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 MNs exhibited an E(GABAAR)10 mV more depolarized tha

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

6 amma (IFN-gamma) and superoxide dismutase 1 (SOD) (P < 0.05).

7 at the core of human superoxide dismutase 1 (SOD) with 0.7 pm precision.

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

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

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

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

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

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

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

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

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

17 ignaling with higher efficiency than CD31 Ab/SOD.

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

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

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

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

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

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

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

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

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

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

28 ogenous antioxidants content (P < 0.001) and SOD activity (P < 0.02) compared to CG meat.

29 [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

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

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

32 e assayed for total antioxidant capacity and SOD activity.

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

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

35 mation, downregulated anti-oxidative GSH and SOD activity;si-TTP upregulated pro-apoptotic cleaved-ca

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

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

38 demonstrated hypoxic induction of Hyal2 and SOD-suppressible hyaluronidase activity, congruent to ou

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

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

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

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

43 of antioxidant enzymes (CAT, APOX, POD, and SOD) all increased in response to drought stress but dec

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

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

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

47 y exchanging metal cofactors for antioxidant SODs.

48 mical (ALB, AMY, TP and GLOB), antioxidants (SOD, GPx and GSH), and immune (IgM and lysozyme) paramet

49 ession of defense-related pine genes such as SOD (superoxide dismutase), LOX (lipoxygenase), PAL (phe

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

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

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

53 Both SODs were monomeric and they exhibited similar binding a

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

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

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

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

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

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

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

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

62 between Fe homeostasis and extracellular Cu-SODs may help many fungi adapt to Fe-limited conditions

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

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

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

66 r results demonstrate the roles of different SODs in miR398b-regulated resistance to rice blast disea

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

70 ntaining peptides, and superoxide dismutase (SOD) activity have been detected in the raw and cooked m

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 ract showed revival in superoxide dismutase (SOD) activity.

74 antioxidant enzymes - superoxide dismutase (SOD) and catalase (CAT), encapsulated in biodegradable n

75 nts (i.e., copper/zinc superoxide dismutase (SOD) and extracellular SOD only in oxidative muscle.

76 uch as catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH).

77 AT), peroxidase (POD), superoxide dismutase (SOD) and glutathione reductase (GR) activities, which le

78 (APX), catalase (CAT), superoxide dismutase (SOD) and peroxidase (POD) in roots and shoots indicate a

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

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 quitous iron/manganese superoxide dismutase (SOD) family exemplifies this deficit, as the specific me

84 sion of CSDs and other superoxide dismutase (SOD) family members, leading to increased total SOD enzy

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

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

87 Copper/zinc superoxide dismutase (SOD) is a homodimeric metalloenzyme that has been extens

88 Superoxide dismutase (SOD) is a key enzyme that plays a primary role in removi

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

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

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

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

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

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

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

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

97 A), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), matrix metalloproteinase-9 (MMP-9)

98 vities of catalase and superoxide dismutase (SOD), compared to the OS strains.

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

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

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

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

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

104 ant enzymes, including superoxide dismutase (SOD).

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

106 F extracts contained 'superoxide dismutase' (SOD), a known food allergen, osmotic shock extract conta

107 BAL superoxide dismutase(SOD), plasma total-antioxidant capacity activity, and sR

108 activity of cytosolic superoxide dismutase, SOD-1.

109 Copper (Cu)-only superoxide dismutases (SOD) represent a newly characterized class of extracellu

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

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

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

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

114 Copper-only superoxide dismutases (SODs) represent a new class of SOD enzymes that are excl

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

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

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

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

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

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

121 be used to distinguish the functions of each SOD for resistance to oxidative stress that changes with

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

123 novel substrate of CatA, which decreased EC-SOD abundance 5-fold.

124 antioxidant enzyme superoxide dismutase (EC-SOD) as a novel substrate of CatA, which decreased EC-SO

125 in of extracellular superoxide dismutase (EC-SOD), with arginine to glycine substitution at position

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

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

128 In conclusion, CatA-mediated EC-SOD reduction in the heart contributes to increased oxid

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

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

131 Redistribution of EC-SOD resolves bleomycin-induced inflammation via increase

132 Loss of EC-SOD-mediated antioxidative activity resulted in signific

133 e provide new evidence that redistributed EC-SOD accelerates the resolution of inflammation through r

134 on at position 213 (R213G), redistributes EC-SOD from the matrix into extracellular fluids.

135 e LV of transgenic mice (CatA-TG) reduced EC-SOD protein levels by 43%.

136 ardiac fibroblasts expressed and secreted EC-SOD protein.

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

138 study, we tested the hypothesis that the EC-SOD R213G SNP promotes resolution via accelerated apopto

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

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

141 superoxide dismutase (SOD) and extracellular SOD only in oxidative muscle.

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

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

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

145 a newly characterized class of extracellular SODs important for virulence of several fungal pathogens

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

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

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

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

150 ively Fe-dependent superoxide dismutases (Fe-SODs).

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

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

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

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

155 c inputs to E17.5 fetal MNs from SOD1(G93A) (SOD) mice in parallel with chloride homeostasis.

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

157 gnificant effect on antioxidant levels (GSH, SOD, and CAT) (P >0.05).

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

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

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

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

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

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

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

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

166 results show that IPSCs are less frequent in SOD animals in accordance with a reduction of synaptic V

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

168 Interestingly, SOD GABAergic/glycinergic IPSCs and evoked GABA(A)R-curr

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

170 gen Candida auris contain a single SOD5-like SOD rather than a pair, and in both fungi, this SOD was

171 Systemic and local SOD levels are lowered in CP.

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

173 tonin-treated plants had significantly lower SOD and POD activities than control plants under drought

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

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

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

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

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

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

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

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

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

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

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

185 We searched B. mori SOD (BmSOD) genes using genome database, and we analyzed

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

187 In conclusion, nano-SOD/CAT mitigated activation of cascade of degenerating

188 sulated in biodegradable nanoparticles (nano-SOD/CAT) - at the lesion site would protect mitochondria

189 o test our hypothesis, a single dose of nano-SOD/CAT in saline was administered intravenously 6 h pos

190 e affected region of the spinal cord of nano-SOD/CAT-treated animals demonstrated significantly reduc

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

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

193 hobic interactions between A and B chains of SOD, and van der Waals interactions occupied a dominant

194 formational locks) between A and B chains of SOD.

195 e dismutases (SODs) represent a new class of SOD enzymes that are exclusively extracellular and uniqu

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

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

198 ations of two differently metalated forms of SOD, namely, the fully mature functional Cu,Zn state and

199 roteins or mRNA) and increased the levels of SOD.

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

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

202 cellular levels of Mn-antioxidant mimics of SOD.

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

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

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

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

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

208 40% PEG solution, we find that the volume of SOD was reduced by 9%.

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

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

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

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

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

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

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

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

217 of a vulnerable active site for copper-only SODs and the possible exploitation of this vulnerability

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

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

220 Fungal copper-only SODs harbor an irregular active site that, unlike their

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

222 ng copper binding, making fungal copper-only SODs highly vulnerable to metal chelators.

223 show here an additional role for copper-only SODs in promoting survival of fungal biofilms.

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

225 Candida albicans expresses three copper-only SODs, and deletion of one of them, SOD5, eradicated cand

226 ake of toxic metals and inhibits copper-only SODs.

227 /Zn-SODs in its animal hosts, making Cu-only SODs a possible target for future antifungal drug design

228 rom the spinal cords of untreated control or SOD/CAT solution treated animals.

229 were randomized to administer either SDD or SOD.

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

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

232 Plasma SOD levels from patients with cALD demonstrated an inver

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

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

235 oxidative stress by increasing GT, CAT, POD, SOD and GR activities and reducing GSSG.

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

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

238 the tear film, scavenging ROS, up-regulating SOD, promoting and maintaining corneal and conjunctival

239 netic analysis of two evolutionarily related SODs with different metal specificity produced by the pa

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

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

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

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

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

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

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

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

248 functioning, anti-oxidative defence system (SOD, CAT, and GR) and Ver-1 gene of aflatoxin B(1) biosy

249 Targeting SOD to endothelial surface vs. intracellular compartment

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

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

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

253 Collectively, we show that SOD-1-mediated H(2)O(2) production regulates the redox e

254 at has not been discovered previously in the SOD family, and they were expressed in different tissues

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

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

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

258 using peroxiredoxin-6 overexpression or the SOD mimetic tempol, prevented chromatin SUMO3 depletion,

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

260 These SODs are essential for virulence of fungal pathogens in

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

262 rather than a pair, and in both fungi, this SOD was induced by Fe starvation.

263 Thus, SOD conjugated with antibodies to cell adhesion molecule

264 Total SOD activity was significantly lowered in the glaucoma g

265 letion, resulting in decreased CSD and total SOD enzyme activity.

266 latory network in which miR398b boosts total SOD activity to upregulate H(2) O(2) concentration and t

267 ) family members, leading to increased total SOD enzyme activity that positively contributed to highe

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

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

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

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

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

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

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

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

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

277 87-amino-acid protein that resembles a Cu-Zn SOD with all of the conserved amino acid residues for bi

278 nosine (8-OHdG), superoxide dismutase (Cu-Zn SOD), and thiobarbituric acid reactive substances (TBARS

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

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

281 regular active site that, unlike their Cu,Zn-SOD counterparts, contains a copper co-factor unusually

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

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

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

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

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

287 e expressions of hepatic antioxidants (Cu/Zn-SOD and GPx-4), inflammatory cytokines (TNF-alpha and TG

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

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

290 ts, with interactions being present in Cu/Zn-SOD, TNF-alpha, TGF-beta1, FASN and IGF-I.

291 y mature functional Cu,Zn state and the E,Zn-SOD state in which the Cu site is empty.

292 ous studies on superoxide dismutases (Cu, Zn-SODs) showed that the dimeric structure contributed to t

293 interactions between two subunits of Cu, Zn-SODs.

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

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

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

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

298 of SOD5 strongly deviate from those of Cu/Zn-SODs in its animal hosts, making Cu-only SODs a possible

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