ライフサイエンスコーパス: 3-nitrotyrosine

1 immunohistochemistry of oxidative potential (3-nitrotyrosine).

2 O with epitopes reactive with an antibody to 3-nitrotyrosine.

3 the levels of 3-chlorotyrosine and levels of 3-nitrotyrosine.

4 esence of H(2)O(2) revealed the formation of 3-nitrotyrosine.

5 positive immunostaining of treated cells for 3-nitrotyrosine.

6 entic 3-chlorotyrosine, 3-bromotyrosine, and 3-nitrotyrosine.

7 mage: 3-chlorotyrosine, 3-bromotyrosine, and 3-nitrotyrosine.

8 OS markers gp91(phox), 4-hydroxynonenal, and 3-nitrotyrosine.

9 e nitrogen species which convert tyrosine to 3-nitrotyrosine.

10 of the anthraniloyl group is quenched by the 3-nitrotyrosine.

11 ethod for quantifying free and protein-bound 3-nitrotyrosine.

12 ent oxidant that can modify proteins to form 3-nitrotyrosine.

13 riiodothyronine, gentisate, rosmarinate, and 3-nitrotyrosine.

14 h AbGSC90 and probed with antibodies against 3-nitrotyrosine.

15 n synthesis, atrial natriuretic peptide, and 3'-nitrotyrosine.

16 phy and dysfunction and increased myocardial 3'-nitrotyrosine.

17 used to quantify 3,3'-dityrosine (diTyr) and 3-nitrotyrosine (3-NO2-Tyr) in four regions of the human

18 The presence of 3-nitrotyrosine (3-NT) adducts in Lewy bodies in Parkins

19 nin-1 receptor in the production of striatal 3-nitrotyrosine (3-NT) and l-citrulline (indirect indice

20 Striatal 3-nitrotyrosine (3-NT) concentrations after MPTP were si

21 utathione depletion, lipid peroxidation, and 3-nitrotyrosine (3-NT) formation were measured as indica

22 er of nitrosative stress is the formation of 3-Nitrotyrosine (3-NT) from Tyrosine (Tyr) by adding a n

23 Treatment of tau with ONOO- results in 3-nitrotyrosine (3-NT) immunoreactivity and the formatio

24 oxygen species (ROS), nitric oxide (NO), and 3-nitrotyrosine (3-NT) in Huh7.5.1 cells.

25 3-Nitrotyrosine (3-NT) is formed by the reaction of pero

26 increases of 4-hydroxy-2-nonenal (4-HNE) and 3-nitrotyrosine (3-NT) protein adducts, whereas the cere

27 ed steatosis, lower NOS2 induction, and less 3-nitrotyrosine (3-NT) protein residues, indicating that

28 the selective fluorogenic derivatization of 3-nitrotyrosine (3-NT) residues in peptides (after reduc

29 Hepatic steatosis, 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE), hypoxi

30 Protein expression of 3-nitrotyrosine (3-NT), a marker for the neurotoxin pero

31 4-HNE significantly increased the level of 3-Nitrotyrosine (3-NT), a marker of oxidative stress, in

32 HVA, as well as the significant formation of 3-nitrotyrosine (3-NT), a marker of peroxynitrite genera

33 ETH resulted in the significant formation of 3-nitrotyrosine (3-NT), an in vivo marker of peroxynitri

34 We then assessed 3-nitrotyrosine (3-NT), an indirect index of NO producti

35 y, but higher levels of dihydrobiopterin and 3-nitrotyrosine (3-NT)-modified proteins compared with a

36 and there was marked cellular labelling for 3-nitrotyrosine (3-NT).

37 xidation by immunohistochemical staining for 3-nitrotyrosine (3-NT).

38 ate free radical (A(.-)), NO metabolites and 3-nitrotyrosine (3-NT).

39 Extensive prevalence of 3-nitrotyrosine (3-NT, a stable biomarker of tissue pero

40 vestigated the association between placental 3-nitrotyrosine (3-NTp), a biomarker of oxidative stress

41 for increasing the impact and assessment of 3-nitrotyrosine (3-Nty) as a biomarker for early diagnos

42 3-nitrotyrosine (3-Nty) quenches the luminescence intens

43 Plasma nitrite/nitrate and renal 3-nitrotyrosine (3-NTyr), indicating peroxynitrite forma

44 Cardiac protein nitration (3-nitrotyrosine [3-NT]) and lipid peroxidation were sign

45 However, the 3-nitrotyrosine/3,3'-dityrosine product ratio depended u

46 ted pNO(2)Phe, sulfotyrosine (SO(3)Tyr), and 3-nitrotyrosine (3NO(2)Tyr) at specific sites in murine

47 ly rise in myocardial and peripheral protein-3-nitrotyrosine (3NT) and protein-carbonyl formation tha

48 ues as determined by antibodies specific for 3-nitrotyrosine (3NT) and via mass spectrometry (MS).

49 diseases, and it is evident by detection of 3-nitrotyrosine (3NT) in inflamed tissues.

50 ies for identification and quantification of 3-nitrotyrosine (3NT) post-translationally modified prot

51 Immunohistochemical determination of 3-nitrotyrosine (3NT) residues in liver sections of the

52 onenal (HNE) [a lipid peroxidation product], 3-nitrotyrosine (3NT), and protein carbonyls in the p50

53 nique by identifying an original FET ligand, 3-nitrotyrosine (3NY), for GluR2 (R(o) approximately 24

54 a of healthy subjects had very low levels of 3-nitrotyrosine (9 +/- 7 micromol/mol of tyrosine).

55 ls of PTEN, LKB1-Ser428 phosphorylation, and 3-nitrotyrosine (a biomarker of ONOO-) were significantl

56 f inducible nitric oxide synthase (iNOS) and 3-nitrotyrosine (a stable biomarker of peroxynitrite), a

57 ein in substantia nigra and colocalized with 3-nitrotyrosine, a marker for oxidative protein damage.

58 line, a marker for NO synthase activity, and 3-nitrotyrosine, a marker for peroxynitrite formation, i

59 stology and immunohistochemical detection of 3-nitrotyrosine, a marker of nitrosative stress, were pe

60 d significant increases in concentrations of 3-nitrotyrosine, a marker of peroxynitrite-mediated nitr

61 our hypothesis, we treated L6 myoblasts with 3-nitrotyrosine, a nontoxic inhibitor that resulted in h

62 3-Nitrotyrosine, a product of tyrosine nitration, is use

63 he aromatic ring of free tyrosine to produce 3-nitrotyrosine, a stable product.

64 ated by increases in 4-hydroxy-2-nonenal and 3-nitrotyrosine adduct formation.

65 by Fe-TMPyP pretreatment, and mitochondrial 3-nitrotyrosine adduct levels (peroxynitrite marker) wer

66 ne (GSH) levels, and increased production of 3-nitrotyrosine adducts and protein carbonyl formation.

67 S) formation (nitrite and nitrate levels and 3-nitrotyrosine adducts) increased more profoundly in FP

68 addition, rhAPC limited the increase in lung 3-nitrotyrosine (after 24 hrs [%]: sham, 7 +/- 2; contro

69 nostaining for the protein nitration product 3-nitrotyrosine (all P<.001).

70 diseases has been implicated by detection of 3-nitrotyrosine, an allegedly characteristic protein oxi

71 tic peptide and the oxidative stress markers 3'-nitrotyrosine and 4-hydroxynonenal.

72 a marker of endothelial function, and plasma 3-nitrotyrosine and 24-h urinary excretion rates of free

73 ltrasensitive determination of protein-bound 3-nitrotyrosine and 3, 4-dihydroxyphenylalanine (3-hydro

74 ine oxidation than ONO2- itself and produced 3-nitrotyrosine and 3,3'-dityrosine as the major oxidati

75 y artery disease contains elevated levels of 3-nitrotyrosine and 3-chlorotyrosine.

76 surements showed increased concentrations of 3-nitrotyrosine and 3-nitro-4-hydroxyphenylacetic acid i

77 of reactive oxygen species and mitochondrial 3-nitrotyrosine and 4-hydroxynonenal protein adducts and

78 ione and the immunohistochemical staining of 3-nitrotyrosine and 4-hydroxynonenal.

79 synthase levels determined by Western blot, 3-nitrotyrosine and 4-hydrpxnonenal both assayed by ELIS

80 amage was assessed by immunofluorescence for 3-nitrotyrosine and 8-hydroxydeoxyguanosine and lipid pe

81 novo expression of iNOS and the presence of 3-nitrotyrosine and 8-oxodG formation in the biliary epi

82 ies production, as evidenced by increases in 3-nitrotyrosine and PGIS nitration.

83 formation of the ion pair associate between 3-nitrotyrosine and the optical sensor binuclear Pt-2-py

84 , in vivo administration of statin increased 3-nitrotyrosine and the phosphorylation of AMPK and ACC

85 e, whereas peroxynitrite increased levels of 3-nitrotyrosine and, to a lesser extent, of ortho-tyrosi

86 crease the oxidative productions of protein (3-nitrotyrosine) and lipid (malondialdehyde) and increas

87 detection of inducible NO. synthase (iNOS), 3-nitrotyrosine, and apoptosis in spleen and lymph nodes

88 f malondialdehyde, 4-hydroxynonenal adducts, 3-nitrotyrosine, and inducible nitric oxide synthase in

89 Plasma levels of 3-chlorotyrosine, 3-nitrotyrosine, and o,o'-dityrosine were markedly eleva

90 rosine oxidation products (3-chlorotyrosine, 3-nitrotyrosine, and o,o'-dityrosine) were quantified by

91 ion, and vascular endothelial growth factor, 3-nitrotyrosine, and poly(adenosine diphosphate ribose)

92 g tissue vascular endothelial growth factor, 3-nitrotyrosine, and poly(ribose) expression were attenu

93 onsible for NO production, the expression of 3-nitrotyrosine, and the presence of CD68(+) and/or myel

94 e oxygen species, collectively determined as 3-nitrotyrosine, are associated with bile duct destructi

95 onary artery disease contained twice as much 3-nitrotyrosine as HDL from plasma of healthy subjects,

96 inciple of this method involves reduction of 3-nitrotyrosine at an upstream gold amalgam electrode an

97 rst time, the site-specific incorporation of 3-nitrotyrosine at different regions of alpha-syn using

98 free and HDL-bound forms, apoA-I harboring a 3-nitrotyrosine at position 166 apoA-I (NO2-Tyr(166)-apo

99 ss spectrometry (LC-MS/MS) method to measure 3-nitrotyrosine at very low (picomolar) levels.

100 amage products 3-chlorotyrosine (Cl-Tyr) and 3-nitrotyrosine, both of which increased with disease du

101 otein (CRP), and the oxidative damage marker 3-nitrotyrosine (BSA-3NT) on a silicon nitride substrate

102 y, peroxynitrite (assessed by measurement of 3-nitrotyrosine by high-pressure liquid chromatography)

103 es acid hydrolysis of proteins, isolation of 3-nitrotyrosine by ion exchange chromatography, and redu

104 Attomole levels of 3-nitrotyrosine can be reproducibly measured in this man

105 uced postischemic induction of phospho-Drp1, 3-nitrotyrosine, cleaved caspase-3, and LC-3 II/I, indic

106 At 24 hrs, pulmonary 3-nitrotyrosine concentrations were negatively correlate

107 protected against 3-NP-induced increases in 3-nitrotyrosine concentrations, a marker of peroxynitrit

108 omeric forms of cyt c positively stained for 3-nitrotyrosine confirming the reactivity of NO toward t

109 nzyme-linked immunosorbent assay (ELISA) for 3-nitrotyrosine consistently overestimated aggrecan nitr

110 l studies have used proteomics to screen for 3-nitrotyrosine-containing proteins in vivo, most of the

111 We identified the 3-nitrotyrosine-containing sequences of 11 proteins, inc

112 r the proteomic characterization of specific 3-nitrotyrosine-containing sequences of nitrated target

113 nase and neurogenic locus notch homolog, two 3-nitrotyrosine-containing sequences were identified, i.

114 ation, as indicated by augmented lung tissue 3-nitrotyrosine content (30 +/- 3 vs. 216 +/- 8 nM; p <

115 , and immunohistochemistry showing increased 3-nitrotyrosine content in A vessels.

116 myeloperoxidase with apoA-I and reduced the 3-nitrotyrosine content of apoA-I.

117 3-Nitrotyrosine content was decreased: 0.04 vs. 0.12 mol

118 d 2.9 vs. 1.9 mol% (P < 0.05), respectively; 3-nitrotyrosine content was higher: 0.10 vs. 0.03 mol% (

119 2 ratio (r = -.882; p < .001) and myocardial 3-nitrotyrosine content with stroke volume indexes (r =

120 In PC12 cells, 3-nitrotyrosine decreases intracellular dopamine levels

121 nt (p < 0.05), and formation of lung protein 3-nitrotyrosine derivatives (p < 0.05) was greatest unde

122 not linoleic acid or the nitrated amino acid 3-nitrotyrosine, dose-dependently (0.2 to 1 micromol/L)

123 Specific immunoglobulins that recognize 3-nitrotyrosine epitopes were identified in human lesion

124 evels of circulating immunoglobulins against 3-nitrotyrosine epitopes were quantified in patients wit

125 and 5 of treatment, increased gp91(phox) and 3-nitrotyrosine expression and persistent activation of

126 ry cell infiltration (P =.0064) and elevated 3-nitrotyrosine expression in BECs (P =.0246) compared w

127 Levels of 3-nitrotyrosine failed to increase in mice infected with

128 ratracheal rhSOD decreased the enhanced lung 3-nitrotyrosine fluorescence observed with iNO therapy.

129 phrine and KCl, lung isoprostane levels, and 3-nitrotyrosine fluorescent intensity were measured.

130 We used 3-nitrotyrosine formation (from peroxynitrite) as an ind

131 lectron microscopy demonstrated an increased 3-nitrotyrosine formation (ONOO(-)-specific protein nitr

132 Furthermore, hyperoxia decreased cardiac 3-nitrotyrosine formation and increased inducible nitric

133 f highly reactive peroxynitrite, as shown by 3-nitrotyrosine formation in diseased liver.

134 3-Nitrotyrosine formation in proteins is considered a ha

135 tein structure and function, suggesting that 3-nitrotyrosine formation may not only be a disease mark

136 c oxide (NO) and utilized nitrite to promote 3-nitrotyrosine formation on IDO.

137 With tyrosine in excess, the rate of 3-nitrotyrosine formation was independent of the tyrosin

138 dative/nitrative stress (lipid peroxidation, 3-nitrotyrosine formation, and expression of reactive ox

139 Ang II promotes a rapid increase in 3-nitrotyrosine formation, and uric acid attenuates Ang

140 Ischemia also increased 3-nitrotyrosine formation, which was significantly reduc

141 n modifications through NO(2) production and 3-nitrotyrosine formation.

142 mitochondrial respiratory capacity and lower 3-nitrotyrosine formation.

143 d by increased striatal protein carbonyl and 3-nitrotyrosine formation.

144 Free 3-nitrotyrosine (free-3NT) is also elevated in these set

145 t sustained activation of NADPH oxidase with 3-nitrotyrosine generation and nuclear factor-kappaB act

146 Detection of 3-nitrotyrosine has served as an in vivo marker for the

147 escence donor (anthranilamide) and quencher (3-nitrotyrosine), has been examined for ATP-dependent de

148 3-Nitrotyrosine-, heme oxygenase-1-, and malondialdehyde

149 2 months, Tg2576 mice demonstrated increased 3-nitrotyrosine immunoreactivity in cholinergic projecti

150 In the present study we found increased 3-nitrotyrosine immunoreactivity in the substantia nigra

151 of reactive oxidant species as indicated by 3-nitrotyrosine immunoreactivity increased in these regi

152 , known to be protected against ischemia, no 3-nitrotyrosine immunoreactivity is detected.

153 In contrast, 3-nitrotyrosine immunoreactivity is restricted to the in

154 Increased 3-nitrotyrosine immunoreactivity was observed in motor n

155 with cerebral ischemia also showed increased 3-nitrotyrosine immunoreactivity.

156 nous ONOO- increased proteasome activity and 3-nitrotyrosine in 26S proteasome.

157 eroxidase association with apoA-I as well as 3-nitrotyrosine in apoA-I.

158 ing HDL but that other pathways also produce 3-nitrotyrosine in atherosclerotic tissue.

159 free 3-chlorotyrosine, 3-bromotyrosine, and 3-nitrotyrosine in biological fluids in a single, rapid

160 ng not only free amino acid but also protein 3-nitrotyrosine in biological fluids.

161 as been developed to determine the levels of 3-nitrotyrosine in biological samples.

162 n2+-superoxide dismutase and the presence of 3-nitrotyrosine in CD4+ and ED-1-positive inflammatory c

163 omotes the formation of 3-chlorotyrosine and 3-nitrotyrosine in circulating HDL but that other pathwa

164 We also detected 3-nitrotyrosine in circulating HDL, and linear regressio

165 The mean level of 3-nitrotyrosine in HDL isolated from human aortic athero

166 The detection of 3-nitrotyrosine in HDL raises the possibility that react

167 free 3-chlorotyrosine, 3-bromotyrosine, and 3-nitrotyrosine in human plasma.

168 - in vivo is based largely upon detection of 3-nitrotyrosine in injured tissues.

169 onary vascular phenotype and the presence of 3-nitrotyrosine in invading inflammatory cells.

170 The detection of 3-nitrotyrosine in LDL isolated from vascular lesions ra

171 ine, a specific product of MPO, and those of 3-nitrotyrosine in lesion HDL.

172 on of PGHS-1 was confirmed by the absence of 3-nitrotyrosine in lesions from ApoE(-/-)iNOS(-/-) mice.

173 presence of bile duct infiltrating cells and 3-nitrotyrosine in PBC with an increase dominant in earl

174 itol, significantly increased superoxide and 3-nitrotyrosine in PGI(2) synthase (PGIS).

175 lts in the formation of 3-chlorotyrosine and 3-nitrotyrosine in ratios that are similar to those obta

176 Detection of 3-nitrotyrosine in the asthmatic lung confirms the prese

177 3 and IK1 protein, superoxide (O(2)(-)), and 3-nitrotyrosine in the endothelium of SMAs.

178 0% oxygen had increased immunopositivity for 3-nitrotyrosine in the hippocampus and increased lipid p

179 itioning of macrophages induced formation of 3-nitrotyrosine in the PP2Ac associated with VCP/p97, a

180 ides additional evidence for the identity of 3-nitrotyrosine in the sample.

181 dly increased levels of o, o'-dityrosine and 3-nitrotyrosine in the striatum and midbrain but not in

182 wo percent of PBC had elevated expression of 3-nitrotyrosine in their bile duct epithelial cells (BEC

183 Immunohistochemistry analysis for 3-nitrotyrosine in tissue after CAS and 1 hour reperfusi

184 chromatography/mass spectrometry to quantify 3-nitrotyrosine in two models of peritoneal inflammation

185 Both MPO and peroxynitrite produce 3-nitrotyrosine in vitro.

186 es hydrogen peroxide and nitrite to generate 3-nitrotyrosine in vitro.

187 oxygen species and the peroxynitrite marker 3-nitrotyrosine in wild-type mice but not in nox2 nulls.

188 yrosine, meta-tyrosine, o,o'-dityrosine, and 3-nitrotyrosine -- in aortic proteins.

189 eloped recombinant apoA-I with site-specific 3-nitrotyrosine incorporation only at position 166 using

190 PGHS-2 was also found in lesions, but 3-nitrotyrosine incorporation was not detected.

191 3-Nitrotyrosine induced loss of tyrosine hydroxylase-pos

192 In NT2 cells, incorporation of 3-nitrotyrosine into alpha-tubulin induces a progressive

193 3-Nitrotyrosine is a relatively specific marker for oxid

194 In both cell lines, 3-nitrotyrosine is a substrate for tyrosine tubulin liga

195 3-Nitrotyrosine is a useful marker for nitric oxide-medi

196 3-Nitrotyrosine is quantified by the amount of the curre

197 Herein, we show that extracellular 3-nitrotyrosine is transported via the l-aromatic amino

198 NO2Tyr (3-Nitrotyrosine) is a modified amino acid that is formed

199 examined for invading inflammatory cells and 3-nitrotyrosine labeling, a marker of oxidative/nitrosat

200 ogen species in atherogenesis, we quantified 3-nitrotyrosine levels in HDL in vivo.

201 ic oxide (NO) synthase, total NO levels, and 3-nitrotyrosine levels in lung tissue.

202 matography and mass spectrometry to quantify 3-nitrotyrosine levels in proteins.

203 Quantifying 3-nitrotyrosine levels of tissues by stable isotope dilu

204 In striking contrast, 3-nitrotyrosine levels rose only in the mice infected wi

205 MPTP-induced increases in free 3-nitrotyrosine levels were blocked in Bcl-2 overexpress

206 Hippocampal 3-nitrotyrosine levels were determined by immunohistoche

207 ressing high levels of wild-type human SOD1, 3-nitrotyrosine levels were elevated by 2- to 3-fold in

208 was found in tissues in which apoptosis and 3-nitrotyrosine levels were highly elevated within speci

209 lung levels of oxidative damage to proteins (3-nitrotyrosine), lipids (8-isoprostane), and nucleic ac

210 drogenase, protein carbonyl (marker of ROS), 3-nitrotyrosine (marker of RNS), poly(adenosine diphosph

211 rkers, among which are protein carbonyls and 3-nitrotyrosine, markers for protein oxidation.

212 ) to PN and identified the major metabolite, 3-nitrotyrosine-methionine-sulfoxide (NSO)-MENK, using l

213 That iNOS-derived NO is essential for 3-nitrotyrosine modification of PGHS-1 was confirmed by

214 al loss of activity is a result of increased 3-nitrotyrosine modification of the Ca-ATPase.

215 entified the active site residue Tyr385 as a 3-nitrotyrosine modification site in purified PGHS-1 exp

216 Ebselen decreased the abundance of 3-nitrotyrosine-modified proteins in ZDF rats.

217 on, liver and kidney NOS2 expression, tissue 3-nitrotyrosine (NO(2)Tyr) formation and apoptosis were

218 rometry we demonstrate a 10-fold increase in 3-nitrotyrosine (NO(2)Y) content, a global marker of pro

219 ET, R2 was synthesized with Y356 replaced by 3-nitrotyrosine (NO(2)Y).

220 3-Nitrotyrosine (NO(2)Y, pK(a) 7.1) has been incorporate

221 lmonary parenchymal inflammation, and tissue 3-nitrotyrosine (NO2 Y) were increased to a greater exte

222 udomonas aeruginosa azurins that incorporate 3-nitrotyrosine (NO2YOH) between Ru(2,2'-bipyridine)2(im

223 of NO with O2- were non-toxic, did not form 3-nitrotyrosine, nor did they elicit any signal transduc

224 l hyperalgesia was associated with increased 3-nitrotyrosine (NT), a PN biomarker, in the RVM.

225 The identification of 15N-labeled 3-nitrotyrosine (NTyr) by gas chromatography/mass spectr

226 ted with myocardial oxidative stress markers 3'-nitrotyrosine or 4-hydroxynonenal expression (P<0.05)

227 rdial and pulmonary tissue concentrations of 3-nitrotyrosine (p = .041 and p = .042 vs. controls, res

228 WI group displayed higher protein carbonyls, 3-nitrotyrosine, PAR, lactate dehydrogenase and proteins

229 de production and greater immunostaining for 3-nitrotyrosine, particularly on the endothelial surface

230 e unaltered and nitric oxide metabolites and 3-nitrotyrosine peptide levels remained unchanged in Cu-

231 Intracellular levels of 133 micromol of 3-nitrotyrosine per mole of tyrosine did not alter NT2 v

232 xidation as detected by Western blotting for 3-nitrotyrosine (peroxynitrite biomarker) and protein ca

233 this hypothesis, we demonstrate that an anti-3-nitrotyrosine polyclonal antibody stains all of the ma

234 ignificantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitri

235 levating reactive oxygen species, increasing 3-nitrotyrosine production by microglia, and reducing th

236 say involves spectrophotometric detection of 3-nitrotyrosine production from 3-nitrophosphotyrosine c

237 ilar effect as NBO treatment on NO(x)(-) and 3-nitrotyrosine production, and when combined with NBO,

238 different peroxynitrite concentrations, and 3-nitrotyrosine products were measured.

239 3-Nitrotyrosine protein adducts were detected only in fa

240 inducible nitric oxide synthase, and higher 3-nitrotyrosine protein adducts were found in livers of

241 Levels of inducible nitric oxide synthase, 3-nitrotyrosine protein adducts, malondialdehyde, and pr

242 of 4-hydroxynonenal (lipid peroxidation) and 3-nitrotyrosine (reactive nitrogen species formation) pr

243 revious in vitro studies have suggested that 3-nitrotyrosine represents a specific marker of protein

244 rs of inhaled NO revealed a 90% reduction in 3-nitrotyrosine residues (P<0.05) in PD156707-treated la

245 at peroxynitrite modification resulting in a 3-nitrotyrosine signature is predominantly associated wi

246 s a critical step toward the production of a 3-nitrotyrosine-specific protease useful for proteomic a

247 administration of metformin, which increased 3-nitrotyrosine staining in hearts of C57BL6, resulted i

248 also improved lung morphology and suppressed 3-nitrotyrosine staining in the lungs after LPS.

249 n that was also reflected in lower levels of 3-nitrotyrosine staining in the SP-A(-/-) group.

250 The 3-nitrotyrosine staining intensity was not different.

251 Both apoptotic nuclei and 3-nitrotyrosine staining were found in cells juxtaposed

252 myocardial oxidative stress, as assessed by 3-nitrotyrosine staining, reduced expression of the adhe

253 itration was not detected in PWMI lesions by 3-nitrotyrosine staining.

254 out mice in which metformin had no effect on 3-nitrotyrosine staining.

255 Levels of 3-nitrotyrosine strongly correlated with levels of 3-chl

256 on exchange chromatography, and reduction of 3-nitrotyrosine to 3-aminotyrosine with dithionite.

257 biguously through the actual localization of 3-nitrotyrosine to specific sequences by mass spectromet

258 In vitro studies demonstrated that 3-nitrotyrosine was a highly specific marker for LDL oxi

259 The presence of 3-nitrotyrosine was closely associated with infiltrating

260 lating immunoglobulins against protein-bound 3-nitrotyrosine was documented in patients with CAD (3.7

261 3-Nitrotyrosine was notably increased in the media of th

262 se of 3- to 10-fold in the levels of protein 3-nitrotyrosine was observed in the blood plasma, and a

263 nitric oxide synthase (iNOS), gp91-phox, and 3-nitrotyrosine were detected in ischemic wounds, indica

264 NO(x)(-) (nitrite plus nitrate) and 3-nitrotyrosine were measured in the ischemic cortex.

265 ncreases in the immunoprevalence of iNOS and 3-nitrotyrosine were not evident until 4 h post-LPS.

266 neuronal nitric oxide synthase and increased 3-nitrotyrosine were observed in striatum of Nurr1 heter

267 Concentrations of 3-nitrotyrosine were significantly increased in the cere

268 ta-tyrosine, and o,o'-dityrosine, but not of 3-nitrotyrosine, were significantly higher in aortic tis

269 undergoes nitration in nitric acid to yield 3-nitrotyrosine, which has a lambdamax of 358 nm.

270 Intrastriatal injection of 3-nitrotyrosine, which is a biomarker for nitrating oxid

271 els of a 32-kDa cellular protein modified by 3-nitrotyrosine, which is a hallmark of NO production, w

272 NOS2-expressing TMCs stained positively for 3-nitrotyrosine, which is a marker for peroxynitrite for

273 T that selectively hydrolyzes peptides after 3-nitrotyrosine while effectively discriminating against

274 )EWL, in which 2-aminobenzoic acid (Abz) and 3-nitrotyrosine (Y(NO2)) were used as the fluorescent do