ライフサイエンスコーパス: MnSOD

1 MnSOD contains a nutrient- and ionizing radiation (IR)-d

2 MnSOD enzyme activity and its mRNA were decreased signif

3 MnSOD expression was significantly (P<0.05) decreased in

4 MnSOD lines had a three-fold increase in MnSOD activity,

5 MnSOD overexpression prevented a glucose-induced increas

6 MnSOD protects the retina from diabetes-induced abnormal

7 MnSOD protein carrying a K89A mutation had significantly

8 MnSOD siRNA also reduced nitric oxide production in supe

9 MnSOD-promoter/enhancer analysis demonstrates that p53 i

10 pression of cytoprotective molecules (Bcl-2, MnSOD, GADD45beta, A1) and suppressing proinflammatory t

11 verexpression of p38K extends life span in a MnSOD-dependent manner, whereas inhibition of p38K cause

12 ochemistry for SIRT3 activity via acetylated MnSOD(K68) Murine AEC SIRT3 and cleaved caspase-9 (CC-9)

13 n cells that were pretreated with adenoviral MnSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosoure

14 Transplantation of diabetic EPCs after MnSOD gene therapy restored their ability to mediate ang

15 Silencing studies using siRNA against MnSOD showed that similar results were observed in MnSOD

16 t ER stress via Akt-dependent PrP(C) and Akt-MnSOD pathway.

17 ndings, LPS induced NF-kappaB activation and MnSOD expression in isolated fetal pulmonary arterial en

18 these residues abrogates MKK4 activation and MnSOD expression.

19 death through downregulation of catalase and MnSOD.

20 iated with upregulation of eNOS, p-eNOS, and MnSOD, which reduce oxidative stress and have anti-infla

21 ing regulation of SIRT1/FoxO3a, MEK/ERK, and MnSOD, resulting in oxidative stress intolerance, thereb

22 ndicate that alterations of nitric oxide and MnSOD contribute to pathological HIF-1alpha expression a

23 e mitochondria contain fidelity proteins and MnSOD constitutes an integral part of the nucleoid compl

24 , were not statistically different in WT and MnSOD-Tg diabetic mice.

25 As MnSOD has been shown to remove superoxide radical with v

26 g expression of ROS scavenger genes, such as MnSOD, catalase and PRDX3.

27 repression of FOXO3a-regulated genes such as MnSOD, p27Kip1, and BIM-1.

28 rotonation" pathway than human and bacterial MnSODs and suggested that this could result from small s

29 MnSODs surpass those of human and bacterial MnSODs, due to very low level of product inhibition.

30 cantly more product-inhibited than bacterial MnSODs at high concentrations of superoxide (O(2)(-)).

31 /-) mice demonstrates an interaction between MnSOD, p53 and Polgamma.

32 onse to NAC exposure was an increase in both MnSOD protein and activity.

33 which leads to AP-1 dissociation followed by MnSOD transcription.

34 e stress and increased antioxidant capacity (MnSOD, CuSOD and Catalase activity).

35 the levels of MnSOD protein did not change, MnSOD activity and mitochondrial respiration decreased i

36 as ScMnSOD > D. radiodurans MnSOD > E. coli MnSOD > human MnSOD.

37 efficiencies scaled as Drad MnSOD > E. coli MnSOD > human MnSOD.

38 ct inhibition was similar to that in E. coli MnSOD, specifically a decrease in the rate constant for

39 ared to those of wild-type human and E. coli MnSOD.

40 roduct inhibition resembling that of E. coli MnSOD.

41 rt the crystal structure of Escherichia coli MnSOD with hydrogen peroxide cryotrapped in the active s

42 4 is different in human and Escherichia coli MnSOD.

43 with that of both human and Escherichia coli MnSODs was undertaken.

44 els of alphaA crystallin, betaB2 crystallin, MnSOD, and aconitase and decreased levels of ATP synthas

45 ion of alphaA crystallin, betaB2 crystallin, MnSOD, and Hsp70.

46 ine (K68Q), mimicking acetylation, decreased MnSOD activity in SNc dopaminergic neurons, whereas muta

47 to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 bin

48 Livers of Sirt3/ mice exhibit decreased MnSOD activity, but not immunoreactive protein, relative

49 RPE-J cells with Rz432 resulted in decreased MnSOD mRNA and protein as well as increased levels of su

50 diomyopathy may be attributable to decreased MnSOD expression.

51 We found that decreasing MnSOD with small interfering RNA in MCF-7 cells resulted

52 wnregulating manganese superoxide dismutase (MnSOD) activity by causing the nitrosylation of tyrosine

53 ane-targeted 30 kDa Mn-superoxide dismutase (MnSOD) and a cytosolic FeSOD.

54 suggest that manganese superoxide dismutase (MnSOD) and calpain may be critical mediators of this pro

55 coding genes manganese superoxide dismutase (MnSOD) and catalase (Cat), thereby decreasing cellular l

56 eacetylating manganese superoxide dismutase (MnSOD) and mitochondrial 8-oxoguanine DNA glycosylase.

57 r 1177), and manganese superoxide dismutase (MnSOD) and reduced serum interleukin (IL)-6 with concomi

58 catalase and manganese superoxide dismutase (MnSOD) antioxidant genes and stimulate their transcripti

59 , increasing manganese superoxide dismutase (MnSOD) can increase intracellular H(2)O(2).

60 idant enzyme manganese superoxide dismutase (MnSOD) exacerbated amyloid pathology.

61 Manganese-dependent superoxide dismutase (MnSOD) expression also increased significantly in respon

62 ad increased manganese superoxide dismutase (MnSOD) expression, a manifestation of mitochondrial dysf

63 ncreased mitochondrial superoxide dismutase (MnSOD) expression, decreased DNA oxidation, reduced REV1

64 Manganese superoxide dismutase (MnSOD) from different species differs in its efficiency

65 Trx induces manganese superoxide dismutase (MnSOD) gene transcription by activating MKK4 via redox c

66 ffect on the manganese superoxide dismutase (MnSOD) gene was investigated.

67 xpression of manganese superoxide dismutase (MnSOD) in EPCs contributes to impaired would healing in

68 xpression of manganese superoxide dismutase (MnSOD) in IPAH-ECs paralleled increased HIF-1alpha level

69 target gene manganese superoxide dismutase (MnSOD) in the pulmonary endothelium.

70 Human manganese superoxide dismutase (MnSOD) is a homotetramer of 22 kDa subunits, a dimer of

71 Manganese superoxide dismutase (MnSOD) is a mitochondrially localized primary antioxidan

72 Manganese superoxide dismutase (MnSOD) is a nuclear encoded and mitochondrial matrix-loc

73 Human manganese superoxide dismutase (MnSOD) is characterized by a product inhibition stronger

74 subunits in manganese superoxide dismutase (MnSOD) is currently under scrutiny.

75 idant enzyme manganese superoxide dismutase (MnSOD) modulates the cellular redox environment by conve

76 ion of human manganese superoxide dismutase (MnSOD) mRNA in human lung carcinoma cells, A549, mediate

77 icotiana mitochondrial superoxide dismutase (MnSOD) or an Escherichia coli glutathione reductase (gor

78 NA levels of manganese superoxide dismutase (MnSOD) or glutamate cysteine ligase (GCL) expression.

79 Manganese superoxide dismutase (MnSOD) plays a critical role in the survival of aerobic

80 whether mitochondrial superoxide dismutase (MnSOD) provides protection.

81 othesis that manganese superoxide dismutase (MnSOD) regulates cellular redox flux and glucose consump

82 ctive enzyme manganese superoxide dismutase (MnSOD) was expressed in RPE-J cells, and adeno-associate

83 xpression of manganese superoxide dismutase (MnSOD) was reduced by 38%, indicating that the susceptib

84 lacking mitochondrial superoxide dismutase (MnSOD) were modestly drug-resistant, and elimination of

85 Manganese superoxide dismutase (MnSOD), a mitochondrial antioxidant enzyme, is necessary

86 ssion of mitochondrial superoxide dismutase (MnSOD), and the consequent inhibition of ROS formation a

87 idant enzyme manganese superoxide dismutase (MnSOD), as a RelA target and potential antinecroptotic g

88 [i.e., p65, manganese superoxide dismutase (MnSOD), phosphorylated extracellular signal-regulated ki

89 e levels, of manganese superoxide dismutase (MnSOD), the mitochondrial enzyme that catalyzes superoxi

90 xpression of manganese superoxide dismutase (MnSOD), when combined with certain chemicals that inhibi

91 deletion of manganese superoxide dismutase (MnSOD).

92 motetrameric manganese superoxide dismutase (MnSOD).

93 a manganese-containing superoxide dismutase (MnSOD).

94 27(kip1) and manganese superoxide dismutase (MnSOD).

95 S scavenging enzyme Mn-superoxide dismutase (MnSOD).

96 activity of manganese superoxide dismutase (MnSOD).

97 ging protein manganese superoxide dismutase (MnSOD); the alpha(1)-AR-p66Shc-dependent pathway involvi

98 nt defenses [manganese superoxide dismutase (MnSOD)P< 0.05; copper/zinc superoxide dismutaseP< 0.05;

99 Manganese superoxide dismutase (MnSOD/SOD2) is a mitochondria-resident enzyme that gover

100 Manganese superoxide-dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD), and

101 d-type (WT) manganese superoxide dismutases (MnSODs) from Saccharomyces cerevisiae and Candida albica

102 the dismutation efficiencies scaled as Drad MnSOD > E. coli MnSOD > human MnSOD.

103 Further, Drad MnSOD is most effective at high superoxide fluxes found

104 ts cellular origin, a comparison of the Drad MnSOD efficiency with that of both human and Escherichia

105 X-ray crystal structures of E162D and E162A MnSOD reveal no significant structural changes compared

106 drogen bond interaction with His163 in E162A MnSOD.

107 In the case of E162D MnSOD, an intervening solvent molecule fills the void cr

108 Elevating MnSOD levels in cells enhances the conversion of superox

109 e methylation of Sod2, the gene that encodes MnSOD, in the development of diabetic retinopathy and in

110 ng the longer transcript enhanced endogenous MnSOD mRNA levels, which was associated with an increase

111 na in diabetes, and their scavenging enzyme, MnSOD, becomes subnormal.

112 whether it is a feature common to eukaryotic MnSODs, we purified MnSOD from Saccharomyces cerevisiae

113 d approximately 5% decrease, males/females), MnSOD ( approximately 16% decrease, males only), cytochr

114 of this study suggest a protective role for MnSOD in retinal capillary cell death and, ultimately, i

115 pathology, strongly implicating the role for MnSOD in the pathogenesis of retinopathy in diabetes.

116 ease the expression of the FOXO target genes MnSOD and catalase.

117 eactive oxygen species (ROS)-reducing genes (MnSOD, catalase).

118 redox and signal transduction related genes, MnSOD, CuZnSOD, Nrf2, Keap1, GPx4 and Catalase was also

119 However, it is not known whether or how MnSOD participates in the mitochondrial repair processes

120 Human MnSOD exhibits a substantially higher level of product i

121 Human MnSOD has two poly(A) sites resulting in two transcripts

122 Human MnSOD is significantly more product-inhibited than bacte

123 gin of product inhibition by comparing human MnSOD with ScMnSOD.

124 D. radiodurans MnSOD > E. coli MnSOD > human MnSOD.

125 scaled as Drad MnSOD > E. coli MnSOD > human MnSOD.

126 Glu162 in homotetrameric human MnSOD spans a dimeric interface and forms a hydrogen bon

127 Glu162 at the tetrameric interface in human MnSOD supports stability and efficient catalysis and has

128 t MnSODs indicate the unique nature of human MnSOD in that it predominantly undergoes the inhibited p

129 erties of two site-specific mutants of human MnSOD in which Glu162 is replaced with Asp (E162D) and A

130 ase reporter gene under the control of human MnSOD promoter-enhancer elements and investigated the ch

131 prepared two site-specific mutants of human MnSOD with replacements of Phe66 with Ala and Leu (F66A

132 f Phe66 to Leu resulted in a mutant of human MnSOD with weakened product inhibition resembling that o

133 J-1 causes decreased expression of the human MnSOD.

134 are more similar to bacterial than to human MnSOD.

135 The results identify MnSOD as a p53-regulated gene that switches between earl

136 D wild-type fibroblasts, which was absent in MnSOD homozygous knockout fibroblasts.

137 ice, the numbers of acellular capillaries in MnSOD-Tg nondiabetic and diabetic mice were similar to t

138 nsumption and percentage of S-phase cells in MnSOD wild-type fibroblasts, which was absent in MnSOD h

139 se and oxygen consumption, and a decrease in MnSOD activity.

140 NAC-induced G(1) arrest is exacerbated in MnSOD heterozygous fibroblasts.

141 , increased MnSOD activity when expressed in MnSOD/ MEFs, suggesting acetylation directly regulates f

142 evention of the exercise-induced increase in MnSOD activity via antisense oligonucleotides greatly at

143 MnSOD lines had a three-fold increase in MnSOD activity, but interestingly a five to nine-fold in

144 peroxide anion generation and an increase in MnSOD compared with untreated CNV eyes.

145 ls, which was associated with an increase in MnSOD protein levels and a decrease in the percentage of

146 of age, there was a 2- to 3-fold increase in MnSOD protein levels in Tg19959-MnSOD mice compared to T

147 hesized that an exercise-induced increase in MnSOD would provide cardioprotection by attenuating IR-i

148 igate the mechanism of product inhibition in MnSOD, two yeast MnSODs, one from Saccharomyces cerevisi

149 1/FoxO3a and MEK/ERK pathway are involved in MnSOD regulation by AC5.

150 showed that similar results were observed in MnSOD knockdown HUVECs following Mn(2+) supplementation,

151 ctor Mef2, and predictably, perturbations in MnSOD modify p38K-dependent phenotypes.

152 small interfering RNA led to a reduction in MnSOD gene expression.

153 through IkappaBalpha degradation resulted in MnSOD upregulation and preserved cell growth, whereas NF

154 However, despite extensive studies in MnSOD regulation and its role in cancer, when and how th

155 mitochondrial protein acetylation, including MnSOD(K68) SIRT3 enforced expression reduced oxidant-ind

156 s lung alveolar type II cells have increased MnSOD(K68) acetylation compared with controls.

157 porphyrin, mimicked the effects of increased MnSOD expression.

158 acetylation (lenti-MnSOD(K122-R)), increased MnSOD activity when expressed in MnSOD/ MEFs, suggesting

159 reducing oxidative stress through increased MnSOD.

160 However, a low level of p53 increases MnSOD gene transcription in the presence of the intronic

161 sing cyclin D1 protein levels and increasing MnSOD activity.

162 trated that p53 can both suppress and induce MnSOD expression depending on the balance of promoter an

163 Finally, IR was unable to induce MnSOD deacetylation or activity in Sirt3/ livers, and th

164 dependent transcriptional pathways to induce MnSOD expression.

165 Our data indicate that TPA-induced MnSOD expression was independent of p53 and most likely

166 and NOXO1 in A549 cells impaired TPA-induced MnSOD expression.

167 (FOXO) 3a led to a reduction in TPA-induced MnSOD gene expression.

168 demonstrate that UVB-induced mtDNA damage is MnSOD dependent.

169 Introduction of K68R MnSOD rescued mitochondrial redox status and membrane po

170 Together, these results show that NF-kappaB, MnSOD, 14-3-3zeta, and cyclin B1 contribute to LDIR-indu

171 rential increase in the levels of the 1.5-kb MnSOD transcript was observed in quiescent cells, wherea

172 tion increases the mRNA levels of the 1.5-kb MnSOD transcript, which was consistent with a significan

173 an arginine, mimicking deacetylation (lenti-MnSOD(K122-R)), increased MnSOD activity when expressed

174 hermore, infection of Sirt3/ MEFs with lenti-MnSOD(K122-R) inhibited in vitro immortalization by an o

175 that are present in the 3'-UTR of the longer MnSOD transcript.

176 esults uncover a muscle-restricted p38K-Mef2-MnSOD signaling module that influences life span and str

177 in Drosophila, a p38 MAP kinase (p38K)/Mef2/MnSOD pathway is a coregulator of stress and life span.

178 mimicked by overexpressing the mitochondrial MnSOD (SOD2), whereas SOD2 depletion with small interfer

179 8K modulates expression of the mitochondrial MnSOD enzyme through the transcription factor Mef2, and

180 the oxidative addition of superoxide to Mn2+MnSOD leading to the formation of the peroxide-inhibited

181 ere determined in mice overexpressing MnSOD (MnSOD-Tg).

182 While most MnSODs rest as the oxidized form, ScMnSOD was isolated i

183 ent with small interfering RNA against mouse MnSOD was shown to inhibit the development of LDIR-induc

184 (iron, manganese [Mn], copper/zinc, nickel), MnSOD is the dominant form in the diatom Thalassiosira p

185 cells is mediated by ROS and ICAM-1, but not MnSOD.

186 Lastly, K68 acetylation of MnSOD was significantly increased in the SNc of PD patie

187 hibited decreased expression and activity of MnSOD.

188 le in cancer, when and how the alteration of MnSOD expression occurs during the process of tumor deve

189 ings, clinical and epidemiologic analyses of MnSOD expression and AMPK activation indicated that the

190 cer elements and investigated the changes of MnSOD transcription using the 7,12-dimethylbenz(alpha)an

191 between the positive and negative control of MnSOD expression.

192 To investigate the effect of MnSOD, retinal mitochondrial oxidative stress and electr

193 Elevation of MnSOD was eliminated by both sirtuin and MEK inhibitors,

194 modestly drug-resistant, and elimination of MnSOD in the phb-2, har-1, and spg-7 mutants enhanced re

195 3 to verify their roles in the expression of MnSOD at each stage of cancer development.

196 Because expression of MnSOD protects against cell death, our findings reveal a

197 nt study showed that increased expression of MnSOD sensitized WEHI7.2 cells to glucocorticoid-induced

198 D-0354 suppressed LDIR-induced expression of MnSOD, 14-3-3zeta, and cyclin B1 and diminished the adap

199 s tolerance offered by the cytosolic form of MnSOD has possibly resulted in retention of only the cyt

200 and the release of cytosolic 24 kDa form of MnSOD was obligatory for developing oxidative stress tol

201 pressing either different molecular forms of MnSOD or MnSOD defective in the cleavage of signal/linke

202 Individual contribution of these forms of MnSOD to total oxidative stress tolerance was analysed u

203 between human and certain bacterial forms of MnSOD.

204 ger than that observed in bacterial forms of MnSOD.

205 e ICAM-1 expression and ROS independently of MnSOD, leading to a decrease in monocyte adhesion to end

206 ys a role in cytokine-dependent induction of MnSOD, IL-6, and FH, we assessed the effect of E1A on NF

207 odels, lentiviral shRNA-induced knockdown of MnSOD caused tumors that grew in the presence of TAM to

208 Conversely, siRNA-mediated knockdown of MnSOD in normal EPCs reduced their activity in diabetic

209 and small interfering (SI) RNA knockdown of MnSOD, but not of the copper-zinc SOD, increased HIF-1 p

210 Although the levels of MnSOD protein did not change, MnSOD activity and mitocho

211 cate that lysine and arginine methylation of MnSOD during quiescence would allow greater accessibilit

212 Site-directed mutagenesis of MnSOD lysine 122 to an arginine, mimicking deacetylation

213 our group have shown that overexpression of MnSOD in MCF-7 cells alters stabilization of HIF-1 alpha

214 Overexpression of MnSOD inhibited diabetes-induced increases in mitochondr

215 Overexpression of MnSOD inhibited IFN-gamma-mediated ROS accumulation and

216 myopathy was suppressed by overexpression of MnSOD, whereas protection afforded by the AC5 knockout (

217 trometry results showed a complex pattern of MnSOD-methylation at both lysine (68, 89, 122, and 202)

218 tage of membrane-targeting and processing of MnSOD in either bacteria or plants.

219 c-jun-mediated repression of MnSOD and catalase occurred via mitochondrial complex I

220 he suppression and subsequent restoration of MnSOD expression were mediated by two transcription-fact

221 serving the visible absorbance of species of MnSOD and under catalytic conditions observing the absor

222 2 and His163 contributes to the stability of MnSOD, with the major unfolding transition occurring at

223 f peroxide in the product-inhibited state of MnSOD.

224 th in MCF7-BK-TR cells due to stimulation of MnSOD activity through agonistic effects at mitochondria

225 34, based upon structure-function studies of MnSOD enzymes with mutations at this site.

226 effect of p65 and led to the suppression of MnSOD gene transcription.

227 Targeting of MnSOD to the membrane and subsequent cleavage to release

228 how that MnSOD deficiency in skin tissues of MnSOD-heterozygous knockout (Sod2(+/-)) mice leads to in

229 We conclude that the 3'-UTR of MnSOD regulates MnSOD expression in response to differen

230 gates if the 3'-untranslated region (UTR) of MnSOD regulates its expression during transitions betwee

231 5 can overcome the negative effect of p53 on MnSOD expression.

232 ent with the bi-directional effect of p53 on MnSOD expression.

233 ce RNA reduces the positive effect of p53 on MnSOD gene transcription.

234 in antioxidant protection afforded by GCL or MnSOD.

235 either different molecular forms of MnSOD or MnSOD defective in the cleavage of signal/linker peptide

236 ntly in the reduced state (unlike most other MnSODs).

237 lexes were determined in mice overexpressing MnSOD (MnSOD-Tg).

238 -induced superoxide production and preserved MnSOD expression in vivo.

239 We propose MnSOD as a new molecular player contributing to the Warb

240 echanisms: induction of antioxidant proteins MnSOD and Nrf1, possibly via stimulation of PGC1alpha, a

241 ure common to eukaryotic MnSODs, we purified MnSOD from Saccharomyces cerevisiae (ScMnSOD).

242 nhibition scales as ScMnSOD > D. radiodurans MnSOD > E. coli MnSOD > human MnSOD.

243 scherichia coli and Deinococcus radiodurans) MnSODs.

244 When delivered by AAV, Rz432 reduced MnSOD protein and increased markers of oxidative damage,

245 conclude that the 3'-UTR of MnSOD regulates MnSOD expression in response to different growth states

246 Sirt3/ MEFs deacetylated lysine and restored MnSOD activity.

247 Restricting MnSOD expression or inhibiting AMPK suppresses the metab

248 Thus, a single MnSOD caters to the reduction of superoxide radical in b

249 f a previously undiscovered plastid-specific MnSOD whose identity we validated immunochemically.

250 etylation of mitochondrial Sirt3 substrates, MnSOD and oligomycin-sensitivity conferring protein (OSC

251 increase while high concentrations suppress MnSOD expression.

252 Tg19959-MnSOD mice also had a 50% increase in catalase protein l

253 were restored to wild-type levels in Tg19959-MnSOD littermates.

254 increase in MnSOD protein levels in Tg19959-MnSOD mice compared to Tg19959 littermates.

255 le Abeta pools or Abeta oligomers in Tg19959-MnSOD mice compared to Tg19959 littermates.

256 ken together, these results demonstrate that MnSOD deletion in adipocytes triggered an adaptive stres

257 xposed to UVB radiation, we demonstrate that MnSOD has a critical role in preventing mtDNA damage by

258 The data also demonstrate that MnSOD has a role along with p53 to prevent mtDNA damage.

259 Here we demonstrate that MnSOD upregulation in cancer cells establishes a steady

260 mitochondrial content in WAT and found that MnSOD deletion increased mitochondrial oxygen consumptio

261 These results support the hypothesis that MnSOD regulates a "metabolic switch" during progression

262 Here, we tested the hypothesis that MnSOD regulates the expression of HIF-1 alpha by modulat

263 Taken together, our results indicate that MnSOD serves as a biomarker of cancer progression and ac

264 Here, we show that MnSOD deficiency in skin tissues of MnSOD-heterozygous k

265 The results show that MnSOD expression was suppressed at a very early stage bu

266 In this study, we showed that MnSOD protein expression was elevated in response to TPA

267 These results suggest that MnSOD provides cardioprotection by attenuating IR-induce

268 results demonstrate for the first time that MnSOD is a fidelity protein that maintains the activity

269 The MnSOD is post-translationally processed to 27 and 24 kDa

270 e, Tyr34, by phenylalanine (Y34F) causes the MnSOD from S. cerevisiae to react exclusively through th

271 Methylation-dependent changes in the MnSOD conformation and subsequent changes in the electro

272 Overexpression of the MnSOD 3'-UTR representing the longer transcript enhanced

273 F-kappaB at the promoter and enhancer of the MnSOD gene in vivo were verified by the presence of the

274 gamma, which is prevented by addition of the MnSOD mimetic Mn(III)TE-2-PyP(5+).

275 ha (PGC-1alpha), in the transcription of the MnSOD.

276 ity of transformed cells indicating that the MnSOD/AMPK axis is critical to support cancer cell bioen

277 ssion and AMPK activation indicated that the MnSOD/AMPK pathway is most active in advanced stage and

278 3-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papil

279 K4 activates NFkappaB for its binding to the MnSOD promoter, which leads to AP-1 dissociation followe

280 for the differences in the activities of the MnSODs that considers the release of peroxide as not alw

281 higher level of product inhibition than the MnSODs from bacteria.

282 f high concentrations of O(2)(-) among these MnSODs.

283 Tumor MnSOD and mitochondrial ERbeta are therefore targets for

284 E162A compared to 90 degrees C for wild-type MnSOD.

285 antly lower activity compared with wild-type MnSOD.

286 ha signaling is a major mechanism underlying MnSOD-dependent UCPs expression that consequently trigge

287 Using MnSOD-deficient mice we demonstrate that UVB-induced mtD

288 ptosis and undergo enzymatic elimination via MnSOD and CuZnSOD with further detoxification via catala

289 ll therapy using diabetic EPCs after ex vivo MnSOD gene transfer accelerates their ability to heal wo

290 When MnSOD is deficient, superoxide radical and its resulting

291 We therefore asked whether MnSOD overexpression would prove beneficial against AD p

292 g the offspring of Tg19959 mice crossed with MnSOD-overexpressing mice.

293 Because WT and the mutant yeast MnSOD both rest in the 2+ state and become six-coordinat

294 e, is slightly further away from Mn in yeast MnSODs, which may result in their unusual resting state.

295 echanistically, the high efficiency of yeast MnSODs could be ascribed to putative translocation of an

296 Our studies on yeast MnSODs indicate the unique nature of human MnSOD in that

297 ], the dismutation efficiencies of the yeast MnSODs surpass those of human and bacterial MnSODs, due

298 sm of product inhibition in MnSOD, two yeast MnSODs, one from Saccharomyces cerevisiae mitochondria (

299 tively function in the mechanism of WT yeast MnSODs.

300 sified by their catalytic metal as Cu/ZnSOD, MnSOD, or FeSOD.