ライフサイエンスコーパス: dismutase

1 e size of a protein complex, SOD (superoxide dismutase).

2 lase, glutathione peroxidase, and superoxide dismutase).

3 hich is crucial for NPs' function as nitrite dismutase.

4 o-STAT3 and loss of extracellular superoxide dismutase.

5 whereas it enhances expression of superoxide dismutase.

6 , with a rate constant similar to superoxide dismutase.

7 making the PEG-HCCs a biomimetic superoxide dismutase.

8 n a mutant lacking the Sod1 Cu,Zn-superoxide dismutase.

9 uperoxide to hydrogen peroxide by superoxide dismutase.

10 nslational modifications of human superoxide dismutase 1 (hSOD1) in the amyotrophic lateral sclerosis

11 lation of chloroplast copper/zinc superoxide dismutase 1 (HvSOD1), whereas loss of function in Rom1 r

12 e G985R and G93A mutated forms of superoxide dismutase 1 (linked to familial amyotrophic lateral scle

13 by expression of a mutant form of superoxide dismutase 1 (SOD1 G93A) that causes astrocyte dysfunctio

14 expressing a mutant form of human superoxide dismutase 1 (SOD1(G93A) ).

15 Mutant superoxide dismutase 1 (SOD1(G93A)) expression in astrocytes is sel

16 l in which a pathogenic mutant of superoxide dismutase 1 (SOD1(G93A)) is expressed in an Aptx-/- mous

17 We administered fenofibrate to superoxide dismutase 1 (SOD1(G93A)) mice daily prior to any detecta

18 se model of ALS expressing mutant superoxide dismutase 1 (SOD1(G93A)), we show that motor neurons for

19 s such as ALS, where mutations of superoxide dismutase 1 (SOD1) account for about 20% of the inherite

20 activity of antioxidant enzymes, superoxide dismutase 1 (SOD1) and peroxiredoxin-4 (PRDX4) during hy

21 Changes in the redox state of superoxide dismutase 1 (SOD1) are associated with the onset and dev

22 ere, we report that inhibition of superoxide dismutase 1 (SOD1) by the small molecule ATN-224 induced

23 opper-dependent activation of the superoxide dismutase 1 (SOD1) during spore germination.

24 h 20% are due to mutations in the superoxide dismutase 1 (SOD1) gene.

25 Superoxide dismutase 1 (Sod1) has been known for nearly half a cent

26 ic mouse models expressing mutant superoxide dismutase 1 (SOD1) have been critical in furthering our

27 ALS-associated mutations in Cu/Zn superoxide dismutase 1 (SOD1) impair axonal transport of mitochondr

28 ructure of a cytotoxic segment of superoxide dismutase 1 (SOD1) in its oligomeric state.

29 ics of the ALS-associated protein superoxide dismutase 1 (SOD1) in vitro and in transgenic mice.

30 nhibition or genetic knockdown of superoxide dismutase 1 (SOD1) inhibits the functional holoenzyme as

31 injection of oligomers of mutant superoxide dismutase 1 (SOD1) into the cytoplasm of invertebrate ne

32 We show that increased plasma superoxide dismutase 1 (SOD1) levels are statistically significant

33 re, we report that placing mutant superoxide dismutase 1 (SOD1) mice in a leptin-deficient background

34 creasing metabolism in the mutant superoxide dismutase 1 (SOD1) mouse model of ALS (G93A SOD1) would

35 re we show that, in vitro, mutant superoxide dismutase 1 (SOD1) mouse oligodendrocytes induce WT moto

36 nd neutralize misfolded and toxic superoxide dismutase 1 (SOD1) mutant proteins may find application

37 the models (polyalanine (37A) and superoxide dismutase 1 (SOD1) mutants A4V and G85R) accumulated int

38 Superoxide dismutase 1 (SOD1) mutations account for up to 20% of fa

39 mechanistic relationship between superoxide dismutase 1 (SOD1) mutations and human disease is contro

40 d by transgenic overexpression of superoxide dismutase 1 (SOD1) or an SOD1 mimetic.

41 al sclerosis-associated cytosolic superoxide dismutase 1 (SOD1) protein between motor neurons could b

42 erosis (ALS)-causing mutations in superoxide dismutase 1 (SOD1) provokes noncell autonomous paralytic

43 G85R is a mutant version of Cu/Zn superoxide dismutase 1 (SOD1) that is unable to reach native form a

44 Superoxide dismutase 1 (SOD1), a key antioxidant enzyme in human ce

45 ence lacking cytoplasmic protein, superoxide dismutase 1 (SOD1), and its mutant form linked to amyotr

46 etermined the in vivo kinetics of superoxide dismutase 1 (SOD1), mutation of which causes amyotrophic

47 y oligomers of mutant human Cu/Zn superoxide dismutase 1 (SOD1), which are associated with motor neur

48 For mutated superoxide dismutase 1 (SOD1), which causes familial amyotrophic la

49 d in astrocytes expressing mutant superoxide dismutase 1 (SOD1), which causes familial amyotrophic la

50 n found to be inhibitors of Cu/Zn superoxide dismutase 1 (SOD1)-dependent protein aggregation, which

51 enotypes in preclinical stages of superoxide dismutase 1 (SOD1)-mutant-mediated disease.

52 by mutations in the gene encoding superoxide dismutase 1 (SOD1).

53 iver, including downregulation of superoxide dismutase 1 (Sod1).

54 reactive oxygen species scavenger superoxide dismutase 1 (SOD1).

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

56 scription factor ERG; antioxidant superoxide dismutase 1 (SOD1); chloride intracellular channel 6 ion

57 tures from a mutant form of human superoxide dismutase 1 (SOD1G93A) mouse model of ALS allow the dete

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

59 cetin increased the expression of superoxide dismutase 1 and 2, and reduced the levels of oxidative s

60 ownstream of Nrf2, levels of oPMN superoxide dismutase 1 and catalase were decreased in severe CP, de

61 lation of the antioxidant enzymes superoxide dismutase 1 and catalase, and activation of the pro-oxid

62 and translation of antioxidants, superoxide dismutase 1 and glutathione peroxidase-1, were significa

63 op DM are homozygous for a common superoxide dismutase 1 gene (SOD1) mutation.

64 ant FUS (Fused in sarcoma), SOD1 (superoxide dismutase 1), TDP43 (TAR DNA-binding protein 43), and ta

65 uch as hemoglobin alpha genes and superoxide dismutase 1, that have network functions associated with

66 ocytes isolated from mutant human superoxide dismutase 1-overexpressing mice as well as human post-mo

67 MN cell bodies from ChAT-eGFP or superoxide dismutase 1-yellow fluorescent protein (SOD1YFP) transge

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

69 are sporadic, mutations in Cu-Zn superoxide dismutase-1 (SOD1) are causative for 10-20% of familial

70 icle investigates how the rate of superoxide dismutase-1 (SOD1) fibrillization is affected by 12 diff

71 e acylation of lysine residues in superoxide dismutase-1 (SOD1) has been previously shown to decrease

72 cases result from impaired mutant superoxide dismutase-1 (SOD1) maturation.

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

74 setup and use the specificity of superoxide dismutase-1 (SOD1) to show, for the first time, that H2O

75 nced the association of DJ-1 with superoxide dismutase-1 (SOD1), paralleled by significant increases

76 of familial ALS expressing mutant superoxide dismutase-1 (SOD1), TAR DNA-binding protein 43 (TDP-43),

77 s has been shown for mutations in superoxide dismutase-1 (SOD1).

78 Both were different from superoxide dismutase-1 aggregates generated in vitro under a variet

79 e oxidative species scavenging by superoxide dismutase-1 and superoxide dismutase-2.

80 ce with high numbers of the Cu/Zn superoxide dismutase-1 G93A transgene (SOD1(G93A) G1H) have become

81 F- and S-type motoneurons in the superoxide dismutase-1 mutant G93A (mSOD1), a mouse model of ALS at

82 tamine, huntingtin, ataxin-1, and superoxide dismutase-1) inhibits clathrin-mediated endocytosis (CME

83 An archetype example of this is superoxide dismutase-1, the first genetic factor to be linked with

84 ulate intracellular aggregates of superoxide dismutase-1.

85 of Sirt1 increased mitochondrial superoxide dismutase 2 (Sod2) acetylation of lysine residue 68, the

86 active oxygen species and reduced superoxide dismutase 2 (SOD2) activity.

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

88 rms of stress, or enzymes such as superoxide dismutase 2 (SOD2) and catalase, which directly detoxify

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

90 ased acetylation of mitochondrial superoxide dismutase 2 (SOD2) and isocitrate dehydrogenase 2 (IDH2)

91 mitochondrial antioxidant enzyme, superoxide dismutase 2 (SOD2) because of hyperacetylation.

92 d induced a rapid upregulation of superoxide dismutase 2 (SOD2) expression and a delayed upregulation

93 protein 70 (hsp70) interacts with superoxide dismutase 2 (SOD2) in the cytosol after synthesis to tra

94 Superoxide dismutase 2 (SOD2) is a crucial antioxidative enzyme tha

95 Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpressed in oral a

96 Ectopic expression of superoxide dismutase 2 (SOD2) reduced ROS and preserved viability o

97 ia possess an antioxidant enzyme, superoxide dismutase 2 (SOD2), to neutralize ROS.

98 derived RPE cell lines identified superoxide dismutase 2 (SOD2)-mediated antioxidative defense in the

99 itrate dehydrogenase 2 (IDH2) and superoxide dismutase 2 (SOD2).

100 r the primary antioxidant enzyme, superoxide dismutase 2 (SOD2).

101 mitochondrial antioxidant enzyme superoxide dismutase 2 (Sod2).

102 oxides, had reduced activities of superoxide dismutase 2 and catalase, and were hypersensitive to hyd

103 sed NADPH oxidase 2 and decreased superoxide dismutase 2 expression; and oxidative stress in the nucl

104 ylation of the antioxidant enzyme superoxide dismutase 2 in muscle but not the liver of MCD(-/-) mice

105 (TRPM2-S) had reduced FOXO3a and superoxide dismutase 2 levels, reduced calcium influx in response t

106 tion of ROS scavengers (catalase, superoxide dismutase 2) in HF keratinocytes.

107 A) isocitrate dehydrogenase 2 and superoxide dismutase 2, concomitant with increases in citrate synth

108 rescued by genetic modulation of superoxide dismutase 2, p53, and apoptotic caspase cascade mediator

109 regulator of oxidative stress and superoxide dismutase 2.

110 OXO3a) and a downstream effector, superoxide dismutase 2.

111 ated with a reduced ratio of mROS/superoxide dismutase 2.

112 nscription factor 3a (FOXO3a) and superoxide dismutase 2.

113 es sirtuin 1 (SIRT1) activity and superoxide dismutase-2 (SOD-2) expression in ECs.

114 mice, induction of HO-1, but not superoxide dismutase-2 (SOD-2), was also observed in response to 5-

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

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

117 thereby enhancing the activity of superoxide dismutase-2 and catalase, two antioxidant enzymes that p

118 al and vascular oxidative stress (superoxide dismutase-2), neuroinflammation (astroglial and microgli

119 d enhanced lung concentrations of superoxide dismutase-2, thereby reducing lung tissue reactive oxida

120 ing by superoxide dismutase-1 and superoxide dismutase-2.

121 lysis with higher MMP-2 and lower superoxide dismutase 3 gene expression, independent of age and aort

122 P-2), MMP-14, endoglin (ENG), and superoxide dismutase 3 in ascending aorta samples from 50 tricuspid

123 .6% of normoxic control), reduced superoxide dismutase (60.7 +/- 6.3%), increased phosphodiesterase t

124 omolecules, e.g., of enzyme Cu/Zn-superoxide dismutase, abnormal aggregation of which is linked to am

125 ng, and the D83G mutation results in loss of dismutase activity and SOD1 protein instability.

126 we show that mitochondrial SOD1 is the main dismutase activity in breast cancer cells but not in non

127 Superoxide dismutase activity in human blood plasma mirrored these

128 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-to-glutathio

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

132 pecies, and reduced activities of superoxide dismutase and catalase enzymes.

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

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

135 enzymes: glutathione peroxidase, superoxide dismutase and catalase.

136 ynamin related protein, manganese superoxide dismutase and Lon protease, respectively, were generated

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

138 itochondrial manganese-containing superoxide dismutase and peroxiredoxin 5 were only upregulated by P

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

140 here the latter had impurities of superoxide dismutase and ubiquitin.

141 ion, oxidative stress protection (superoxide dismutases) and iron and nitrogen metabolism varied amon

142 including glutathione peroxidase, superoxide dismutase, and catalase, were evaluated in each of the i

143 ldehyde (MDA), nitric oxide (NO), superoxide dismutase, and glutathione peroxidase (GPX) levels in se

144 es, increased levels of manganese superoxide dismutase, and NADPH oxidase-complex adaptor cytochrome

145 e proteins such as cyclophilin D, superoxide dismutase, and PEPCK1 were not deacetylated.

146 ymes, namely tyrosinase and Cu-Zn superoxide dismutase, are decreased significantly following the con

147 antioxidant proteins catalase and superoxide dismutase as well as the antiapoptotic proteins Bcl-2 an

148 However, the superoxide dismutase C (SodC) protein of the M. leprae cell wall wa

149 a new human recombinant manganese superoxide dismutase can enter cells and carry molecules.

150 and S.EPS significantly improved superoxide dismutase, catalase and glutathione peroxidase activitie

151 enzyme expression, such as Cu/Zn-superoxide dismutase, catalase, and glutathione peroxidase, but als

152 The GS diet improved superoxide dismutase, catalase, glutathione peroxidase and GR activ

153 TNF-alpha) and oxidative stress (superoxide dismutase, catalase, glutathione peroxidase, lipidic and

154 aded with EUK-134 (EUK), a potent superoxide dismutase/catalase mimetic.

155 exaggerated in the presence of a superoxide dismutase/catalase mimetic.

156 and the Cu(+)-chaperone for Cu/Zn superoxide dismutase (CCS), uncovering a Cu(+) network that has evo

157 The copper chaperone for superoxide dismutase (Ccs1) activates immature copper-zinc superoxi

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

159 for miR398 in an isoform of Cu/Zn superoxide dismutase (CSD1) is eliminated by alternative splicing t

160 the gain of aberrant function of superoxide dismutase, Cu,Zn-SOD1 upon protein misfolding.

161 CuZn-superoxide dismutase (CuZn-SOD) and ascorbate peroxidase (APX) cons

162 reduction using PTR, homodimeric superoxide dismutase/CuZn (31.4 kDa) was subjected to PTR in order

163 Deletion of copper-zinc superoxide dismutase (CuZnSOD) in Sod1(-/-) mice leads to accelerat

164 Copper/zinc superoxide dismutase (CuZnSOD; SOD1) is widely considered as a pote

165 Ras-related nuclear, p53, PEPCK1, superoxide dismutase, cyclophilin D, and Hsp10, and analyzed the de

166 revealed a range of phenotypes of superoxide dismutase deficiency not observed in previous studies of

167 meric beta-lactoglobulin, dimeric superoxide dismutase, dimeric and tetrameric concanavalin A, and he

168 acids, and has an iron/manganese superoxide dismutase domain.

169 7 is able to induce extracellular superoxide dismutase during differentiation of monocytes but not in

170 The enzyme extracellular superoxide dismutase (EC-SOD; SOD3) is a major antioxidant defense

171 h varying levels of extracellular superoxide dismutase (ecSOD) activity, we have recently shown that

172 e training enhances extracellular superoxide dismutase (EcSOD) expression in skeletal muscle and elic

173 ed the reduction of extracellular superoxide dismutase (EcSOD) protein expression, as well as the ind

174 geted expression of extracellular superoxide dismutase (EcSOD) via the cardiac troponin-T promoter wo

175 ssing lung-specific extracellular superoxide dismutase (ecSOD) were exposed to HEPA-filtered air or t

176 Activities of catalase and superoxide dismutase enzymes, levels of total anthocyanins, DPPH ra

177 HSM also restores superoxide dismutase expression in TGF-beta1-treated lung fibroblas

178 activated catalase and manganese superoxide dismutase expression, indicating that this pathway is co

179 scavenging species, and enzymes (superoxide dismutase family, hydrogen peroxide, and catalase) until

180 ntains exclusively iron-dependent superoxide dismutases (Fe-SODs) located in different subcellular co

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

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

183 substrate (tryparedoxin) and iron superoxide dismutase in COL and SYL (versus TCC) trypomastigotes.

184 de and package a functional Cu-Zn superoxide dismutase in the virion that presumably lowers the conce

185 an functionally replace cytosolic superoxide dismutase in yeast, indicating that the pool of Mn displ

186 F-alpha), CXCL10, CCL5, IL-6, and superoxide dismutase, in human macrophages infected with 3 ATCC and

187 t mice with SOD1(G85R) mice, which express a dismutase-inactive mutant of SOD1 and are considered a m

188 so led to decreased expression of superoxide dismutase isoform 2 and glutathione peroxidase.

189 We used a superoxide dismutase knockout mouse to demonstrate that oxidative s

190 able radical and showed superoxide (O2 (*-)) dismutase-like properties yet were inert to nitric oxide

191 reatment with the small-molecule, superoxide dismutase mimetic (GC4419; 0.25 mumol/L) significantly m

192 A superoxide dismutase mimetic made superoxide levels subnormal, redu

193 Coadministration of tempol, a superoxide dismutase mimetic, ameliorated the exaggerated inflammat

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

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

196 r stress proteins (e.g. manganese superoxide dismutase, mitochondrial KATP channels and peroxisome pr

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

198 part, by deacetylating manganese superoxide dismutase (MnSOD) and mitochondrial 8-oxoguanine DNA gly

199 ers of the catalase and manganese superoxide dismutase (MnSOD) antioxidant genes and stimulate their

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

201 Trx induces manganese superoxide dismutase (MnSOD) gene transcription by activating MKK4

202 Manganese superoxide dismutase (MnSOD) is a mitochondrially localized primary

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

204 d decreased activity of manganese superoxide dismutase (MnSOD).

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

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

207 ut associated with maintenance of superoxide dismutase mRNA expression in the absence of IL-17 in the

208 ated the amidate ligand in nickel superoxide dismutase (NiSOD) in stabilizing Ni-centered redox catal

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

210 ellular antioxidants (sulfhydryl, superoxide dismutase) of zebrafish brain were assessed after recove

211 or by overexpression of manganese superoxide dismutase or catalase.

212 ial ALS patients with mutation in superoxide dismutase or hexanucleotide expansion in C9orf72 (ORF 72

213 th polyethylene glycol-conjugated superoxide dismutase, or NOX4 inhibitors fulvene-5, 6-dimethylamino

214 anine aminotransferase, catalase, superoxide dismutase, ornithine decarboxylase, glutamate receptor,

215 y high abundance of extracellular superoxide dismutase produced by Synechococcus and a dynamic secret

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

217 utathione S-transferase (GST) and superoxide dismutase (SOD) activities.

218 study investigates the levels of superoxide dismutase (SOD) activity in serum and saliva of patients

219 ulation, which result from higher superoxide dismutase (SOD) activity, associated with lower catalase

220 ic or mitochondrial ROS scavenger superoxide dismutase (SOD) caused a significant increase in segrega

221 dase (PPO), peroxidase (POX), and superoxide dismutase (SOD) enzymes activities were measured during

222 toma cells the beneficial role of superoxide dismutase (SOD) enzymes against paraquat-induced toxicit

223 n eukaryotes the bimetallic Cu/Zn superoxide dismutase (SOD) enzymes play important roles in the biol

224 n and colonization by controlling superoxide dismutase (SOD) gene expression.

225 The activity of superoxide dismutase (SOD) in Brassica rapa also displayed a growth

226 Superoxide dismutase (SOD) level in the blood samples expressed sig

227 ences in antioxidant capacity and superoxide dismutase (SOD) levels between phenotypes may allow for

228 k alterations in heritable Cu, Zn superoxide dismutase (SOD) mutants cause misassembly and aggregatio

229 racellular superoxide by specific superoxide dismutase (SOD) showed the applicability for selective i

230 (glutathione-S-transferase (GST), superoxide dismutase (SOD)), and fish health (condition factor (K),

231 IL10, reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT).

232 ehyde (MDA) and activity of total superoxide dismutase (SOD), and its mitochondrial (Mn-SOD) and cyst

233 Activities of superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD) dec

234 sociation of baseline erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx), and catal

235 KO MEFs exhibit reduced levels of superoxide dismutase (Sod), glutathione peroxidase 4 (Gpx4) and per

236 activities of antioxidant enzymes superoxide dismutase (SOD), glutathione reductase (GR), and catalas

237 V-A also inhibits the activity of superoxide dismutase (SOD), magnifying the imbalance of redox statu

238 cytokines only when stimulated by superoxide dismutase (SOD)-1.

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

240 of antioxidant enzymes, including superoxide dismutase (SOD).

241 ant strains lacking mitochondrial superoxide dismutase (sod-2) showed oxidative stress for two FeOx a

242 thione S-transferase P (GSTP) and superoxide dismutases (SOD).

243 The dismutase SOD1 also acts as an antioxidant, but it local

244 t the activity of the copper/zinc superoxide dismutase Sod1 and that loss of Sod1 activity contribute

245 gical deposition of mutated Cu/Zn superoxide dismutase (SOD1) accounts for approximately 20% of the f

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

247 between homodimeric mutant Cu, Zn superoxide dismutase (SOD1) and wild-type (WT) SOD1 is suspected to

248 1) activates immature copper-zinc superoxide dismutase (Sod1) by delivering copper and facilitating t

249 an inhibit the amyloidogenesis of superoxide dismutase (SOD1) by increasing the intrinsic net negativ

250 lation (nanozyme) for copper/Zinc superoxide dismutase (SOD1) by polyion condensation with a conventi

251 Mutations in superoxide dismutase (SOD1) cause amyotrophic lateral sclerosis (AL

252 Mutations in superoxide dismutase (SOD1) cause amyotrophic lateral sclerosis (AL

253 ions in the metallo-protein Cu/Zn-superoxide dismutase (SOD1) cause amyotrophic lateral sclerosis (AL

254 tional modifications within Cu,Zn-superoxide dismutase (SOD1) cause this otherwise protective enzyme

255 rences among apo-, Zn-, and Cu,Zn-superoxide dismutase (SOD1) dimers.

256 hout the brain and spinal cord of superoxide dismutase (SOD1) G93A transgenic mice.

257 tients with mutation in the Cu/Zn superoxide dismutase (SOD1) gene, we show that spinal MNs, but rare

258 expresses a Cu-requiring form of superoxide dismutase (Sod1) in the cytosol; but when Cu levels decl

259 Aggregation of copper-zinc superoxide dismutase (SOD1) is a defining feature of familial ALS c

260 ously, we found that human Cu, Zn-superoxide dismutase (SOD1) is S-acylated (palmitoylated) in vitro

261 rodents expressing ALS-associated superoxide dismutase (SOD1) mutations develop spontaneous blood-spi

262 Cu/Zn superoxide dismutase (SOD1) reduction prolongs survival in SOD1-tra

263 uitous expression of mutant Cu/Zn-superoxide dismutase (SOD1) selectively affects motor neurons in th

264 port on the conformation of Cu-Zn superoxide dismutase (SOD1) through the sensitive measurement of di

265 Delivery of copper-zinc superoxide dismutase (SOD1), an efficient ROS scavenger, to the sit

266 transgenic for mutant human Cu/Zn superoxide dismutase (SOD1), G85R SOD1YFP and G93A SOD1, little or

267 ALS model mice expressing mutant superoxide dismutase (SOD1), reduction of MMP-9 function using gene

268 ing pathway of mutant copper-zinc superoxide dismutase (SOD1), the protein known to be a cause of fam

269 We focused on Cu-Zn superoxide dismutase (SOD1), which protects cells from oxidative st

270 to the antioxidant metalloenzyme superoxide dismutase (SOD1).

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

272 f cases, including those in Cu/Zn superoxide dismutase (SOD1).

273 ed for ALS-linked forms of Cu, Zn superoxide dismutase (SOD1).

274 chrome c oxidase (CcO), and Cu/Zn superoxide dismutase (SOD1); (c) metal ion misregulation has also b

275 The dismutase SOD2 localizes in the matrix and is a major an

276 XO3, an important regulator of Mn-superoxide dismutase (SOD2) expression, a tumor suppressor, and a c

277 Manganese superoxide dismutase (SOD2) is a primary defense against mitochondr

278 study, we show that mitochondrial superoxide dismutase (Sod2) is highly expressed in OCCC compared wi

279 upregulation of the antioxidants superoxide dismutase (SOD2), catalase, methionine sulfoxide reducta

280 on of ROS-producing extracellular superoxide dismutase (SOD3) in thyroid cancer cell lines although a

281 nzymes that detoxify ROS, such as superoxide dismutase (SodA).

282 t lacking the manganese-dependent superoxide dismutase, SodA, was significantly less virulent than wi

283 ine-pyruvate transaminase (avtA), superoxide dismutase (sodB), and 2 hypothetical proteins.

284 eliver the metal ion to the Cu/Zn superoxide dismutase SodCII.

285 Superoxide dismutases (SODs) are metalloproteins that protect organ

286 stems that include iron-dependent superoxide dismutases (SODs) in mitochondria and glycosomes.

287 The copper-containing superoxide dismutases (SODs) represent a large family of enzymes th

288 tosolic and chloroplast-localized superoxide dismutases (SODs), which are known to be dependent on co

289 tems, including a nascent form of superoxide dismutase that is implicated in neurodegenerative diseas

290 organisms employ a separate enzyme, chlorite dismutase, to prevent accumulation of the destructive Cl

291 atalase, ascorbate peroxidase and superoxide dismutase together with xanthophyll cycle and non-photoc

292 Erythrocyte Mn-superoxide dismutase was also reduced at 6 (0.154 vs. 0.096, P = 0.

293 , and mRNA levels of catalase and superoxide dismutase were increased, whereas those of nitric oxide

294 xidase, glutathione reductase and superoxide dismutase were measured.

295 component, biotin carboxylase and superoxide dismutase were related to energy and carbon metabolism,

296 alase, glutathione peroxidase and superoxide dismutase were significantly lower in PSE-induced sample

297 ctor acetylhydrolase [PAF-AH] and superoxide dismutase) were measured from samples collected before d

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

299 culated the kon rate constant for superoxide dismutase with its natural substrate, O2-, in a validati

300 mes viz. catalase, peroxidase and superoxide dismutase with the excess accumulation of proline.