ライフサイエンスコーパス: superoxide dismutase

1 wding on the size of a protein complex, SOD (superoxide dismutase).

2 zymes (catalase, glutathione peroxidase, and superoxide dismutase).

3 ased phospho-STAT3 and loss of extracellular superoxide dismutase.

4 g tissues, whereas it enhances expression of superoxide dismutase.

5 e scavenger, with a rate constant similar to superoxide dismutase.

6 2 and H2O2, making the PEG-HCCs a biomimetic superoxide dismutase.

7 elevated in a mutant lacking the Sod1 Cu,Zn-superoxide dismutase.

8 of toxic superoxide to hydrogen peroxide by superoxide dismutase.

9 argely dependent on MSD1, a mitochondrial Mn-superoxide dismutase.

10 antioxidant enzymes peroxiredoxin-3 and CuZn-superoxide-dismutase.

11 ve post-translational modifications of human superoxide dismutase 1 (hSOD1) in the amyotrophic latera

12 uced accumulation of chloroplast copper/zinc superoxide dismutase 1 (HvSOD1), whereas loss of functio

13 ssion of the G985R and G93A mutated forms of superoxide dismutase 1 (linked to familial amyotrophic l

14 e enhanced by expression of a mutant form of superoxide dismutase 1 (SOD1 G93A) that causes astrocyte

15 ouse model expressing a mutant form of human superoxide dismutase 1 (SOD1(G93A) ).

16 Mutant superoxide dismutase 1 (SOD1(G93A)) expression in astroc

17 murine model in which a pathogenic mutant of superoxide dismutase 1 (SOD1(G93A)) is expressed in an A

18 We administered fenofibrate to superoxide dismutase 1 (SOD1(G93A)) mice daily prior to

19 Using a mouse model of ALS expressing mutant superoxide dismutase 1 (SOD1(G93A)), we show that motor

20 ive diseases such as ALS, where mutations of superoxide dismutase 1 (SOD1) account for about 20% of t

21 storing the activity of antioxidant enzymes, superoxide dismutase 1 (SOD1) and peroxiredoxin-4 (PRDX4

22 Changes in the redox state of superoxide dismutase 1 (SOD1) are associated with the on

23 Here, we report that inhibition of superoxide dismutase 1 (SOD1) by the small molecule ATN-

24 uired for copper-dependent activation of the superoxide dismutase 1 (SOD1) during spore germination.

25 ed, of which 20% are due to mutations in the superoxide dismutase 1 (SOD1) gene.

26 Superoxide dismutase 1 (Sod1) has been known for nearly

27 Transgenic mouse models expressing mutant superoxide dismutase 1 (SOD1) have been critical in furt

28 shown that ALS-associated mutations in Cu/Zn superoxide dismutase 1 (SOD1) impair axonal transport of

29 rew-like structure of a cytotoxic segment of superoxide dismutase 1 (SOD1) in its oligomeric state.

30 ation kinetics of the ALS-associated protein superoxide dismutase 1 (SOD1) in vitro and in transgenic

31 cological inhibition or genetic knockdown of superoxide dismutase 1 (SOD1) inhibits the functional ho

32 e find that injection of oligomers of mutant superoxide dismutase 1 (SOD1) into the cytoplasm of inve

33 We show that increased plasma superoxide dismutase 1 (SOD1) levels are statistically s

34 Here, we report that placing mutant superoxide dismutase 1 (SOD1) mice in a leptin-deficient

35 asked if decreasing metabolism in the mutant superoxide dismutase 1 (SOD1) mouse model of ALS (G93A S

36 Here we show that, in vitro, mutant superoxide dismutase 1 (SOD1) mouse oligodendrocytes ind

37 ally bind and neutralize misfolded and toxic superoxide dismutase 1 (SOD1) mutant proteins may find a

38 Two of the models (polyalanine (37A) and superoxide dismutase 1 (SOD1) mutants A4V and G85R) accu

39 Superoxide dismutase 1 (SOD1) mutations account for up t

40 owever, the mechanistic relationship between superoxide dismutase 1 (SOD1) mutations and human diseas

41 as abrogated by transgenic overexpression of superoxide dismutase 1 (SOD1) or an SOD1 mimetic.

42 ophic lateral sclerosis-associated cytosolic superoxide dismutase 1 (SOD1) protein between motor neur

43 lateral sclerosis (ALS)-causing mutations in superoxide dismutase 1 (SOD1) provokes noncell autonomou

44 Notably, G85R is a mutant version of Cu/Zn superoxide dismutase 1 (SOD1) that is unable to reach na

45 Superoxide dismutase 1 (SOD1), a key antioxidant enzyme

46 signal sequence lacking cytoplasmic protein, superoxide dismutase 1 (SOD1), and its mutant form linke

47 ction and determined the in vivo kinetics of superoxide dismutase 1 (SOD1), mutation of which causes

48 uppressed by oligomers of mutant human Cu/Zn superoxide dismutase 1 (SOD1), which are associated with

49 For mutated superoxide dismutase 1 (SOD1), which causes familial amy

50 was enriched in astrocytes expressing mutant superoxide dismutase 1 (SOD1), which causes familial amy

51 viously been found to be inhibitors of Cu/Zn superoxide dismutase 1 (SOD1)-dependent protein aggregat

52 croglial phenotypes in preclinical stages of superoxide dismutase 1 (SOD1)-mutant-mediated disease.

53 nly caused by mutations in the gene encoding superoxide dismutase 1 (SOD1).

54 ys in the liver, including downregulation of superoxide dismutase 1 (Sod1).

55 ion of the reactive oxygen species scavenger superoxide dismutase 1 (SOD1).

56 racellular proteins with similarity to Cu/Zn superoxide dismutase 1 (SOD1).

57 S100; transcription factor ERG; antioxidant superoxide dismutase 1 (SOD1); chloride intracellular ch

58 c slice cultures from a mutant form of human superoxide dismutase 1 (SOD1G93A) mouse model of ALS all

59 Co-expression of wild-type human superoxide dismutase 1 (WT-hSOD1) with ALS mutant hSOD1

60 Quercetin increased the expression of superoxide dismutase 1 and 2, and reduced the levels of

61 Downstream of Nrf2, levels of oPMN superoxide dismutase 1 and catalase were decreased in se

62 th downregulation of the antioxidant enzymes superoxide dismutase 1 and catalase, and activation of t

63 anscription and translation of antioxidants, superoxide dismutase 1 and glutathione peroxidase-1, wer

64 that develop DM are homozygous for a common superoxide dismutase 1 gene (SOD1) mutation.

65 cluding mutant FUS (Fused in sarcoma), SOD1 (superoxide dismutase 1), TDP43 (TAR DNA-binding protein

66 proteins, such as hemoglobin alpha genes and superoxide dismutase 1, that have network functions asso

67 rimary astrocytes isolated from mutant human superoxide dismutase 1-overexpressing mice as well as hu

68 cent lumbar MN cell bodies from ChAT-eGFP or superoxide dismutase 1-yellow fluorescent protein (SOD1Y

69 Here, we show superoxide dismutase-1 (SOD-1), an enzyme that converts

70 f ALS cases are sporadic, mutations in Cu-Zn superoxide dismutase-1 (SOD1) are causative for 10-20% o

71 This article investigates how the rate of superoxide dismutase-1 (SOD1) fibrillization is affected

72 The acylation of lysine residues in superoxide dismutase-1 (SOD1) has been previously shown

73 osis (ALS) cases result from impaired mutant superoxide dismutase-1 (SOD1) maturation.

74 Rodent models in which the superoxide dismutase-1 (SOD1) mutation is overexpressed

75 trochemical setup and use the specificity of superoxide dismutase-1 (SOD1) to show, for the first tim

76 ))ATSM enhanced the association of DJ-1 with superoxide dismutase-1 (SOD1), paralleled by significant

77 use models of familial ALS expressing mutant superoxide dismutase-1 (SOD1), TAR DNA-binding protein 4

78 disease, as has been shown for mutations in superoxide dismutase-1 (SOD1).

79 Both were different from superoxide dismutase-1 aggregates generated in vitro und

80 es, reactive oxidative species scavenging by superoxide dismutase-1 and superoxide dismutase-2.

81 Mice with high numbers of the Cu/Zn superoxide dismutase-1 G93A transgene (SOD1(G93A) G1H) h

82 identified F- and S-type motoneurons in the superoxide dismutase-1 mutant G93A (mSOD1), a mouse mode

83 ns (polyglutamine, huntingtin, ataxin-1, and superoxide dismutase-1) inhibits clathrin-mediated endoc

84 An archetype example of this is superoxide dismutase-1, the first genetic factor to be l

85 which accumulate intracellular aggregates of superoxide dismutase-1.

86 ic deletion of Sirt1 increased mitochondrial superoxide dismutase 2 (Sod2) acetylation of lysine resi

87 ncreased reactive oxygen species and reduced superoxide dismutase 2 (SOD2) activity.

88 deacetylase activity of sirtuin 3 to inhibit superoxide dismutase 2 (SOD2) activity.

89 nd other forms of stress, or enzymes such as superoxide dismutase 2 (SOD2) and catalase, which direct

90 regulation of the oxidative stress enzymes, superoxide dismutase 2 (SOD2) and catalase.

91 f the increased acetylation of mitochondrial superoxide dismutase 2 (SOD2) and isocitrate dehydrogena

92 y of a key mitochondrial antioxidant enzyme, superoxide dismutase 2 (SOD2) because of hyperacetylatio

93 nged ROS and induced a rapid upregulation of superoxide dismutase 2 (SOD2) expression and a delayed u

94 heat shock protein 70 (hsp70) interacts with superoxide dismutase 2 (SOD2) in the cytosol after synth

95 Superoxide dismutase 2 (SOD2) is a crucial antioxidative

96 Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpresse

97 Ectopic expression of superoxide dismutase 2 (SOD2) reduced ROS and preserved

98 mitochondria possess an antioxidant enzyme, superoxide dismutase 2 (SOD2), to neutralize ROS.

99 ecific iPS-derived RPE cell lines identified superoxide dismutase 2 (SOD2)-mediated antioxidative def

100 vating isocitrate dehydrogenase 2 (IDH2) and superoxide dismutase 2 (SOD2).

101 the gene for the primary antioxidant enzyme, superoxide dismutase 2 (SOD2).

102 encodes the mitochondrial antioxidant enzyme superoxide dismutase 2 (Sod2).

103 id hydroperoxides, had reduced activities of superoxide dismutase 2 and catalase, and were hypersensi

104 ion; increased NADPH oxidase 2 and decreased superoxide dismutase 2 expression; and oxidative stress

105 educed acetylation of the antioxidant enzyme superoxide dismutase 2 in muscle but not the liver of MC

106 ort isoform (TRPM2-S) had reduced FOXO3a and superoxide dismutase 2 levels, reduced calcium influx in

107 e transcription of ROS scavengers (catalase, superoxide dismutase 2) in HF keratinocytes.

108 d cycle (TCA) isocitrate dehydrogenase 2 and superoxide dismutase 2, concomitant with increases in ci

109 otypes were rescued by genetic modulation of superoxide dismutase 2, p53, and apoptotic caspase casca

110 , a master regulator of oxidative stress and superoxide dismutase 2.

111 actor 3a (FOXO3a) and a downstream effector, superoxide dismutase 2.

112 was associated with a reduced ratio of mROS/superoxide dismutase 2.

113 ead box transcription factor 3a (FOXO3a) and superoxide dismutase 2.

114 uld be identified, including upregulation of superoxide dismutase 2.

115 UnAG rescues sirtuin 1 (SIRT1) activity and superoxide dismutase-2 (SOD-2) expression in ECs.

116 o 5-LO(-/-) mice, induction of HO-1, but not superoxide dismutase-2 (SOD-2), was also observed in res

117 oxidative stress resistance enzymes such as superoxide dismutase-2 (SOD2).

118 There was a 34% increase in superoxide dismutase-2 activity, along with a 3.5-fold i

119 as ATF-2, thereby enhancing the activity of superoxide dismutase-2 and catalase, two antioxidant enz

120 d to neuronal and vascular oxidative stress (superoxide dismutase-2), neuroinflammation (astroglial a

121 synthase and enhanced lung concentrations of superoxide dismutase-2, thereby reducing lung tissue rea

122 ies scavenging by superoxide dismutase-1 and superoxide dismutase-2.

123 ariable analysis with higher MMP-2 and lower superoxide dismutase 3 gene expression, independent of a

124 inase-2 (MMP-2), MMP-14, endoglin (ENG), and superoxide dismutase 3 in ascending aorta samples from 5

125 41.1 +/- 17.6% of normoxic control), reduced superoxide dismutase (60.7 +/- 6.3%), increased phosphod

126 gates of biomolecules, e.g., of enzyme Cu/Zn-superoxide dismutase, abnormal aggregation of which is l

127 Superoxide dismutase activity in human blood plasma mirr

128 bread and mixed bread, a marked decrease in superoxide dismutase activity was found.

129 The superoxide dismutase activity was relatively insensitive

130 Superoxide dismutase activity, the reduced glutathione-t

131 The results showed that the liver superoxide dismutase and catalase activities (FA200), er

132 ve oxygen species, and reduced activities of superoxide dismutase and catalase enzymes.

133 Furthermore, the synthetic superoxide dismutase and catalase mimetic EUK-134 also a

134 ing, which restored NO production, increased superoxide dismutase and catalase, and suppressed NADPH

135 antioxidant enzymes: glutathione peroxidase, superoxide dismutase and catalase.

136 oxidase, dynamin related protein, manganese superoxide dismutase and Lon protease, respectively, wer

137 se through higher activities of antioxidant (superoxide dismutase and peroxidase) and defense enzymes

138 s such as mitochondrial manganese-containing superoxide dismutase and peroxiredoxin 5 were only upreg

139 ulation of GR and up-regulation of manganese superoxide dismutase and reduced glutathione levels.

140 nhydrase, where the latter had impurities of superoxide dismutase and ubiquitin.

141 arbon fixation, oxidative stress protection (superoxide dismutases) and iron and nitrogen metabolism

142 t enzymes, including glutathione peroxidase, superoxide dismutase, and catalase, were evaluated in ea

143 Malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase, and glutathione peroxidase (GPX) l

144 The activity of catalase, superoxide dismutase, and glutathione peroxidase in atri

145 thetase genes, increased levels of manganese superoxide dismutase, and NADPH oxidase-complex adaptor

146 in substrate proteins such as cyclophilin D, superoxide dismutase, and PEPCK1 were not deacetylated.

147 pendent enzymes, namely tyrosinase and Cu-Zn superoxide dismutase, are decreased significantly follow

148 ulates the antioxidant proteins catalase and superoxide dismutase as well as the antiapoptotic protei

149 However, the superoxide dismutase C (SodC) protein of the M. leprae c

150 peptide of a new human recombinant manganese superoxide dismutase can enter cells and carry molecules

151 lly, S.PEPS and S.EPS significantly improved superoxide dismutase, catalase and glutathione peroxidas

152 antioxidant enzyme expression, such as Cu/Zn-superoxide dismutase, catalase, and glutathione peroxida

153 The GS diet improved superoxide dismutase, catalase, glutathione peroxidase a

154 L-6, IL-10, TNF-alpha) and oxidative stress (superoxide dismutase, catalase, glutathione peroxidase,

155 iposomes loaded with EUK-134 (EUK), a potent superoxide dismutase/catalase mimetic.

156 , which was exaggerated in the presence of a superoxide dismutase/catalase mimetic.

157 hylakoids, and the Cu(+)-chaperone for Cu/Zn superoxide dismutase (CCS), uncovering a Cu(+) network t

158 The copper chaperone for superoxide dismutase (Ccs1) activates immature copper-zi

159 ious studies have shown that levels of Cu/Zn superoxide dismutase (CSD) are down-regulated by miR398.

160 nding site for miR398 in an isoform of Cu/Zn superoxide dismutase (CSD1) is eliminated by alternative

161 resembles the effects of antioxidants Cu,Zn-superoxide dismutase (Cu,Zn-SOD) in platelet function.

162 n linked to the gain of aberrant function of superoxide dismutase, Cu,Zn-SOD1 upon protein misfolding

163 CuZn-superoxide dismutase (CuZn-SOD) and ascorbate peroxidase

164 d by charge reduction using PTR, homodimeric superoxide dismutase/CuZn (31.4 kDa) was subjected to PT

165 Deletion of copper-zinc superoxide dismutase (CuZnSOD) in Sod1(-/-) mice leads t

166 Copper/zinc superoxide dismutase (CuZnSOD; SOD1) is widely considere

167 ns, namely Ras-related nuclear, p53, PEPCK1, superoxide dismutase, cyclophilin D, and Hsp10, and anal

168 s, we also revealed a range of phenotypes of superoxide dismutase deficiency not observed in previous

169 stigated dimeric beta-lactoglobulin, dimeric superoxide dismutase, dimeric and tetrameric concanavali

170 f 215 amino acids, and has an iron/manganese superoxide dismutase domain.

171 e that IL-27 is able to induce extracellular superoxide dismutase during differentiation of monocytes

172 The enzyme extracellular superoxide dismutase (EC-SOD; SOD3) is a major antioxida

173 ic mice with varying levels of extracellular superoxide dismutase (ecSOD) activity, we have recently

174 Exercise training enhances extracellular superoxide dismutase (EcSOD) expression in skeletal musc

175 mice blocked the reduction of extracellular superoxide dismutase (EcSOD) protein expression, as well

176 ed that targeted expression of extracellular superoxide dismutase (EcSOD) via the cardiac troponin-T

177 e overexpressing lung-specific extracellular superoxide dismutase (ecSOD) were exposed to HEPA-filter

178 Activities of catalase and superoxide dismutase enzymes, levels of total anthocyani

179 HSM also restores superoxide dismutase expression in TGF-beta1-treated lun

180 r-cGMP also activated catalase and manganese superoxide dismutase expression, indicating that this pa

181 s, reactive scavenging species, and enzymes (superoxide dismutase family, hydrogen peroxide, and cata

182 disease, contains exclusively iron-dependent superoxide dismutases (Fe-SODs) located in different sub

183 Since the linking of mutations in the Cu,Zn superoxide dismutase gene (sod1) to amyotrophic lateral

184 complexes, not antioxidant enzymes (e.g., Mn superoxide dismutase), govern IR survival.

185 and their substrate (tryparedoxin) and iron superoxide dismutase in COL and SYL (versus TCC) trypoma

186 often encode and package a functional Cu-Zn superoxide dismutase in the virion that presumably lower

187 ut NRAMP2 can functionally replace cytosolic superoxide dismutase in yeast, indicating that the pool

188 r alpha (TNF-alpha), CXCL10, CCL5, IL-6, and superoxide dismutase, in human macrophages infected with

189 pression also led to decreased expression of superoxide dismutase isoform 2 and glutathione peroxidas

190 We used a superoxide dismutase knockout mouse to demonstrate that

191 ortantly, treatment with the small-molecule, superoxide dismutase mimetic (GC4419; 0.25 mumol/L) sign

192 A superoxide dismutase mimetic made superoxide levels subn

193 Coadministration of tempol, a superoxide dismutase mimetic, ameliorated the exaggerate

194 is could be partially inhibited by Tempol (a superoxide dismutase-mimetic agent) and by glyburide (an

195 the addition of 4-hydroxy-TEMPO (TEMPOL), a superoxide dismutase mimic that reacts with superoxide,

196 adaptive or stress proteins (e.g. manganese superoxide dismutase, mitochondrial KATP channels and pe

197 20 encodes for a membrane-targeted 30 kDa Mn-superoxide dismutase (MnSOD) and a cytosolic FeSOD.

198 species, in part, by deacetylating manganese superoxide dismutase (MnSOD) and mitochondrial 8-oxoguan

199 the promoters of the catalase and manganese superoxide dismutase (MnSOD) antioxidant genes and stimu

200 Manganese-dependent superoxide dismutase (MnSOD) expression also increased s

201 Trx induces manganese superoxide dismutase (MnSOD) gene transcription by activ

202 Manganese superoxide dismutase (MnSOD) is a mitochondrially locali

203 an adipocyte-selective deletion of manganese superoxide dismutase (MnSOD).

204 tylation and decreased activity of manganese superoxide dismutase (MnSOD).

205 itochondrial antioxidant defenses [manganese superoxide dismutase (MnSOD)P< 0.05; copper/zinc superox

206 Manganese superoxide dismutase (MnSOD/SOD2) is a mitochondria-resi

207 neration, but associated with maintenance of superoxide dismutase mRNA expression in the absence of I

208 have implicated the amidate ligand in nickel superoxide dismutase (NiSOD) in stabilizing Ni-centered

209 Nickel-containing superoxide dismutase (NiSOD) is a mononuclear cysteinate

210 city) and cellular antioxidants (sulfhydryl, superoxide dismutase) of zebrafish brain were assessed a

211 r, TEMPOL, or by overexpression of manganese superoxide dismutase or catalase.

212 from familial ALS patients with mutation in superoxide dismutase or hexanucleotide expansion in C9or

213 embryos with polyethylene glycol-conjugated superoxide dismutase, or NOX4 inhibitors fulvene-5, 6-di

214 thetase, alanine aminotransferase, catalase, superoxide dismutase, ornithine decarboxylase, glutamate

215 surprisingly high abundance of extracellular superoxide dismutase produced by Synechococcus and a dyn

216 Small heat shock proteins, superoxide dismutase, quinone oxidoreductase, UDP-glucos

217 In contrast, RBC superoxide dismutase seemed to be a trait marker for sch

218 ation of glutathione S-transferase (GST) and superoxide dismutase (SOD) activities.

219 This study investigates the levels of superoxide dismutase (SOD) activity in serum and saliva

220 H2O2 accumulation, which result from higher superoxide dismutase (SOD) activity, associated with low

221 e cytoplasmic or mitochondrial ROS scavenger superoxide dismutase (SOD) caused a significant increase

222 yphenol oxidase (PPO), peroxidase (POX), and superoxide dismutase (SOD) enzymes activities were measu

223 Y neuroblastoma cells the beneficial role of superoxide dismutase (SOD) enzymes against paraquat-indu

224 In eukaryotes the bimetallic Cu/Zn superoxide dismutase (SOD) enzymes play important roles

225 suppression and colonization by controlling superoxide dismutase (SOD) gene expression.

226 The activity of superoxide dismutase (SOD) in Brassica rapa also display

227 Superoxide dismutase (SOD) level in the blood samples ex

228 ning differences in antioxidant capacity and superoxide dismutase (SOD) levels between phenotypes may

229 in framework alterations in heritable Cu, Zn superoxide dismutase (SOD) mutants cause misassembly and

230 ging of extracellular superoxide by specific superoxide dismutase (SOD) showed the applicability for

231 ive stress (glutathione-S-transferase (GST), superoxide dismutase (SOD)), and fish health (condition

232 IL-6, IL-8, IL10, reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT).

233 malondialdehyde (MDA) and activity of total superoxide dismutase (SOD), and its mitochondrial (Mn-SO

234 Activities of superoxide dismutase (SOD), catalase (CAT) and peroxidas

235 e (LDH) levels along with reduction in liver superoxide dismutase (SOD), catalase (CAT), reduced glut

236 ated the association of baseline erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx)

237 TKO MEFs exhibit reduced levels of superoxide dismutase (Sod), glutathione peroxidase 4 (Gp

238 ntitis, on activities of antioxidant enzymes superoxide dismutase (SOD), glutathione reductase (GR),

239 tly, GA + UV-A also inhibits the activity of superoxide dismutase (SOD), magnifying the imbalance of

240 uced these cytokines only when stimulated by superoxide dismutase (SOD)-1.

241 responsive MRI contrast agent and a mimic of superoxide dismutase (SOD).

242 regulation of antioxidant enzymes, including superoxide dismutase (SOD).

243 mpaired wound healing, we tested a synthetic superoxide dismutase (SOD)/catalase mimetic, EUK-207, in

244 ts with mutant strains lacking mitochondrial superoxide dismutase (sod-2) showed oxidative stress for

245 dants glutathione S-transferase P (GSTP) and superoxide dismutases (SOD).

246 y to support the activity of the copper/zinc superoxide dismutase Sod1 and that loss of Sod1 activity

247 Pathological deposition of mutated Cu/Zn superoxide dismutase (SOD1) accounts for approximately 2

248 and nitrate (NO3(-)) ions using copper, zinc superoxide dismutase (SOD1) and nitrate reductase (NaR)

249 f subunits between homodimeric mutant Cu, Zn superoxide dismutase (SOD1) and wild-type (WT) SOD1 is s

250 mutase (Ccs1) activates immature copper-zinc superoxide dismutase (Sod1) by delivering copper and fac

251 harmacon) can inhibit the amyloidogenesis of superoxide dismutase (SOD1) by increasing the intrinsic

252 nano-formulation (nanozyme) for copper/Zinc superoxide dismutase (SOD1) by polyion condensation with

253 Mutations in superoxide dismutase (SOD1) cause amyotrophic lateral sc

254 Mutations in superoxide dismutase (SOD1) cause amyotrophic lateral sc

255 Mutations in the metallo-protein Cu/Zn-superoxide dismutase (SOD1) cause amyotrophic lateral sc

256 ost-translational modifications within Cu,Zn-superoxide dismutase (SOD1) cause this otherwise protect

257 s and differences among apo-, Zn-, and Cu,Zn-superoxide dismutase (SOD1) dimers.

258 YFP throughout the brain and spinal cord of superoxide dismutase (SOD1) G93A transgenic mice.

259 Cs) from patients with mutation in the Cu/Zn superoxide dismutase (SOD1) gene, we show that spinal MN

260 C. albicans expresses a Cu-requiring form of superoxide dismutase (Sod1) in the cytosol; but when Cu

261 Aggregation of copper-zinc superoxide dismutase (SOD1) is a defining feature of fam

262 Previously, we found that human Cu, Zn-superoxide dismutase (SOD1) is S-acylated (palmitoylated

263 transgenic rodents expressing ALS-associated superoxide dismutase (SOD1) mutations develop spontaneou

264 Cu/Zn superoxide dismutase (SOD1) reduction prolongs survival

265 Ubiquitous expression of mutant Cu/Zn-superoxide dismutase (SOD1) selectively affects motor ne

266 (PDS) to report on the conformation of Cu-Zn superoxide dismutase (SOD1) through the sensitive measur

267 Delivery of copper-zinc superoxide dismutase (SOD1), an efficient ROS scavenger,

268 se strains transgenic for mutant human Cu/Zn superoxide dismutase (SOD1), G85R SOD1YFP and G93A SOD1,

269 In ALS model mice expressing mutant superoxide dismutase (SOD1), reduction of MMP-9 function

270 the misfolding pathway of mutant copper-zinc superoxide dismutase (SOD1), the protein known to be a c

271 We focused on Cu-Zn superoxide dismutase (SOD1), which protects cells from o

272 h mutations to the antioxidant metalloenzyme superoxide dismutase (SOD1).

273 involving cytotoxic conformations of Cu, Zn superoxide dismutase (SOD1).

274 in 5-10% of cases, including those in Cu/Zn superoxide dismutase (SOD1).

275 also reported for ALS-linked forms of Cu, Zn superoxide dismutase (SOD1).

276 luding cytochrome c oxidase (CcO), and Cu/Zn superoxide dismutase (SOD1); (c) metal ion misregulation

277 n factor FOXO3, an important regulator of Mn-superoxide dismutase (SOD2) expression, a tumor suppress

278 Manganese superoxide dismutase (SOD2) is a primary defense against

279 he present study, we show that mitochondrial superoxide dismutase (Sod2) is highly expressed in OCCC

280 /aP2 is the upregulation of the antioxidants superoxide dismutase (SOD2), catalase, methionine sulfox

281 ownregulation of ROS-producing extracellular superoxide dismutase (SOD3) in thyroid cancer cell lines

282 encoding enzymes that detoxify ROS, such as superoxide dismutase (SodA).

283 A mutant lacking the manganese-dependent superoxide dismutase, SodA, was significantly less virul

284 (glxK), valine-pyruvate transaminase (avtA), superoxide dismutase (sodB), and 2 hypothetical proteins

285 quired to deliver the metal ion to the Cu/Zn superoxide dismutase SodCII.

286 Superoxide dismutases (SODs) are metalloproteins that pr

287 -oxidant systems that include iron-dependent superoxide dismutases (SODs) in mitochondria and glycoso

288 The copper-containing superoxide dismutases (SODs) represent a large family of

289 of both cytosolic and chloroplast-localized superoxide dismutases (SODs), which are known to be depe

290 protein systems, including a nascent form of superoxide dismutase that is implicated in neurodegenera

291 eductase, catalase, ascorbate peroxidase and superoxide dismutase together with xanthophyll cycle and

292 Erythrocyte Mn-superoxide dismutase was also reduced at 6 (0.154 vs. 0.

293 ize, number, and mRNA levels of catalase and superoxide dismutase were increased, whereas those of ni

294 thione peroxidase, glutathione reductase and superoxide dismutase were measured.

295 ogenase E1 component, biotin carboxylase and superoxide dismutase were related to energy and carbon m

296 ties of catalase, glutathione peroxidase and superoxide dismutase were significantly lower in PSE-ind

297 tivating factor acetylhydrolase [PAF-AH] and superoxide dismutase) were measured from samples collect

298 diminished by polyethylene glycol-conjugated superoxide dismutase, whereas its inhibitor KN93 or AIP

299 We also calculated the kon rate constant for superoxide dismutase with its natural substrate, O2-, in

300 xidant enzymes viz. catalase, peroxidase and superoxide dismutase with the excess accumulation of pro