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 expression was significantly (P<0.05) decreased in

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

4 MnSOD protein carrying a K89A mutation had significantly

5 MnSOD siRNA also reduced nitric oxide production in supe

6 MnSOD(K68Q) expressing cells exhibit resistance to tamox

7 MnSOD-promoter/enhancer analysis demonstrates that p53 i

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

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

10 These results suggest a MnSOD-K68-Ac metabolic pathway for Tam resistance, carci

11 e MnSOD-K68Q Ac-mimic, or physically K68-Ac (MnSOD-K68-Ac), suggest that these monomers function as a

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

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

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

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

39 roduct inhibition resembling that of E. coli MnSOD.

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

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

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

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

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

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

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

47 diomyopathy may be attributable to decreased MnSOD expression.

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

49 However, how defective MnSOD impacts the chain of events that lead to cell tran

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

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

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

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

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

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

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

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

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

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

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

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

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

63 Manganese superoxide dismutase (MnSOD) functions as a tumor suppressor; however, once tu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 , manganese-containing superoxide dismutase (MnSOD), has dual roles in early- and late-carcinogenesis

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

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

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

89 motetrameric manganese superoxide dismutase (MnSOD).

90 a manganese-containing superoxide dismutase (MnSOD).

91 activity of manganese superoxide dismutase (MnSOD).

92 27(kip1) and manganese superoxide dismutase (MnSOD).

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

94 deletion of manganese superoxide dismutase (MnSOD).

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

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

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

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

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

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

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

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

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

104 drogen bond interaction with His163 in E162A MnSOD.

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

106 Elevating MnSOD levels in cells enhances the conversion of superox

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

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

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

110 the genes coding for the antioxidant enzymes MnSOD and GPx, as evaluated by qRT-PCR.

111 drial-specific anti-oxidant defence enzymes (MnSOD; P < 0.01).

112 a peroxidase, distinct from the established MnSOD superoxide dismutase activity.

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

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

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

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

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

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

119 Human MnSOD exhibits a substantially higher level of product i

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

121 Human MnSOD is significantly more product-inhibited than bacte

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

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

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

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

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

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

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

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

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

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

132 are more similar to bacterial than to human MnSOD.

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

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

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

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

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

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

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

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

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

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

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

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

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

146 1/FoxO3a and MEK/ERK pathway are involved in MnSOD regulation by AC5.

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

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

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

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

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

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

153 porphyrin, mimicked the effects of increased MnSOD expression.

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

155 reducing oxidative stress through increased MnSOD.

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

157 sing cyclin D1 protein levels and increasing MnSOD activity.

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

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

160 dependent transcriptional pathways to induce MnSOD expression.

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

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

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

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

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

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

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

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

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

170 eractions involving adiposity and LEP, LEPR, MnSOD, PPARgamma, PPARgamma2, and IRS-1 polymorphisms we

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

172 ochondrial health and show that UVB-mediated MnSOD inactivation promotes mitophagy and thereby preven

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

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

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

176 8K modulates expression of the mitochondrial MnSOD enzyme through the transcription factor Mef2, and

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

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

179 nce exhibited increased K68-Ac and monomeric MnSOD.

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

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

182 the MnSOD-K68 acetylation (Ac) mimic mutant (MnSOD(K68Q)) functions as a tumor promoter.

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

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

185 hibited decreased expression and activity of MnSOD.

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

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

188 MnSOD(K68Q) is accompanied with a change of MnSOD's stoichiometry from a known homotetramer complex

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

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

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

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

193 3 to verify their roles in the expression of MnSOD at each stage of cancer development.

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

195 cer and primary cell types the expression of MnSOD(K68Q) is accompanied with a change of MnSOD's stoi

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

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

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

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

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

201 between human and certain bacterial forms of MnSOD.

202 ger than that observed in bacterial forms of MnSOD.

203 umors, implying a potential dual function of MnSOD in the regulation of metabolism.

204 diation causes nitration and inactivation of MnSOD leading to mitochondrial injury and mitophagy.

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

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

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

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

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

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

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

212 Overexpression of MnSOD inhibited diabetes-induced increases in mitochondr

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

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

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

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

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

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

219 2 and His163 contributes to the stability of MnSOD, with the major unfolding transition occurring at

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

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

222 34, based upon structure-function studies of MnSOD enzymes with mutations at this site.

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

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

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

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

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

228 5 can overcome the negative effect of p53 on MnSOD expression.

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

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

231 in antioxidant protection afforded by GCL or MnSOD.

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

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

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

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

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

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

238 FXN, HAX-1 and antioxidant defence proteins MnSOD and Nrf2 was observed both in PBMCs and AC16 cardi

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

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

241 scherichia coli and Deinococcus radiodurans) MnSODs.

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

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

244 Sirt3/ MEFs deacetylated lysine and restored MnSOD activity.

245 Restricting MnSOD expression or inhibiting AMPK suppresses the metab

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

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

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

249 tumorigenesis occurs, clinical data suggest MnSOD levels correlate with more aggressive human tumors

250 increase while high concentrations suppress MnSOD expression.

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

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

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

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

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

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

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

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

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

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

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

262 These results indicate that MnSOD is a major redox regulator that maintains mitochon

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

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

275 rmation and xenograft growth assays that the MnSOD-K68 acetylation (Ac) mimic mutant (MnSOD(K68Q)) fu

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 Biochemical experiments using the MnSOD-K68Q Ac-mimic, or physically K68-Ac (MnSOD-K68-Ac)

281 Importantly, pretreatment with the MnSOD mimic MnTnBuOE-2-PyP(5+) (MnP) attenuates mTORC2 a

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

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

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

285 Tumor MnSOD and mitochondrial ERbeta are therefore targets for

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

287 antly lower activity compared with wild-type MnSOD.

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

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

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

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

292 When MnSOD is deficient, superoxide radical and its resulting

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

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

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

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

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

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

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

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

301 tively function in the mechanism of WT yeast MnSODs.

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