ライフサイエンスコーパス: superoxide dismutase

1 oxidant markers (Glutathione peroxidase, and superoxide dismutase).

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

3 of toxic superoxide to hydrogen peroxide by superoxide dismutase.

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

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

6 le such as strongly donating thiolates in Ni superoxide dismutase.

7 orms of either Tar DNA-binding protein 43 or superoxide dismutase.

8 erwise functionally redundant SoxR-regulated superoxide dismutase.

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

10 L-6, IL-17, interferon-gamma (IFN-gamma) and superoxide dismutase 1 (SOD) (P < 0.05).

11 II) coordination sphere at the core of human superoxide dismutase 1 (SOD) with 0.7 pm precision.

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

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

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

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

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

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

18 ta, mitochondrial dysfunction, and disturbed superoxide dismutase 1 (SOD1) and Keap1/Nrf2 antioxidant

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

20 Mutations in the gene encoding superoxide dismutase 1 (SOD1) are the second most common

21 Non-natively folded variants of superoxide dismutase 1 (SOD1) are thought to contribute

22 Mutations in superoxide dismutase 1 (SOD1) cause 15-20% of familial a

23 Mutations in Cu-Zn superoxide dismutase 1 (SOD1) cause familial forms of am

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

25 and ALS patients harboring mutations in the superoxide dismutase 1 (SOD1) gene.

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

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

28 throughout the sequence of the gene encoding superoxide dismutase 1 (SOD1) have been linked to toxic

29 the activity and release of a model enzyme, superoxide dismutase 1 (SOD1) immobilized by polyion cou

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

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

32 genic proteins amyloid-beta (Abeta), tau and superoxide dismutase 1 (SOD1) in the cerebrospinal fluid

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

34 cid to lysine (E40K) residue substitution in superoxide dismutase 1 (SOD1) is associated with canine

35 Superoxide dismutase 1 (SOD1) is the principal cytoplasm

36 onucleotide that mediates the degradation of superoxide dismutase 1 (SOD1) messenger RNA to reduce SO

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

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

39 yotrophic lateral sclerosis (ALS)-associated superoxide dismutase 1 (SOD1) mutant protein induces cha

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

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

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

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

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

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

46 Here, we examined potential inhibitors of superoxide dismutase 1 (SOD1) using ThT-fluorescence inc

47 sis (ALS) and mutations in the gene encoding superoxide dismutase 1 (SOD1) were treated with a single

48 trophic lateral sclerosis (ALS) mouse model, superoxide dismutase 1 (SOD1)(G93A), revealed that these

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

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

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

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

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

54 form transiently during aggregation of human superoxide dismutase 1 (SOD1), which is known to form mi

55 lateral sclerosis-associated protein variant superoxide dismutase 1 (SOD1)-A4V, whereas HSPA1L enhanc

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

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

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

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

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

61 nts for TAR DNA-binding protein (TDP-43) and superoxide dismutase 1 (SOD1).

62 al-sequence-lacking Acb1 and the antioxidant superoxide dismutase 1 (SOD1).

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

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

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

66 cardial expression of free radical scavenger superoxide dismutase 1 and aldehyde dehydrogenase 2 was

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

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

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

70 ed with mitochondrial dysfunction, disturbed superoxide dismutase 1 and Keap1/Nrf2 antioxidant respon

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

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

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

74 (ALS), in which astrocytes expressing mutant superoxide dismutase-1 (mutSOD1) kill wild-type motor ne

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

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

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

78 Superoxide dismutase-1 (SOD1) maturation comprises a str

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

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

81 cells in mice expressing the ALS-associated superoxide dismutase-1 (SOD1)(G93A) mutant decreased spi

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

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

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

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

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

87 hase II enzymes (heme oxygenase-1, catalase, superoxide dismutase-1) in a time-dependent manner.

88 which accumulate intracellular aggregates of superoxide dismutase-1.

89 egulation in messenger RNA of shared targets superoxide dismutase 2 (P <= 0.001) and heme oxygenase 1

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

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

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

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

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

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

96 , we observed that inhibitory acetylation of superoxide dismutase 2 (SOD2) at K122 was increased in W

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

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

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

100 Superoxide dismutase 2 (SOD2) is a crucial antioxidative

101 Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpresse

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

103 drial morphology, elevated protein levels of superoxide dismutase 2 (SOD2), and increased levels of p

104 d proteins and increased antioxidant enzymes superoxide dismutase 2 (SOD2), catalase, glutathione per

105 f specific mitochondrial proteins, including superoxide dismutase 2 (SOD2), depended on 4E-BP1/2.

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

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

108 iR-145-5p caused significant upregulation of superoxide dismutase 2 and heme oxygenase 1 protein foll

109 increased the levels of peroxiredoxin 3 and superoxide dismutase 2 in adipose tissue, indicating inc

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

111 on of oxidative damage markers, and of SOD2 (superoxide dismutase 2), PGC1alpha [peroxisome prolifera

112 elongation in rice (Oryza sativa) (FSD2, Fe-superoxide dismutase 2).

113 polymorphisms were discovered in relation to superoxide dismutase 2, ATP binding cassette subfamily A

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

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

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

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

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

119 nd its target genes (including mitochondrial superoxide dismutase), (2) enhanced phagocytic activity

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

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

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

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

124 In this study, we investigated the effect of superoxide dismutase 3 (SOD3) on LL-37- or KLK-5-induced

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

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

127 41.1 +/- 17.6% of normoxic control), reduced superoxide dismutase (60.7 +/- 6.3%), increased phosphod

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

129 ABA caused further increases in catalase and superoxide dismutase activities, which led to a signific

130 Superoxide dismutase activity in human blood plasma mirr

131 tain wild-type levels of manganese-dependent superoxide dismutase activity in the presence of calprot

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

133 The superoxide dismutase activity was relatively insensitive

134 oxidase, distinct from the established MnSOD superoxide dismutase activity.

135 a higher activity of the antioxidant enzyme superoxide dismutase and a different regulation of the g

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

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

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

139 ated genes, including one of three copies of superoxide dismutase and five novel members of its regul

140 hermore, Sch A lowered DON-induced catalase, superoxide dismutase and glutathione peroxidase antioxid

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

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

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

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

145 In B. asiatica, high superoxide dismutase and significantly enhanced (p < 0.0

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

147 by well-promoted antioxidant enzymes (i.e., superoxide dismutase, and catalase), strong DPPH-scaveng

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

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

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

151 O USNPs simultaneously possessing catalase-, superoxide dismutase-, and glutathione peroxidase-mimick

152 ies were characterized by higher activity of superoxide dismutase, ascorbate peroxidase and phenylala

153 (H(2) O(2) ) is produced, via superoxide and superoxide dismutase, by electron transport in chloropla

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

155 larly, 10 mmol L(-1) treatment showed higher superoxide dismutase, catalase and ascorbate peroxidase

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

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

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

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

160 contrast, mutations in Copper Chaperone for Superoxide Dismutase (CCSD) resulted in enhanced suscept

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

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

163 o ALS pathogenesis (RNA-binding protein FUS, superoxide dismutase Cu-Zn and neurofilaments light poly

164 arkers 8-hydroxy-2'-deoxyguanosine (8-OHdG), superoxide dismutase (Cu-Zn SOD), and thiobarbituric aci

165 The previous studies on superoxide dismutases (Cu, Zn-SODs) showed that the dime

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

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

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

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 ntified the extracellular antioxidant enzyme superoxide dismutase (EC-SOD) as a novel substrate of Ca

173 n the matrix-binding domain of extracellular superoxide dismutase (EC-SOD), with arginine to glycine

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

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

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

177 polyphenol oxidase and increased activity of superoxide dismutase enzyme.

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 ease (CD), contains exclusively Fe-dependent superoxide dismutases (Fe-SODs).

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

183 target genes and demonstrated that multiple superoxide dismutase genes contribute to miR398b-regulat

184 ive (SynCav1(+)) mouse with the mutant human superoxide dismutase glycine to alanine point mutation a

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

186 Scavengers of superoxide radical anion (superoxide dismutase), hydrogen peroxide (catalase), hyd

187 to the stability of the ALS related protein superoxide dismutase I (SOD1) in mammalian cells, we sho

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

189 mutase 1 (SOD1) is the principal cytoplasmic superoxide dismutase in humans and plays a major role in

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

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

192 se inactivation are similar, suggesting that superoxide dismutase is calibrated so the oxygen- and su

193 n of defense-related pine genes such as SOD (superoxide dismutase), LOX (lipoxygenase), PAL (phenylal

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

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

196 ve stress, because treatment with Tempol, an superoxide dismutase mimetic, rescued kidney injury in k

197 compare the efficacy and safety of GC4419, a superoxide dismutase mimetic, with placebo to reduce the

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

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

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

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

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

203 Manganese superoxide dismutase (MnSOD) functions as a tumor suppre

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

205 Manganese superoxide dismutase (MnSOD) is a mitochondrially locali

206 fic antioxidant enzyme, manganese-containing superoxide dismutase (MnSOD), has dual roles in early- a

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

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

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

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

211 ction of a stable monomeric variant of Cu/Zn superoxide dismutase (mSOD1), an enzyme responsible for

212 ial fusion and increasing cytoplasmic ROS in superoxide dismutase mutants.

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

214 d against the proteotoxicity of mutant Cu/Zn superoxide dismutase or C9orf72 dipeptide repeat protein

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

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

217 phenols, histidine-containing peptides, and superoxide dismutase (SOD) activity have been detected i

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

219 while 400 ug/ml of extract showed revival in superoxide dismutase (SOD) activity.

220 exogenous delivery of antioxidant enzymes - superoxide dismutase (SOD) and catalase (CAT), encapsula

221 increases of antioxidants (i.e., copper/zinc superoxide dismutase (SOD) and extracellular SOD only in

222 ogenous antioxidants such as catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH).

223 one (GSH), catalase (CAT), peroxidase (POD), superoxide dismutase (SOD) and glutathione reductase (GR

224 ascorbate peroxidase (APX), catalase (CAT), superoxide dismutase (SOD) and peroxidase (POD) in roots

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

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

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

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

229 The ubiquitous iron/manganese superoxide dismutase (SOD) family exemplifies this defic

230 splayed altered expression of CSDs and other superoxide dismutase (SOD) family members, leading to in

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

232 Copper/zinc superoxide dismutase (SOD) is a homodimeric metalloenzym

233 Superoxide dismutase (SOD) is a key enzyme that plays a

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

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

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

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

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

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

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

241 of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), matrix metal

242 icantly increased activities of catalase and superoxide dismutase (SOD), compared to the OS strains.

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

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

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

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

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

248 Copper (Cu)-only superoxide dismutases (SOD) represent a newly characteri

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

250 The PEF extracts contained 'superoxide dismutase' (SOD), a known food allergen, osmo

251 BAL superoxide dismutase(SOD), plasma total-antioxidant capa

252 , which depends on the activity of cytosolic superoxide dismutase, SOD-1.

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

254 S. cerevisiae) Cu chaperone for Cu-zinc (Zn) superoxide dismutase (SOD1) activates by directly promot

255 S) homeostasis by repressing a Cu-containing superoxide dismutase (SOD1) and inducing Mn-containing S

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

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

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

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

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

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

262 Here, we examine the trajectory that Cu/Zn superoxide dismutase (SOD1) dimers take over the unfoldi

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

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

265 Mutations in Cu/Zn superoxide dismutase (Sod1) have been reported in both f

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

267 Here, we show that Cu, Zn superoxide dismutase (SOD1) is unique among proteins in

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

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

270 on of BMAA into the ALS-linked protein Cu,Zn superoxide dismutase (SOD1) upon translation promotes pr

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

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

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

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

275 mutations in the metallo-enzyme copper-zinc superoxide dismutase (SOD1).

276 Mitochondrial superoxide dismutase (SOD2) suppresses tumor initiation

277 tional coactivator PGC-1alpha, mitochondrial superoxide dismutase (SOD2), and chemical antioxidants a

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

279 ess due to hyperacetylation of mitochondrial superoxide dismutase (SOD2), increases HIF1alpha (hypoxi

280 n detached cells by regulating the manganese superoxide dismutase (SOD2).

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

282 The antioxidant enzyme extracellular superoxide dismutase (SOD3) protects against hypoxia-ind

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

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

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

288 Copper-only superoxide dismutases (SODs) represent a new class of SO

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

290 responses in catalase, guaiacol peroxidase, superoxide dismutase, soluble protein, lignin, chlorophy

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

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

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

294 sporter 2, NADP-dependent glyceraldehyde and superoxide dismutase were found significantly upregulate

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

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

297 one contents, and activities of catalase and superoxide dismutase were significantly deteriorated in

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

299 Among these was the SodA superoxide dismutase, which is essential for mammalian i

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