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1 -dependent conformational change, to form an S-nitrosothiol.
2 ysteine thiol (or thiolate anion) 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 o form thionitrous acid (HSNO), the smallest S-nitrosothiol.
6 ction that converts a protein Cys thiol to a S-nitrosothiol.
7 ical effects of nitric oxide are mediated by S-nitrosothiols.
8 ay be involved in the regulation of cellular S-nitrosothiols.
9 obes and the instability of cellular protein S-nitrosothiols.
10 ur species and related modifications such as S-nitrosothiols.
11 yl anion, the nitric oxide free radical, and S-nitrosothiols.
12 esult in decreased rates of decomposition of S-nitrosothiols.
13 f intracellular glutathione and formation of S-nitrosothiols.
14 ed that NO reacts with ---SH groups, forming S-nitrosothiols.
15 volvement of superoxide in the metabolism of S-nitrosothiols.
16 associated with low concentrations of airway S-nitrosothiols.
17 s from reaction of copper(II) thiolates with S-nitrosothiols.
18 ted in release of nitric oxide (NO) from the S-nitrosothiols.
19 in is promoted by the erythrocytic export of S-nitrosothiols.
20 ric methods for the reliable quantitation of S-nitrosothiols.
21 roducts, with a decrease in the formation of S-nitrosothiols.
22 the presence of nitrite to form N(2)O(3) and S-nitrosothiols.
23 y can be achieved through rational design of S-nitrosothiols.
24 trite versus chemical intermediates, such as S-nitrosothiols.
25 sms encompassing the cellular homeostasis of S-nitrosothiols.
26 his release occurs due to NO liberation from S-nitrosothiols.
27 enerate high levels of intracellular protein S-nitrosothiols.
28 significantly higher concentrations of total S-nitrosothiols (11.1+/-2.9 nmol/mL) than normal pregnan
29 osation, did not change total red blood cell S-nitrosothiol abundance but did shift S-nitrosothiol di
30 , manually curated data set of proteins with S-nitrosothiols, accounting for a variety of biochemical
31 ition of NO provides the fully characterized S-nitrosothiol adduct [Cu(I)](kappa(1)-N(O)SR), which re
34 Further reaction of HNO with the remaining S-nitrosothiol and thiol results in the generation of ot
36 esulted in a time-dependent decomposition of S-nitrosothiols and accumulation of nitrite/nitrate in r
40 n could facilitate nitric oxide release from S-nitrosothiols and represents a potential physiological
42 through exposure to cell membrane-permeable S-nitrosothiols and that sGC is S-nitrosylated and desen
43 tes to be more susceptible to NO (especially S-nitrosothiols) and subsequent necrotic cell death.
44 e to the anaerobic regulon protected against S-nitrosothiols, and anaerobic growth of E. coli lacking
45 ycerin (GTN) and nitric oxide donors such as S-nitrosothiols are clinically vasoactive through stimul
53 indicates that hypoxic vasodilation entails S-nitrosothiol-based (SNO-based) vasoactivity (rather th
56 focus is on oxidized nitrogen in the form of S-nitrosothiol bond-containing species, which are now ap
57 creased sensitivity to acidified nitrite and S-nitrosothiols, both of which produce nitric oxide.
58 and was evaluated as a fluorescence probe of S-nitrosothiol-bound NO transfer in human umbilical vein
59 first gel-based method to identify not only S-nitrosothiols but also other labile NO-based modificat
60 ity of ascorbate to generate a thiol from an S-nitrosothiol, but not from alternatively S-oxidized th
62 and ascorbate can stimulate decomposition of S-nitrosothiol by chemical reduction of contaminating tr
63 nonaphthalene and nitrous acid released from S-nitrosothiols by treatment with mercuric chloride in a
64 100% as documented by simultaneous assays of S-nitrosothiols by uv spectrophotometry and by Saville m
68 showed that exposure to nitric oxide and to S-nitrosothiols causes S-nitrosylation of sGC, which dir
70 We conclude that S-nitrosoalbumin and total S-nitrosothiol concentrations are significantly increase
75 Compared to similar measurements of total S-nitrosothiol content in bulk solution, use of the micr
76 151+/-25 pmol/mg protein, respectively) when S-nitrosothiol content was expressed per milligram prote
77 tylcysteine (SNOAC), decreasing erythrocytic S-nitrosothiol content, both during whole-blood deoxygen
79 IPC and GSNO both significantly increased S-nitrosothiol contents and S-nitrosylation levels of th
80 reatment with NO donors (increasing cellular S-nitrosothiol contents) substantially enhanced the init
86 CRT externalization occurred together in an S-nitrosothiol-dependent and caspase-independent manner.
88 renitrosylated RBCs than during infusion of S-nitrosothiol-depleted RBCs, and this difference in cor
90 cell S-nitrosothiol abundance but did shift S-nitrosothiol distribution to lower molecular weight sp
91 m within endothelial cells from an exogenous S-nitrosothiol donor or from endogenous production of NO
92 sponse in proportion to the concentration of S-nitrosothiols (e.g., nitrosocysteine, nitrosoglutathio
93 hysiological levels of nitric oxide (NO) and S-nitrosothiols (e.g., S-nitrosoglutathione, GSNO) and a
94 nosine monophosphate (cGMP) generation after S-nitrosothiol exposure (65.4 +/- 26.7% reduction compar
95 e thiols modified using nitric oxide, termed S-nitrosothiols, facilitate the hypersensitive response
97 involved both S- and N-nitrosation, and RBC S-nitrosothiol formation emerged as a sensitive indicato
98 nor, is much less effective at intracellular S-nitrosothiol formation in the presence of L-cystine or
99 is study was to investigate the mechanism of S-nitrosothiol formation under physiological conditions.
100 presented for the quantitative detection of S-nitrosothiols formed by model biological thiols, cyste
103 talytic Cu(II)/(I)-mediated decomposition of S-nitrosothiols generates NO(g) in the thin polymeric fi
104 ators (including a.NO donor [DeaNonoate], an S-nitrosothiol [GSNO], and the nitroxyl anion donor, Ang
106 rstanding the biosynthesis and catabolism of S-nitrosothiols has proven to be difficult, in part beca
114 ions .NO reacts directly with thiols to form S-nitrosothiol in the presence of an electron acceptor.
115 e contention that the transient formation of S-nitrosothiols in biological systems may protect NO fro
116 que offers simple and rapid determination of S-nitrosothiols in complex reaction mixtures with the de
118 (6) enhanced the therapeutic actions of oral S-nitrosothiols in mouse models of C. difficile infectio
119 ontrol samples and 53.7% and 56.8% of plasma S-nitrosothiols in normal pregnancy and preeclampsia, re
121 P, but not SNP or SIN-1, increased levels of S-nitrosothiols in SN56 proteins, consistent with the tr
122 min fraction contained 49.4% of total plasma S-nitrosothiols in the control samples and 53.7% and 56.
124 etic analysis showed that the degradation of S-nitrosothiols in the presence of superoxide proceeded
126 an approximately 50% reduction in perfusate [S-nitrosothiol], in association with an increase in perf
127 n of dynamin2 or treatment with the NO donor S-nitrosothiols increases, whereas targeted reduction of
128 constituted domain peptides demonstrate that S-nitrosothiols indeed release zinc from both the alpha-
129 mine whether the hemodynamic effects of this S-nitrosothiol involves the activation of stereoselectiv
131 S-nitrosothiol decomposition if the product S-nitrosothiol is more susceptible to transition metal i
133 sults suggest that inactivation of papain by S-nitrosothiols is due to a direct attack of the highly
134 study, we demonstrate that the transport of S-nitrosothiols is essential for these compounds to affe
135 ed in the modification of the thiol group by S-nitrosothiols is important for understanding the role
136 hway responsible for the cellular effects of S-nitrosothiols is specific for S-nitrosocysteine (CSNO)
137 ts whereas the BJR responses elicited by the S-nitrosothiol, L-S-nitrosocysteine (5 micromol/kg, i.v.
139 sothiol uptake, increasing the intracellular S-nitrosothiol level from approximately 60 pmol/mg of pr
142 eine biosynthesis pathway and an increase in S-nitrosothiol levels suggest S-nitrosylation to be a co
143 restored intracardiac nitrite and increased S-nitrosothiol levels, decreased pathological cardiac mi
144 s was accompanied by an increase in cellular S-nitrosothiol levels, modification of cysteines residue
146 ocysteine-sensitive metH gene indicated that S-nitrosothiols may directly deplete intracellular homoc
147 Accordingly, mutation of Cys 890 compromised S-nitrosothiol-mediated control of AtRBOHD activity, per
150 e, and provide insight into the aetiology of S-nitrosothiols, methaemoglobin and its related valency
154 Reduced metal ion (e.g. Cu+) decomposes S-nitrosothiols more rapidly than oxidized metal ion (e.
155 te bioactivation, nitrite was reduced to NO, S-nitrosothiols, N-nitros-amines, and iron-nitrosylated
156 bone marrow-derived CD31(+)/CD45(-), plasma S-nitrosothiols, nitrite, and skeletal tissue cGMP level
157 egulated by redox reactions involving NO and S-nitrosothiols (nitrosative stress), emphasizing a vers
158 de that in the HEK293 expression system, the S-nitrosothiol NO donors inhibit L-type Ca2+ channels by
159 um conferred specific hypersusceptibility to S-nitrosothiol NO-donor compounds and attenuated virulen
160 on mass spectrometry, we found that NO forms S-nitrosothiols on Cys67 and Cys95 of HIV-PR which direc
161 pid method for analyzing protein and peptide S-nitrosothiols on gels using the fluorescent probes 4,5
162 logical event when NO-dependent formation of S-nitrosothiols or peroxynitrite structurally modifies c
164 ese data demonstrate for the first time that S-nitrosothiols oxidatively modify PTEN, leading to reve
167 try effected by NO(g) with the use of trityl-S-nitrosothiol (Ph3CSNO) as the nitric oxide source.
168 peripheral circulation, and (iii) SNO-Hb and S-nitrosothiols play a minimal role in the regulation of
169 cal concentrations of nitrite and deoxyHb, a S-nitrosothiol precursor is formed within seconds and pr
170 The potential physiological importance of S-nitrosothiols prompted us to examine their reaction wi
171 chemical mechanism by which nitric oxide and S-nitrosothiols react with cysteine residues in ornithin
172 ovide tentative evidence that membrane-bound S-nitrosothiol receptors may exist within the cardiovasc
173 l involves the activation of stereoselective S-nitrosothiol receptors within the cardiovascular syste
174 involve its interaction with stereoselective S-nitrosothiol recognition sites within the vasculature
175 n vivo Using this approach, called SNOxICAT (S-nitrosothiol redox isotope-coded affinity tag), we fou
176 lly slower reaction rates of superoxide with S-nitrosothiols relative to the reaction rate with NO ar
180 O2N) that leads to S-nitrosation to give the S-nitrosothiol RSNO and copper(II) hydroxide [Cu(II)]-OH
182 O oxidation leads to formation of vasoactive S-nitrosothiols (RSNO) in vitro and in vivo as detected
192 ested the effects of one class of NO donors, S-nitrosothiols (RSNOs), on expressed cardiovascular L-t
193 t with the low molecular mass cell-permeable S-nitrosothiol S-nitrosocysteine ethyl ester (SNCEE).
194 otein S-nitrosylation, the colocalization of S-nitrosothiol (S-NO) and protein-tyrosine phosphatase 1
195 t the specific transport of amino acid-based S-nitrosothiols (S-nitroso-L-cysteine and S-nitrosohomoc
197 rate that zinc thiolate bonds are targets of S-nitrosothiol signaling and further indicate that MT-II
198 tHb) on HPV, expired NO (eNO), and perfusate S-nitrosothiol (SNO) concentration in isolated, perfused
204 at in human erythrocytes haemoglobin-derived S-nitrosothiol (SNO), generated from imported NO, is ass
205 (betaCys93) that has been assigned a role in S-nitrosothiol (SNO)-based hypoxic vasodilation by RBCs.
210 x 10(-4) at 3 h vs. 6.5 x 10(-4) (fresh) mol S-nitrosothiol (SNO)/mol Hb tetramer (P = 0.032, mercuri
211 fied 1,276 S-nitrosylated cysteine residues [S-nitrosothiol (SNO)] on 491 proteins in resting hearts
213 hemical reaction products [nitrite, nitrate, S-nitrosothiols (SNO), and nitrotyrosine] before, immedi
214 radigm is well exemplified in bacteria where S-nitrosothiols (SNO)-compounds identified with antimicr
216 ron (iron nitrosyl, FeNO) to cysteine thiol (S-nitrosothiol, SNO) that subserves bioactivation, and i
217 es a family of NO-related molecules and that S-nitrosothiols (SNOs) are central to signal transductio
219 whereas treatments favoring stabilization of S-nitrosothiols (SNOs) decreased its cytotoxic potency.
220 nce that nitric oxide (NO) and/or endogenous S-nitrosothiols (SNOs) exert protective effects in a var
221 chemical data demonstrate a pivotal role for S-nitrosothiols (SNOs) in mediating the actions of nitri
222 ntly through protein S-nitrosylation to form S-nitrosothiols (SNOs) in target proteins, operates coor
224 ward nitric oxide (NO) leads to formation of S-nitrosothiols (SNOs) that play important roles in path
226 modified the biotin switch assay for protein S-nitrosothiols (SNOs), using resin-assisted capture (SN
227 st NO bioactivity is packaged in the form of S-nitrosothiols (SNOs), which are relatively resistant t
228 de synthase (NOS), superoxide dismutase, and S-nitrosothiols (SNOs), which have recently been identif
235 e source of this NO is the already available S-nitrosothiol store rather than de novo synthesis by NO
236 gy through intracellular NO by modulation of S-nitrosothiol stores and stimulation of NOS activity.
237 function as a generator for the formation of S-nitrosothiols such as S-nitrosoglutathione and, as suc
238 y to cause vasodilation as compared to other S-nitrosothiols suggests potential application in biolog
239 ur data provide evidence for a physiological S-nitrosothiol synthase activity of tetrameric Hb that d
240 sothiols was used to explore the kinetics of S-nitrosothiol/thiol transnitrosation and was evaluated
241 RSNO2) intermediate and yields low levels of S-nitrosothiols (thionitrites; RSNO), both of which are
243 -nitroso-L-cysteine (1) and six other simple S-nitrosothiols to Cys 34 of bovine serum albumin (2) ha
244 ) in the enzyme active site on the sulfur of S-nitrosothiols to form a mixed disulfide between the in
246 ncluded ultraviolet-induced decomposition of S-nitrosothiols to liberate NO captured by a florigenic
247 This reaction converts unstable primary S-nitrosothiols to stable disulfide-iminophosphorane pro
248 ormational changes in the toxin enabled host S-nitrosothiols to transnitrosylate the toxin catalytic
250 as to be incompatible with life were all the S-nitrosothiols transformed into bioactive equivalents d
251 n this study, we have examined the effect of S-nitrosothiol transport on intracellular thiol status a
252 resence of L-cystine enhanced GSNO-dependent S-nitrosothiol uptake, increasing the intracellular S-ni
254 urate determination of low concentrations of S-nitrosothiols, utilizing conventional spectroscopic te
258 rred by yeast flavohemoglobin against NO and S-nitrosothiols was seen under both anaerobic and aerobi
260 ackground nitrite and stabilizes erythrocyte S-nitrosothiols, we find the levels of SNO-Hb in the bas
261 a nitrate, nitrite, and low-molecular-weight S-nitrosothiol were in the normal range; however, enhanc
267 nificantly more reactive than MT-I/II toward S-nitrosothiols, whereas the reactivity of all three iso
268 B is reflected in the level of intracellular S-nitrosothiols, which are constitutively metabolized.
269 lowed by reductive generation of thiols from S-nitrosothiols, which are then labeled with either a bi
271 on and thiols, furnishing iron nitrosyls and S-nitrosothiols with wide-ranging stabilities and reacti
272 hanges that occur after exposure of cells to S-nitrosothiol, with respect to thiol chemistry, are dis
273 ing reactive cysteines, we hypothesized that S-nitrosothiols would oxidize PTEN and inhibit its phosp
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