ライフサイエンスコーパス: SOD

1 SOD achieved the best peptide recovery ( approximately 2

2 SOD activity in both serum (P <0.05) and saliva (P <0.00

3 SOD activity was determined using an SOD assay and enzym

4 SOD, CAT, GST, GSH, vitamin E and C levels were high in

5 SOD, GR, and CAT activities in red blood cell lysate and

6 SOD, which catalyses the dismutation of superoxide into

7 antioxidant enzymes: superoxide-dismutase 1 (SOD-1), SOD-2, and catalase through different mechanisms

8 Here, we show superoxide dismutase-1 (SOD-1), an enzyme that converts superoxide into less tox

9 ant enzymes: superoxide-dismutase 1 (SOD-1), SOD-2, and catalase through different mechanisms, which

10 (SIRT1) activity and superoxide dismutase-2 (SOD-2) expression in ECs.

11 ion of HO-1, but not superoxide dismutase-2 (SOD-2), was also observed in response to 5-LO (AA861) or

12 2+)-substituted superoxide dismutase (Co(2+)-SOD).

13 Deletion of a SOD-encoding gene under MoSir2 control generated Deltaso

14 ymal transition, cancer cells also undergo a SOD switch during transformation.

15 Ab/SOD enlargement from about 100 to 300nm enhanced amount

16 thway, we conjugated SOD with antibodies (Ab/SOD, size 10nm) to plasmalemmal vesicle-associated prot

17 Both Ab/SOD conjugates targeted to Plvap and CD31 accumulated in

18 ulture with much lower efficacy than CD31 Ab/SOD, yet blocked the effects of LPS signaling with highe

19 ignaling with higher efficiency than CD31 Ab/SOD.

20 ast, enlargement inhibited endocytosis of Ab/SOD and diminished mitigation of inflammatory signaling

21 , both geometry and targeting features of Ab/SOD conjugates control delivery to cell surface vs. endo

22 face vs. endosomal delivery and effect of Ab/SOD, focusing on conjugate size and targeting to PECAM v

23 tibodies to cell adhesion molecule PECAM (Ab/SOD) inhibits pro-inflammatory signaling mediated by end

24 Plvap Ab/SOD bound to endothelial cells in culture with much lowe

25 embrane domains by filipin inhibits Plvap Ab/SOD endocytosis and LPS signaling, implicating the caveo

26 ICAM-targeted Ab/SOD more effectively mitigated inflammatory signaling by

27 ke was inferior to that of PECAM-targeted Ab/SOD.

28 ncounters pathogenic bacteria P. aeruginosa, SOD-1 is induced in the ASER neuron.

29 In Fisher 344 rats, VWR increased eNOS, all SOD isoforms and TAC in kidney.

30 SOD activity was determined using an SOD assay and enzyme-linked immunosorbent assay reader a

31 [exp(beta) = 1.09-1.78, p < 0.01-0.04)] and SOD activity [exp(beta) = 1.13-1.48, p < 0.01-0.05)] lev

32 bic acid (AA), antioxidant capacity (AC) and SOD activity decreased while POX activity increased duri

33 fragments of MAP antigens (Ag85A, Ag85B and SOD) that imparted protection against challenge in a mou

34 ns in the levels of antioxidant capacity and SOD activity between ALD phenotypes in patients with cAL

35 e assayed for total antioxidant capacity and SOD activity.

36 lly available total antioxidant capacity and SOD assays were performed on samples of monocytes and bl

37 gulate the antioxidant proteins catalase and SOD and the antiapoptotic proteins Bcl-2 and Bcl-xL.

38 Furthermore, GST and SOD activities of trout exposed to both Se-Met and paras

39 ose of enzymes from erythrocytes of hens and SOD standard.

40 der and no correlation between E2 levels and SOD activity was found using multiple linear regression.

41 inverse relationship between HsrA levels and SOD activity, suggesting that HsrA may serve as a repres

42 esent study was to investigate E2 levels and SOD erythrocyte activity in patients with age-related ca

43 rms of changes in periodontal parameters and SOD activity in patients with CP.

44 Periodontal parameters and SOD activity were evaluated after 3 months.

45 re performed with radioimmunoassay (RIA) and SOD activity was measured in erythrocyte lysates.

46 Unit-wide application of SDD and SOD was associated with low levels of antibiotic resista

47 nstrate that miR-126 also controls SIRT1 and SOD-2 expression, thus confirming its role in driving Un

48 y exchanging metal cofactors for antioxidant SODs.

49 Average SOD activity in egg yolk was 98.5+/-19.5U.g(-1) while in

50 No correlation was seen between SOD activity and age or gender and no correlation betwee

51 dels] showed the integrity of the Zn-binding SOD/ADH under the OFFGEL electrophoretic conditions.

52 sis as a unifying general mechanism for both SOD aggregation and ALS disease progression, with implic

53 t 100 to 300nm enhanced amount of cell-bound SOD and protection against extracellular superoxide.

54 ring salt stress gets converted into H2O2 by SOD and its optimum level was maintained by APX.

55 1DM mesenteric arteries, which is rescued by SOD mimetic tempol or gene transfer of SOD3.

56 redox-active copper ion, and in most cases, SODs also harbor a zinc at the active site that enhances

57 s (ethoxyresorufin-O-deethylase (EROD), CAT, SOD, and GR) were also determined.

58 of Shh expression in the hypothalamus cause SOD.

59 r crowding on the size of a protein complex, SOD (superoxide dismutase).

60 mpaired rice defence suppression, confirming SOD activity as a downstream output of MoSir2.

61 bit this pathological pathway, we conjugated SOD with antibodies (Ab/SOD, size 10nm) to plasmalemmal

62 ensures that C. albicans maintains constant SOD activity for cytosolic antioxidant protection despit

63 However, a new class of copper-containing SODs has recently emerged that function without zinc.

64 CuZn-superoxide dismutase (CuZn-SOD) and ascorbate peroxidase (APX) constitute first lin

65 C. albicans adjusted its cytosolic SODs accordingly and expressed Cu-Sod1 at early stages o

66 and selective oropharyngeal decontamination (SOD) are prophylactic antibiotic regimens used in intens

67 ant-aided precipitation/on-pellet digestion (SOD) method, and MAM proteome was quantified by an ion-c

68 ant-aided-precipitation/on-pellet-digestion (SOD) strategy that provides effective sample cleanup and

69 ivity and expression), superoxide dismutase (SOD) (activity and expression) and glutathione peroxidas

70 -transferase (GST) and superoxide dismutase (SOD) activities.

71 stigates the levels of superoxide dismutase (SOD) activity in serum and saliva of patients with chron

72 ich result from higher superoxide dismutase (SOD) activity, associated with lower catalase (CAT) and

73 etal-binding proteins [superoxide dismutase (SOD) and alcohol dehydrogenase (ADH) as protein models]

74 idant enzyme activity, superoxide dismutase (SOD) and glutathione peroxidase (GPx), vitamin E, lipid

75 but they were not when superoxide dismutase (SOD) and tert-butyl alcohol were used.

76 Finally, direct superoxide dismutase (SOD) assays showed an inverse relationship between HsrA

77 The antioxidant enzyme superoxide dismutase (SOD) catalyzes the dismutation of highly reactive O2 (-)

78 hondrial ROS scavenger superoxide dismutase (SOD) caused a significant increase in segregation errors

79 membrane delivery of a superoxide dismutase (SOD) enzyme embedded in MSN was demonstrated.

80 peroxidase (POX), and superoxide dismutase (SOD) enzymes activities were measured during storage.

81 the beneficial role of superoxide dismutase (SOD) enzymes against paraquat-induced toxicity, as well

82 s the bimetallic Cu/Zn superoxide dismutase (SOD) enzymes play important roles in the biology of reac

83 y to activate the SodA superoxide dismutase (SOD) essential for virulence.

84 ization by controlling superoxide dismutase (SOD) gene expression.

85 The activity of superoxide dismutase (SOD) in Brassica rapa also displayed a growth-stage depe

86 ARS), and catalase and superoxide dismutase (SOD) in liver, heart and kidney decreased significantly

87 Cu,Zn-superoxide dismutase (SOD) is a key antioxidant enzyme that detoxifies intrace

88 Superoxide dismutase (SOD) level in the blood samples expressed significant po

89 tioxidant capacity and superoxide dismutase (SOD) levels between phenotypes may allow for the generat

90 Accordingly, a superoxide dismutase (SOD) mimetic compound and SOD2 overexpression provided a

91 ns in heritable Cu, Zn superoxide dismutase (SOD) mutants cause misassembly and aggregation in cells

92 dition of catalase and superoxide dismutase (SOD) prevented the hydroxyl radical driven-degradation o

93 superoxide by specific superoxide dismutase (SOD) showed the applicability for selective in vitro ROS

94 e-S-transferase (GST), superoxide dismutase (SOD)), and fish health (condition factor (K), hepatosoma

95 through the action of superoxide dismutase (SOD), and against hydrogen peroxide (H2O2) via peroxidas

96 ced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT).

97 ies of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) and the levels of

98 luding catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) in vivo.

99 and activity of total superoxide dismutase (SOD), and its mitochondrial (Mn-SOD) and cystolic (Cu,Zn

100 tioxidant enzymes viz. superoxide dismutase (SOD), ascorbate peroxidase (APX), guaiacol peroxidase (G

101 Activities of superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD) decreased at a

102 ant activities such as superoxide dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST) an

103 ith reduction in liver superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and glut

104 f baseline erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) a

105 of antioxidant enzymes superoxide dismutase (SOD), glutathione reductase (GR), and catalase (CAT) as

106 and the activities of superoxide dismutase (SOD), glutathione S-transferase (GST) and total glutathi

107 hibits the activity of superoxide dismutase (SOD), magnifying the imbalance of redox status of E. col

108 nsor method based on a superoxide dismutase (SOD), while the increasing toxicity was monitored using

109 nly when stimulated by superoxide dismutase (SOD)-1.

110 t agent and a mimic of superoxide dismutase (SOD).

111 ant enzymes, including superoxide dismutase (SOD).

112 we tested a synthetic superoxide dismutase (SOD)/catalase mimetic, EUK-207, in a rat model of combin

113 nsferase P (GSTP) and superoxide dismutases (SOD).

114 Superoxide dismutases (SODs) are metalloproteins that protect organisms from to

115 nclude iron-dependent superoxide dismutases (SODs) in mitochondria and glycosomes.

116 The copper-containing superoxide dismutases (SODs) represent a large family of enzymes that participa

117 chloroplast-localized superoxide dismutases (SODs), which are known to be dependent on copper, were n

118 racellular membranes, cells express distinct SOD isoforms in the cytosol (Cu,Zn-SOD) and mitochondria

119 Day 28-mortality was 25.4% and 24.1% during SOD and SDD, respectively (adjusted odds ratio, 0.96 [95

120 g SDD and 11.8% (95% CI, 10.3%-13.2%) during SOD (P < .001).

121 .02) and 4% per month (95% CI, 0%-8%) during SOD (P = .046; P = .40 for difference).

122 rred in 5.9% and 4.6% of the patients during SOD and SDD, respectively (odds ratio, 0.77 [95% CI, 0.6

123 ld concept of sphincter of Oddi dysfunction (SOD) type III is discarded.

124 ficance of pancreatic sphincter dysfunction (SOD).

125 Septo-optic dysplasia (SOD) is a congenital brain anomaly that results in pitui

126 Both strains increased eNOS and EC SOD in lung with VWR.

127 Sprague-Dawley rats, VWR reduced eNOS and EC SOD, but increased Mn SOD in kidney.

128 the effect of exercise on kidney eNOS and EC SOD, which in turn influence the susceptibility to AKI.

129 ) and extracellular superoxide dismutase (EC SOD), in kidney and lung, and other SOD isoforms and tot

130 EC-SOD plays a key role in preserving angiogenesis by scave

131 nzyme extracellular superoxide dismutase (EC-SOD KO) showed reduced sensitivity to radiation-induced

132 Extracellular superoxide dismutase (EC-SOD) is the main antioxidant enzyme in the extracellular

133 nzyme extracellular superoxide dismutase (EC-SOD; SOD3) is a major antioxidant defense in lung and va

134 tivity correlates closely with endogenous EC-SOD expression, although several interesting differences

135 is in agreement with published endogenous EC-SOD gene expression studies.

136 onomous single-nucleotide polymorphism in EC-SOD (rs1799895) leads to an arginine to glycine amino ac

137 cognitive functions, and that high-level EC-SOD may provide protection against irradiation-related d

138 Thus, the 5'-flanking region of mouse EC-SOD gene is responsible, at least in part, for cell spec

139 ents flanking the 5' region of the murine EC-SOD gene.

140 activity, but shifted the distribution of EC-SOD from lung and vascular tissue to extracellular fluid

141 ative stress: thus, the redistribution of EC-SOD from the lung and pulmonary circulation to the extra

142 However, high levels of EC-SOD in the granule cell layer supported normal maturatio

143 Taken together, our data suggest that EC-SOD plays an important role in all stages of hippocampal

144 We conclude that EC-SOD provides optimal protection when localized to the co

145 developed transgenic mice to analyze the EC-SOD promoter activity in vivo in real time and to identi

146 organelle-specific overexpression of either SOD in Jurkat T cell lines increases intracellular produ

147 ble to compensate for the loss of endogenous SOD enzymes, acting both at a cytosolic and mitochondria

148 ion for the mitochondrial antioxidant enzyme SOD-2 during hepatic inflammatory stress.

149 0 nmol/liter), as reported for extracellular SOD.

150 It is the only form of extracellular SOD in fungi and oomycetes, in stark contrast to the ext

151 vascular-specific deletion of extracellular SOD) and have shown that these animals develop vascular

152 e copper-only enzymes serve as extracellular SODs in specific bacteria (i.e. Mycobacteria), throughou

153 Structural analysis comparing both Fe-SOD isoforms reveals differences in key cysteines and tr

154 d previously for Escherichia coli Mn- and Fe-SODs and mammalian Mn-SOD, whereas Fe-SODB was exception

155 nitrite-mediated inactivation of T. cruzi Fe-SODs is due to the site-specific nitration of the critic

156 ely iron-dependent superoxide dismutases (Fe-SODs) located in different subcellular compartments.

157 by defining the size and shape of fibrillar SOD aggregates after mild biochemical perturbations.

158 ncluded in the clinical outcome analysis for SOD and SDD, respectively.

159 A technology, that SIRT1 is also crucial for SOD-2 expression.

160 roups for all the enzymes studied except for SOD in blood.

161 ving the framework types FAU, LTA, EMT, GIS, SOD, ANA, CAN, and JBW.

162 a, IL-6, and IL-8, and increased IL-10, GSH, SOD, and CAT levels.

163 tivities with an elevation in levels of GSH, SOD, GST and t-GPx activities.

164 fish protein groups had lower GSH and higher SOD activities, the pork protein group showed lower Grx1

165 associated with 1-standard deviation higher SOD, GPx, and CAT activities were 1.07 (95% confidence i

166 sical techniques to six ALS mutants at human SOD hotspot glycine 93.

167 nism catalyzed by the NiSOD maquette {Ni(II)(SOD(m1))} (SOD(m1) = HCDLP CGVYD PA).

168 These studies suggest that the {Ni(II)(SOD(m1))} active-site possesses a Ni(II)-S(H(+))-Cys(6)

169 formulated active-site structure of {Ni(II)(SOD(m1))} suggests that O2(-) reduction takes place thro

170 he detailed active-site structure of {Ni(II)(SOD(m1))}.

171 Changes in SOD activity of the egg yolk during its storage for 200d

172 during meiosis I is significantly greater in SOD knockdown oocytes than in controls.

173 The L(OH) complex maintains its SOD activity in the presence of (*)OH and Mn(IV)-oxo spe

174 Sneaky little SOD!

175 Systemic and local SOD levels are lowered in CP.

176 ar oxidation level, but higher GSH and lower SOD activities.

177 zed by the NiSOD maquette {Ni(II)(SOD(m1))} (SOD(m1) = HCDLP CGVYD PA).

178 nt enzyme expression through Nfe2l2-mediated SOD-2 expression in sepsis.

179 is protective role, Leishmania mitochondrial SOD may also initiate H2O2-mediated redox signaling that

180 the specific role of SODA, the mitochondrial SOD isoform in Leishmania amazonensis Our inability to g

181 WR reduced eNOS and EC SOD, but increased Mn SOD in kidney.

182 e but not by azide, which inhibits Fe and Mn SODs.

183 richia coli Mn- and Fe-SODs and mammalian Mn-SOD, whereas Fe-SODB was exceptionally resistant to oxid

184 the cytosol (Cu,Zn-SOD) and mitochondria (Mn-SOD), where they locally scavenge O2 (-) leading to prod

185 e dismutase (SOD), and its mitochondrial (Mn-SOD) and cystolic (Cu,Zn-SOD) isoform were measured.

186 We report that overexpression of Mn-SOD enhances tyrosine phosphorylation of TCR-associated

187 laucoma group (p = 0.003); serum level of Mn-SOD was significantly lower in glaucoma patients (p = 0.

188 y antioxidant enzymes, such as Cu/Zn-SOD, Mn-SOD, CAT, GR, and guaiacol peroxidase, were also determi

189 verall homology with other members of the Mn-SOD family, but computer-assisted modeling revealed some

190 This toggling between Cu- and Mn-SODs is controlled by the Cu-sensing regulator Mac1 and

191 oor environment, the opposite is true for Mn-SODs of organisms such as Escherichia coli and bakers' y

192 These Mn-SODs still capture manganese in an iron-rich cell, and w

193 tify distinguishing attributes of ALS mutant SOD proteins that correlate with clinical severity by ap

194 T and MDA along with decreased activities of SOD and CAT were significantly (p<0.01) ameliorated by S

195 Overall, activities of SOD, GPx, and CAT were not associated with CHD among wom

196 All rice grains increased the activity of SOD and GPx.

197 Further analysis of SOD activity in biobank samples showed significant reduc

198 Controlled endothelial delivery of SOD may alleviate abnormal local surplus of superoxide i

199 e results indicate that targeted delivery of SOD to specific cellular compartments may offer effectiv

200 pective hypothalamus exhibit key features of SOD, including pituitary hypoplasia and absence of the o

201 that an adjunct to the accepted mechanism of SOD catalysed dismutation of superoxide operates, with C

202 (NiSOD maquettes) to probe the mechanism of SOD catalysis facilitated by NiSOD, we computationally e

203 r molecules impact the rate and mechanism of SOD catalysis.

204 cellular levels of Mn-antioxidant mimics of SOD.

205 mized crossover trial comparing 12 months of SOD with 12 months of SDD in 16 Dutch ICUs between Augus

206 The performance of SOD was systematically compared against in-solution-dige

207 arly established an antioxidant potential of SOD-MC that exhibited the highest radical-scavenging act

208 I of 6.30+/-0.15 was confirmed in samples of SOD extracted from egg yolk.

209 are a cheap and easily obtainable source of SOD, this enzymatic protein could be used in food, cosme

210 s of gyration to changes in the structure of SOD.

211 40% PEG solution, we find that the volume of SOD was reduced by 9%.

212 not support a role for E2-induced effects on SOD in cataract formation.

213 SOD, while MALDI-TOF analysis confirmed only SOD from erythrocytes.

214 we demonstrate that this curious copper-only SOD occurs throughout the fungal kingdom as well as in p

215 ODs and discuss the evolution of copper-only SOD protein domains in animals and fungi.

216 Copper-only SOD sequences similar to those seen in fungi and oomycet

217 ndida albicans expresses a novel copper-only SOD, known as SOD5, that lacks the zinc cofactor and ele

218 lypeptides we refer to as CSRPs (copper-only SOD-repeat proteins).

219 re and contrast the Cu,Zn versus copper-only SODs and discuss the evolution of copper-only SOD protei

220 The eukaryotic copper-only SODs are particularly unique in that they lack an electr

221 Copper-only SODs are virulence factors for certain fungal pathogens;

222 oaches we demonstrate that these copper-only SODs have evolved with a specialized active site consist

223 n Cu/Zn-SODs and have evolved in copper-only SODs to control catalysis and copper binding in lieu of

224 were randomized to administer either SDD or SOD.

225 tase (EC SOD), in kidney and lung, and other SOD isoforms and total antioxidant capacity (TAC), in ki

226 Bax-caspase-3 proteins and by increasing p53-SOD-2 co-localization; (iii) accelerated germ cell cyst

227 Physiological parameters, SOD, POD, PPO, CAT activity, free proline, soluble prote

228 Plasma SOD levels from patients with cALD demonstrated an inver

229 Plasma SOD may serve as a potential biomarker for cerebral dise

230 Longitudinal plasma SOD samples from the same patients (n = 4) showed decrea

231 evidence for biliary obstruction (previously SOD type II, now called "Functional Biliary Sphincter Di

232 idation and pharmacokinetic studies in rats, SOD outperformed other methods and provided highly accur

233 Serum and salivary SOD activity in 38 patients with CP were compared with t

234 Only salivary SOD and GR activities were significantly different in th

235 Serum SOD levels in TG-2 increased even above the level of the

236 ochondrial (Fe-SODA) and cytosolic (Fe-SODB) SODs with second order rate constants of 4.6 +/- 0.2 x 1

237 longed P. aeruginosa exposure, ASER-specific SOD-1 expression is diminished.

238 es postulated for the propensity of specific SOD mutants to cause ALS.

239 cilitate the PCET necessary for outer-sphere SOD activity.

240 ical parameters, such as antioxidant status (SOD, CAT, GPX and GSH) and lipid peroxidation was also s

241 Targeting SOD to endothelial surface vs. intracellular compartment

242 The effectiveness of FMSN-TAT-SOD as an agent against ROS was investigated, which incl

243 Results suggested that FMSN-TAT-SOD may provide a strategy for the therapeutic delivery

244 ristic nonendosomal distribution of FMSN-TAT-SOD.

245 was conjugated to FITC-MSN forming FMSN-TAT-SOD.

246 The purified TAT-SOD was conjugated to FITC-MSN forming FMSN-TAT-SOD.

247 The His-tagged TAT-SOD fusion protein was expressed in E. coli using IPTG i

248 to produce a genetic in-frame His-tagged TAT-SOD fusion protein.

249 fy the associations, with the exception that SOD activity was positively associated with the risk of

250 To test the hypothesis that SOD delivery to caveolae may specifically inhibit this p

251 FISH analysis indicated that SOD knockdown moderately increased the percentage of ooc

252 Administration of the SOD mimetic mito-tempol or the NADPH oxidase inhibitor a

253 lear accumulation and high expression of the SOD-3 gene (a DAF-16-specific target gene) were observed

254 as well as the therapeutic potential of the SOD-mimetic compound M40403.

255 was no evidence for iron inactivation of the SOD.

256 In summary, the SOD method has proven to be highly robust, efficient and

257 ly captures extracellular copper, make these SODs well suited to meet challenges in zinc and copper a

258 Thus, SOD conjugated with antibodies to cell adhesion molecule

259 However, stability of Cu bound to SOD is not guaranteed.

260 Total SOD activity was significantly lowered in the glaucoma g

261 After 3 months of follow-up, SOD activity improved in both treatment groups; however,

262 pled electron transfer (PCET) reactions, (v) SOD activity and reductive activity toward both oxygen a

263 t group in the same clade as the other virus SODs but instead groups in an expanded clade that includ

264 nzymatic protein described in this study was SOD, while MALDI-TOF analysis confirmed only SOD from er

265 x was found to be positively associated with SOD activity, and PCB-138, PCB-180, and beta-HCH were th

266 Compared with SOD, SDD was associated with lower rectal carriage of an

267 significantly lower during SDD compared with SOD; for aminoglycoside resistance, average prevalence w

268 Among the 69 patients with SOD, 48.5% who received BES and 47.2% who received DES h

269 Cu-Zn SOD homologs have been described to occur in 3 other fam

270 de gel assay, which was blocked by the Cu-Zn SOD inhibitor cyanide but not by azide, which inhibits F

271 87-amino-acid protein that resembles a Cu-Zn SOD with all of the conserved amino acid residues for bi

272 that the PDH45 protein interacts with Cu/Zn SOD, adenosine-5'-phosphosulfate-kinase, cysteine protei

273 ups in an expanded clade that includes Cu-Zn SODs from many cellular organisms.

274 veals that although the beta-barrel of Cu/Zn SODs is largely preserved, SOD5 is a monomeric copper pr

275 T, is needed to activate a periplasmic Cu,Zn-SOD (SodCII) in Salmonella enterica serovar Typhimurium.

276 Biochemical characteristics of Cu,Zn-SOD derived from hen egg white and egg yolk were determi

277 In this study, we fused a human Cu,Zn-SOD gene with TAT in a bacterial expression vector to pr

278 K/cJun pathway, whereas overexpressing Cu,Zn-SOD had no effect on any of these TCR-mediated signaling

279 Furthermore, overexpression of Cu,Zn-SOD in mice resulted in a profibrotic environment and ac

280 Cu,Zn-SOD isolated from egg yolk had an optimum at pH 6.

281 lmonary fibrosis, we hypothesized that Cu,Zn-SOD modulated the macrophage phenotype.

282 In this study, we demonstrate that Cu,Zn-SOD polarized macrophages to an M2 phenotype, and Cu,Zn-

283 glaucoma patients (p = 0.048) however, Cu,Zn-SOD was not.

284 distinct SOD isoforms in the cytosol (Cu,Zn-SOD) and mitochondria (Mn-SOD), where they locally scave

285 tioxidants Cu,Zn-superoxide dismutase (Cu,Zn-SOD) in platelet function.

286 s mitochondrial (Mn-SOD) and cystolic (Cu,Zn-SOD) isoform were measured.

287 ochondrial Cu,Zn-superoxide dismutase (Cu,Zn-SOD)-mediated H2O2 is crucial for development of pulmona

288 spectroscopy revealed that DMAV, like Cu,Zn-SOD, interacts with Cu(2+), which provides redox potenti

289 ervations provide a novel mechanism of Cu,Zn-SOD-mediated and Th2-independent M2 polarization and pro

290 ed macrophages to an M2 phenotype, and Cu,Zn-SOD-mediated H2O2 levels modulated M2 gene expression at

291 ase (CAT), Cu/Zn-superoxide-dismutase (Cu/Zn-SOD), and glutathione reductase (GR), were quantified us

292 es of key antioxidant enzymes, such as Cu/Zn-SOD, Mn-SOD, CAT, GR, and guaiacol peroxidase, were also

293 etals and metalloproteins, such as MT, Cu/Zn-SOD, or Mn-CA, the breakdown of membrane phospholipids,

294 Such bimetallic Cu,Zn-SODs are widespread, from the periplasm of bacteria to v

295 riplasmic Cu,Zn-superoxide dismutases (Cu,Zn-SODs) are implicated in bacterial virulence.

296 a manner similar to that of the ESL in Cu/Zn-SODs and assists in copper cofactor binding.

297 positions are zinc binding ligands in Cu/Zn-SODs and have evolved in copper-only SODs to control cat

298 and electrostatic loop (ESL) domain of Cu/Zn-SODs for substrate guidance.

299 in stark contrast to the extracellular Cu/Zn-SODs of plants and animals.

300 Similar to the zinc ion in Cu/Zn-SODs, SOD5 Glu-110 helps orient a key copper-coordinatin