing r
53 l studied, the response elements specific to S-nitrosothiols are less clear.
54                                              S-nitrosothiols are naturally occurring bronchodilators,
55                                              S-Nitrosothiols are stable compounds at 37 degrees C and
56 mechanism of inactivation was reported using S-nitrosothiols as the NO donor.
57 r to those reported for low-molecular-weight S-nitrosothiols, as well as from nitrite.
58  indicates that hypoxic vasodilation entails S-nitrosothiol-based (SNO-based) vasoactivity (rather th
59                  Our results suggest that an S-nitrosothiol-based signal originating from RBCs mediat
60              These observations suggest that S-nitrosothiol biochemistry is of central importance to
61 focus is on oxidized nitrogen in the form of S-nitrosothiol bond-containing species, which are now ap
62 creased sensitivity to acidified nitrite and S-nitrosothiols, both of which produce nitric oxide.
63 and was evaluated as a fluorescence probe of S-nitrosothiol-bound NO transfer in human umbilical vein
64  first gel-based method to identify not only S-nitrosothiols but also other labile NO-based modificat
65 ity of ascorbate to generate a thiol from an S-nitrosothiol, but not from alternatively S-oxidized th
66             A fraction (25%) was exported as S-nitrosothiol, but this fraction was not increased at l
67 and ascorbate can stimulate decomposition of S-nitrosothiol by chemical reduction of contaminating tr
68 nonaphthalene and nitrous acid released from S-nitrosothiols by treatment with mercuric chloride in a
69 100% as documented by simultaneous assays of S-nitrosothiols by uv spectrophotometry and by Saville m
70        We have investigated the breakdown of S-nitrosothiols by wild-type (WT) SOD and two common FAL
71                             Nitric oxide and S-nitrosothiols can be metabolized by bacteria, but only
72                                 We find that S-nitrosothiols can react with thiols to generate nitrox
73  showed that exposure to nitric oxide and to S-nitrosothiols causes S-nitrosylation of sGC, which dir
74  by binding to cysteine residues and forming S-nitrosothiol complexes.
75  We conclude that S-nitrosoalbumin and total S-nitrosothiol concentrations are significantly increase
76                                     Tracheal S-nitrosothiol concentrations from eight asthmatic child
77                                         Mean S-nitrosothiol concentrations in asthmatic children were
78 more pronounced effect of protecting against S-nitrosothiols, confirms this finding.
79  plants, as NO-releasing nanomaterials (e.g. S-nitrosothiol-containing chitosan nanoparticles) have m
80                                  Erythrocyte S-nitrosothiol content (reflecting mainly S-nitrosohemog
81    Compared to similar measurements of total S-nitrosothiol content in bulk solution, use of the micr
82 151+/-25 pmol/mg protein, respectively) when S-nitrosothiol content was expressed per milligram prote
83 tylcysteine (SNOAC), decreasing erythrocytic S-nitrosothiol content, both during whole-blood deoxygen
84  occurs in tandem with increased erythrocyte S-nitrosothiol content, EM, and O2 unloading.
85    IPC and GSNO both significantly increased S-nitrosothiol contents and S-nitrosylation levels of th
86 reatment with NO donors (increasing cellular S-nitrosothiol contents) substantially enhanced the init
87 the fluorescence intensity of dansyl-labeled S-nitrosothiols could be enhanced up to 30-fold.
88                       We now report that (1) S-nitrosothiols covalently modify both NBT and TNBT, but
89                The mechanism and products of S-nitrosothiol decomposition are of great significance t
90          Transnitrosation can also stimulate S-nitrosothiol decomposition if the product S-nitrosothi
91                  The biological relevance of S-nitrosothiol decomposition is discussed.
92 epresented >90% of nitrosonium equivalent of S-nitrosothiols degraded during the incubation.
93  S-nitrosohaemoglobin consumption and plasma S-nitrosothiol delivery during apnoea (all P >= 0.05).
94  CRT externalization occurred together in an S-nitrosothiol-dependent and caspase-independent manner.
95           We observed that PDI catalyzes the S-nitrosothiol-dependent oxidation of the heme group of
96  renitrosylated RBCs than during infusion of S-nitrosothiol-depleted RBCs, and this difference in cor
97               S-nitrosohemoglobin and plasma S-nitrosothiols did not change with NO inhalation.
98 r alpha-NADP did not produce diformazan, (5) S-nitrosothiols did not promote NADPH-dependent reductio
99  cell S-nitrosothiol abundance but did shift S-nitrosothiol distribution to lower molecular weight sp
100 m within endothelial cells from an exogenous S-nitrosothiol donor or from endogenous production of NO
101 sponse in proportion to the concentration of S-nitrosothiols (e.g., nitrosocysteine, nitrosoglutathio
102 hysiological levels of nitric oxide (NO) and S-nitrosothiols (e.g., S-nitrosoglutathione, GSNO) and a
103 nosine monophosphate (cGMP) generation after S-nitrosothiol exposure (65.4 +/- 26.7% reduction compar
104 e thiols modified using nitric oxide, termed S-nitrosothiols, facilitate the hypersensitive response
105                                The selective S-nitrosothiol formation at Cys-81 led to a doubling of
106  involved both S- and N-nitrosation, and RBC S-nitrosothiol formation emerged as a sensitive indicato
107 nor, is much less effective at intracellular S-nitrosothiol formation in the presence of L-cystine or
108 is study was to investigate the mechanism of S-nitrosothiol formation under physiological conditions.
109  presented for the quantitative detection of S-nitrosothiols formed by model biological thiols, cyste
110          GSNO is a low molecular weight SNO (S-nitrosothiol) formed during oxidation of NO.
111 itatively transferring the thiol groups into S-nitrosothiol functionalities.
112 talytic Cu(II)/(I)-mediated decomposition of S-nitrosothiols generates NO(g) in the thin polymeric fi
113 ators (including a.NO donor [DeaNonoate], an S-nitrosothiol [GSNO], and the nitroxyl anion donor, Ang
114          Transnitrosation between thiols and S-nitrosothiols has been suggested to be a mechanism of
115 rstanding the biosynthesis and catabolism of S-nitrosothiols has proven to be difficult, in part beca
116                                              S-nitrosothiols have been implicated as intermediary tra
117                                              S-Nitrosothiols have been implicated to play key roles i
118                                              S-nitrosothiols have been shown to affect a number of ph
119                                              S-nitrosothiols have been suggested to play an important
120                                              S-Nitrosothiols have generated considerable interest due
121                                              S-Nitrosothiols have many biological activities and have
122                                       Airway S-nitrosothiols have not been studied in asthma.
123 ions .NO reacts directly with thiols to form S-nitrosothiol in the presence of an electron acceptor.
124 e contention that the transient formation of S-nitrosothiols in biological systems may protect NO fro
125 que offers simple and rapid determination of S-nitrosothiols in complex reaction mixtures with the de
126                 Detection of NO2-, NO3-, and S-nitrosothiols in lung epithelial lining fluids confirm
127 (6) enhanced the therapeutic actions of oral S-nitrosothiols in mouse models of C. difficile infectio
128 ontrol samples and 53.7% and 56.8% of plasma S-nitrosothiols in normal pregnancy and preeclampsia, re
129                               In analysis of S-nitrosothiols in protein-containing mixtures, HgCl2-me
130 P, but not SNP or SIN-1, increased levels of S-nitrosothiols in SN56 proteins, consistent with the tr
131 min fraction contained 49.4% of total plasma S-nitrosothiols in the control samples and 53.7% and 56.
132 ha,we obtained evidence for the formation of S-nitrosothiols in the ER molecule.
133 etic analysis showed that the degradation of S-nitrosothiols in the presence of superoxide proceeded
134 letely accounted for the increased levels of S-nitrosothiols in total plasma.
135 an approximately 50% reduction in perfusate [S-nitrosothiol], in association with an increase in perf
136 t couple NAD(P)H oxidation with reduction of S-nitrosothiols, including protein and low-molecular-wei
137 n of dynamin2 or treatment with the NO donor S-nitrosothiols increases, whereas targeted reduction of
138 constituted domain peptides demonstrate that S-nitrosothiols indeed release zinc from both the alpha-
139 mine whether the hemodynamic effects of this S-nitrosothiol involves the activation of stereoselectiv
140                    Finally, the formation of S-nitrosothiol is demonstrated in an anaerobic environme
141  S-nitrosothiol decomposition if the product S-nitrosothiol is more susceptible to transition metal i
142                             Concentration of S-nitrosothiols is determined from the difference in flu
143 sults suggest that inactivation of papain by S-nitrosothiols is due to a direct attack of the highly
144  study, we demonstrate that the transport of S-nitrosothiols is essential for these compounds to affe
145 ed in the modification of the thiol group by S-nitrosothiols is important for understanding the role
146 hway responsible for the cellular effects of S-nitrosothiols is specific for S-nitrosocysteine (CSNO)
147        Thionitrous acid (HSNO), the smallest S-nitrosothiol, is emerging as a potential key intermedi
148 ts whereas the BJR responses elicited by the S-nitrosothiol, L-S-nitrosocysteine (5 micromol/kg, i.v.
149 th mutated thioredoxin reductase denitrosate S-nitrosothiols less efficiently.
150 sothiol uptake, increasing the intracellular S-nitrosothiol level from approximately 60 pmol/mg of pr
151 a nitrate, nitrite, and low-molecular-weight S-nitrosothiol levels by chemiluminescence.
152 provide new insight into the determinants of S-nitrosothiol levels in subcellular compartments.
153 eine biosynthesis pathway and an increase in S-nitrosothiol levels suggest S-nitrosylation to be a co
154  restored intracardiac nitrite and increased S-nitrosothiol levels, decreased pathological cardiac mi
155 s was accompanied by an increase in cellular S-nitrosothiol levels, modification of cysteines residue
156                                 In parallel, S-nitrosothiol-linked probes enable enrichment and detec
157  procedures that accelerate decomposition of S-nitrosothiols, markedly reduced NADPH diaphorase stain
158 ocysteine-sensitive metH gene indicated that S-nitrosothiols may directly deplete intracellular homoc
159 Accordingly, mutation of Cys 890 compromised S-nitrosothiol-mediated control of AtRBOHD activity, per
160                              We suggest that S-nitrosothiol metabolism may be a target for the develo
161 sents a potential physiological mechanism of S-nitrosothiol metabolism.
162 e, and provide insight into the aetiology of S-nitrosothiols, methaemoglobin and its related valency
163                                 Importantly, S-nitrosothiol-MIF formation was measured both in vitro
164            This decrease was paralleled by a S-nitrosothiol-MIF- but not Cys81 serine (Ser)-MIF mutan
165 roversies surrounding the proposal that this S-nitrosothiol modulates blood flow in vivo.
166      Reduced metal ion (e.g. Cu+) decomposes S-nitrosothiols more rapidly than oxidized metal ion (e.
167 te bioactivation, nitrite was reduced to NO, S-nitrosothiols, N-nitros-amines, and iron-nitrosylated
168  bone marrow-derived CD31(+)/CD45(-), plasma S-nitrosothiols, nitrite, and skeletal tissue cGMP level
169 egulated by redox reactions involving NO and S-nitrosothiols (nitrosative stress), emphasizing a vers
170 de that in the HEK293 expression system, the S-nitrosothiol NO donors inhibit L-type Ca2+ channels by
171 um conferred specific hypersusceptibility to S-nitrosothiol NO-donor compounds and attenuated virulen
172 on mass spectrometry, we found that NO forms S-nitrosothiols on Cys67 and Cys95 of HIV-PR which direc
173 pid method for analyzing protein and peptide S-nitrosothiols on gels using the fluorescent probes 4,5
174 l of NBT after modification, (2) addition of S-nitrosothiols or beta- or alpha-NADPH to solutions of
175 logical event when NO-dependent formation of S-nitrosothiols or peroxynitrite structurally modifies c
176          However, the mechanisms by which an S-nitrosothiol (or the S-nitroso functional group) is tr
177 ese data demonstrate for the first time that S-nitrosothiols oxidatively modify PTEN, leading to reve
178                   Plasma nitrite (P = 0.01), S-nitrosothiols (P = 0.03) and total red blood cell NO (
179 umption and corresponding delivery of plasma S-nitrosothiols (P>0.05).
180 ely, with a stoichiometric ratio of 1 mol of S-nitrosothiol per 2 mol of superoxide.
181 try effected by NO(g) with the use of trityl-S-nitrosothiol (Ph3CSNO) as the nitric oxide source.
182 peripheral circulation, and (iii) SNO-Hb and S-nitrosothiols play a minimal role in the regulation of
183 cal concentrations of nitrite and deoxyHb, a S-nitrosothiol precursor is formed within seconds and pr
184    The potential physiological importance of S-nitrosothiols prompted us to examine their reaction wi
185 chemical mechanism by which nitric oxide and S-nitrosothiols react with cysteine residues in ornithin
186 ovide tentative evidence that membrane-bound S-nitrosothiol receptors may exist within the cardiovasc
187 l involves the activation of stereoselective S-nitrosothiol receptors within the cardiovascular syste
188 involve its interaction with stereoselective S-nitrosothiol recognition sites within the vasculature
189 n vivo Using this approach, called SNOxICAT (S-nitrosothiol redox isotope-coded affinity tag), we fou
190 lly slower reaction rates of superoxide with S-nitrosothiols relative to the reaction rate with NO ar
191                                              S-Nitrosothiol resistance was restored by exogenous homo
192                                Photolysis of S-nitrosothiols results in the formation of .NO and disu
193 es can be preserved in a more stable form of S-nitrosothiols (RS-NO).
194 O2N) that leads to S-nitrosation to give the S-nitrosothiol RSNO and copper(II) hydroxide [Cu(II)]-OH
195  nitric oxide (NO) delivery is achieved from S-nitrosothiol (RSNO) type NO donor doped silicone rubbe
196 in the reaction of H(2) S with NO as well as S-nitrosothiols (RSNO) and nitrite (NO(2)(-) ) that serv
197                         The decomposition of S-nitrosothiols (RSNO) in solution under oxidative condi
198 O oxidation leads to formation of vasoactive S-nitrosothiols (RSNO) in vitro and in vivo as detected
199 d metabolites with thiols and metals to form S-nitrosothiols (RSNOs) and metal nitrosyls.
200                                              S-Nitrosothiols (RSNOs) are carriers of nitric oxide (NO
201                                              S-Nitrosothiols (RSNOs) are important exogenous and endo
202                    Amperometric detection of S-nitrosothiols (RSNOs) at submicromolar levels in blood
203                                     Although S-nitrosothiols (RSNOs) have been frequently implicated
204                  Here we report that certain S-nitrosothiols (RSNOs) impose what we term a "nitrosati
205 widely used methodology for the detection of S-nitrosothiols (RSNOs) in biological samples.
206                                              S-Nitrosothiols (RSNOs) serve as air-stable reservoirs f
207                                              S-nitrosothiols (RSNOs) serve as ready sources of biolog
208                         The concentration of S-nitrosothiols (RSNOs), endogenous transporters of the
209 ested the effects of one class of NO donors, S-nitrosothiols (RSNOs), on expressed cardiovascular L-t
210 t with the low molecular mass cell-permeable S-nitrosothiol S-nitrosocysteine ethyl ester (SNCEE).
211 otein S-nitrosylation, the colocalization of S-nitrosothiol (S-NO) and protein-tyrosine phosphatase 1
212 uding protein and low-molecular-weight (LMW) S-nitrosothiols (S-nitroso-GSH (GSNO) and S-nitroso-CoA
213 t the specific transport of amino acid-based S-nitrosothiols (S-nitroso-L-cysteine and S-nitrosohomoc
214 sidues in ornithine decarboxylase to form an S-nitrosothiol(s) on the protein.
215 rate that zinc thiolate bonds are targets of S-nitrosothiol signaling and further indicate that MT-II
216 tHb) on HPV, expired NO (eNO), and perfusate S-nitrosothiol (SNO) concentration in isolated, perfused
217  kidney injury (AKI), double knockout (-/-), S-nitrosothiol (SNO) condition at a nitrosylation level
218 eases the rate at which low-molecular-weight S-nitrosothiol (SNO) decomposes in vitro.
219                                  The role of S-nitrosothiol (SNO) formation and turnover in governing
220                                              S-nitrosothiol (SNO) formation was increased in isoprote
221                                Disruption of S-nitrosothiol (SNO) homeostasis may result not only fro
222                            Further, this Trx S-nitrosothiol (SNO) reductase activity was potentiated
223 na zinc finger transcription factor (ZF-TF), S-nitrosothiol (SNO) Regulated 1 (SRG1), is a central ta
224 at in human erythrocytes haemoglobin-derived S-nitrosothiol (SNO), generated from imported NO, is ass
225 (betaCys93) that has been assigned a role in S-nitrosothiol (SNO)-based hypoxic vasodilation by RBCs.
226                                              S-nitrosothiol (SNO)-deficient RBCs produce impaired vas
227 oxic vasodilation is recapitulated by native S-nitrosothiol (SNO)-replete RBCs and by SNO-Hb itself,
228 rotein cysteine (Cys) thiol (-SH) to form an S-nitrosothiol (SNO).
229 oiety to a protein cysteine thiol forming an S-nitrosothiol (SNO).
230 oiety to a protein cysteine thiol to form an S-nitrosothiol (SNO).
231 cysteine thiol by an NO group to generate an S-nitrosothiol (SNO).
232 x 10(-4) at 3 h vs. 6.5 x 10(-4) (fresh) mol S-nitrosothiol (SNO)/mol Hb tetramer (P = 0.032, mercuri
233 fied 1,276 S-nitrosylated cysteine residues [S-nitrosothiol (SNO)] on 491 proteins in resting hearts
234                     We demonstrate here that S-nitrosothiols (SNO) caused a dose-dependent inhibition
235 hemical reaction products [nitrite, nitrate, S-nitrosothiols (SNO), and nitrotyrosine] before, immedi
236 radigm is well exemplified in bacteria where S-nitrosothiols (SNO)-compounds identified with antimicr
237 ttachment of NO to cysteine residues to form S-nitrosothiols (SNO).
238 ron (iron nitrosyl, FeNO) to cysteine thiol (S-nitrosothiol, SNO) that subserves bioactivation, and i
239 es a family of NO-related molecules and that S-nitrosothiols (SNOs) are central to signal transductio
240                     Nitric oxide (NO) and/or S-nitrosothiols (SNOs) can prevent the loss of beta-AR s
241 whereas treatments favoring stabilization of S-nitrosothiols (SNOs) decreased its cytotoxic potency.
242 nce that nitric oxide (NO) and/or endogenous S-nitrosothiols (SNOs) exert protective effects in a var
243 chemical data demonstrate a pivotal role for S-nitrosothiols (SNOs) in mediating the actions of nitri
244 sylation reflects dynamic equilibria between S-nitrosothiols (SNOs) in proteins and small molecules (
245 ntly through protein S-nitrosylation to form S-nitrosothiols (SNOs) in target proteins, operates coor
246  dehydrogenase involved in the regulation of S-nitrosothiols (SNOs) in vivo.
247 ward nitric oxide (NO) leads to formation of S-nitrosothiols (SNOs) that play important roles in path
248                                              S-nitrosothiols (SNOs), formed by nitric oxide (NO)-medi
249 modified the biotin switch assay for protein S-nitrosothiols (SNOs), using resin-assisted capture (SN
250 st NO bioactivity is packaged in the form of S-nitrosothiols (SNOs), which are relatively resistant t
251 de synthase (NOS), superoxide dismutase, and S-nitrosothiols (SNOs), which have recently been identif
252 O reductase (GSNOR) and are depleted of lung S-nitrosothiols (SNOs).
253 fer of NO from Hb to form other (vasoactive) S-nitrosothiols (SNOs).
254 idative modification of Cys residues to form S-nitrosothiols (SNOs).
255 E ) is signalled by deoxyhaemoglobin-derived S-nitrosothiols (SNOs).
256 ioactivity in mammals is largely mediated by S-nitrosothiols (SNOs).
257 rosylation by biologically relevant low-mass S-nitrosothiols (SNOs).
258         The direct amperometric detection of S-nitrosothiol species (RSNOs) is realized by modifying
259 e source of this NO is the already available S-nitrosothiol store rather than de novo synthesis by NO
260 gy through intracellular NO by modulation of S-nitrosothiol stores and stimulation of NOS activity.
261 function as a generator for the formation of S-nitrosothiols such as S-nitrosoglutathione and, as suc
262 y to cause vasodilation as compared to other S-nitrosothiols suggests potential application in biolog
263 ur data provide evidence for a physiological S-nitrosothiol synthase activity of tetrameric Hb that d
264 sothiols was used to explore the kinetics of S-nitrosothiol/thiol transnitrosation and was evaluated
265 RSNO2) intermediate and yields low levels of S-nitrosothiols (thionitrites; RSNO), both of which are
266 ffers) stimulates the catalytic breakdown of S-nitrosothiols to .NO and disulfide.
267 -nitroso-L-cysteine (1) and six other simple S-nitrosothiols to Cys 34 of bovine serum albumin (2) ha
268 ) in the enzyme active site on the sulfur of S-nitrosothiols to form a mixed disulfide between the in
269       Here, we report that H(2)S reacts with S-nitrosothiols to form thionitrous acid (HSNO), the sma
270 ncluded ultraviolet-induced decomposition of S-nitrosothiols to liberate NO captured by a florigenic
271 T did not elicit diformazan, (3) addition of S-nitrosothiols to solutions of NBT plus beta- or alpha-
272 resence of paraformaldehyde, (4) addition of S-nitrosothiols to solutions of NBT plus beta- or alpha-
273      This reaction converts unstable primary S-nitrosothiols to stable disulfide-iminophosphorane pro
274 ormational changes in the toxin enabled host S-nitrosothiols to transnitrosylate the toxin catalytic
275             However, the mechanisms by which S-nitrosothiols transduce their activity across cell mem
276 as to be incompatible with life were all the S-nitrosothiols transformed into bioactive equivalents d
277 n this study, we have examined the effect of S-nitrosothiol transport on intracellular thiol status a
278 resence of L-cystine enhanced GSNO-dependent S-nitrosothiol uptake, increasing the intracellular S-ni
279                   A bis-ligation reaction of S-nitrosothiols using triaryl substituted phosphine-thio
280 urate determination of low concentrations of S-nitrosothiols, utilizing conventional spectroscopic te
281                        The resultant protein-S-nitrosothiol was found to be unstable and to decompose
282                  The inhibition of papain by S-nitrosothiol was rapidly reversed by dithiothreitol, b
283                Intracellular accumulation of S-nitrosothiols was observed with 2a but not with 2b.
284 rred by yeast flavohemoglobin against NO and S-nitrosothiols was seen under both anaerobic and aerobi
285       In addition, one of the dansyl-labeled S-nitrosothiols was used to explore the kinetics of S-ni
286 ackground nitrite and stabilizes erythrocyte S-nitrosothiols, we find the levels of SNO-Hb in the bas
287 a nitrate, nitrite, and low-molecular-weight S-nitrosothiol were in the normal range; however, enhanc
288                                              S-Nitrosothiols were barely detectable.
289            Moreover, a variety of additional S-nitrosothiols were catabolized more readily by A4V SOD
290         Surprisingly, when concentrations of S-nitrosothiols were high, nitric oxide function also go
291              A series of fluorophore-labeled S-nitrosothiols were synthesized, and their fluorescence
292           We found that low-molecular-weight S-nitrosothiols were undetectable and S-nitroso-albumin
293 nificantly more reactive than MT-I/II toward S-nitrosothiols, whereas the reactivity of all three iso
294 helium induces a precipitous decline in cell S-nitrosothiol, which depends upon enhanced Trx activity
295 B is reflected in the level of intracellular S-nitrosothiols, which are constitutively metabolized.
296 lowed by reductive generation of thiols from S-nitrosothiols, which are then labeled with either a bi
297 hanism, we here investigate the reactions of S-nitrosothiols with different isoforms of MT.
298 on and thiols, furnishing iron nitrosyls and S-nitrosothiols with wide-ranging stabilities and reacti
299 hanges that occur after exposure of cells to S-nitrosothiol, with respect to thiol chemistry, are dis
300 ing reactive cysteines, we hypothesized that S-nitrosothiols would oxidize PTEN and inhibit its phosp

 
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