ライフサイエンスコーパス: Mn-SOD

1 Mn SOD activity was unaffected by treatment.

2 Mn-SOD activity in late preconditioning was considerably

3 Mn-SOD contains a GC-rich and TATA/CAAT-less promoter ch

4 Mn-SOD expression and activity of Ad.SOD2 in liver mitoc

5 Mn-SOD expression is tightly regulated in a manner that

6 Mn-SOD has tumor suppressor activity in a wide variety o

7 Mn-SOD is a nuclear-encoded mitochondrial matrix protein

8 Mn-SOD overexpression and low oxygen alter IL-1alpha mRN

9 Mn-SOD protein content was negatively correlated to the

10 Mn-SOD serves as the primary cellular defense against ox

11 In addition, Mn-SOD blocked the TNF-mediated activation of activated

12 Although Mn-SOD could enhance HQ-induced cytotoxicity to stromal

13 dy used a human tissue microarray to analyze Mn-SOD expression in primary ovarian cancer tissues, ben

14 nide but not by azide, which inhibits Fe and Mn SODs.

15 ly no effect on the expression of VCAM-1 and Mn-SOD.

16 d the expression of iNOS, COX-2, VCAM-1, and Mn-SOD in a time-dependent manner, but with different pa

17 nhibiting NF-kappaB DNA binding activity and Mn-SOD expression, and increasing paclitaxel-induced apo

18 unchanged (GFAP) or depressed (beta APP and Mn-SOD) in level, despite elevations in corresponding mR

19 Cu/Zn-SOD in the cytosol and Mn-SOD in mitochondria each are capable of protecting He

20 e overexpressed Cu/Zn-SOD in the cytosol and Mn-SOD in the mitochondria was confirmed by assaying the

21 lders' blood and chemiluminescence, GPx, and Mn-SOD, and between lead levels and albumin, TAS, GPx, a

22 in albumin, TAS, chemiluminescence, GPx, and Mn-SOD.

23 tween lead levels and albumin, TAS, GPx, and Mn-SOD.

24 Protein contents of Bcl-2, HSP70, and Mn-SOD increased in both soleus and ventricle muscles of

25 91(phox) and p47(phox) and decreased IC- and Mn-SOD.

26 with diminished renal expression of IC- and Mn-SOD.

27 We measured Cu,Zn-SOD and Mn-SOD activities in peripheral lymphocytes of 43 newly

28 a 2- and 3.5-fold elevation in CuZn-SOD and Mn-SOD activities in the cytoplasm and mitochondria, res

29 ance of selegiline on measured Cu,Zn-SOD and Mn-SOD activity in peripheral lymphocytes.

30 Overexpression of Cu/Zn-SOD and Mn-SOD also partially protected E47 cells from the incre

31 Infection with Cu/Zn-SOD and Mn-SOD also protected the E47 cells against AA toxicity

32 nd thus to allow assay of both Cu,Zn-SOD and Mn-SOD in mixtures of the two was also explored, as was

33 Both Cu,Zn-SOD and Mn-SOD inhibited the aerobic oxidation of NADPH by AS, b

34 The significant changes in Cu,Zn-SOD and Mn-SOD mRNA indicate that SOD is primarily expressed by

35 ellular levels and activity of Cu/Zn-SOD and Mn-SOD were increased about 2- and 3-fold, respectively.

36 anti-oxidant enzymes catalase, Cu/Zn-SOD and Mn-SOD, compared to vehicle.

37 or both Cu,Zn-superoxide dismutase (SOD) and Mn-SOD by exploiting the cyanide sensitivity of the form

38 Cu/Zn-superoxide dismutase (SOD) and Mn-SOD were modestly induced, and Bcl-2 was modestly red

39 , heat shock protein (HSP)70, Cu/Zn-SOD, and Mn-SOD protein levels were determined by Western analyse

40 n-SOD complementary DNA (cDNA) (Ad.SOD1) and Mn-SOD cDNA (Ad.SOD2).

41 ofactored superoxide dismutase [Mn-SOD]) and Mn-SOD were used as a reporter gene and endogenous repor

42 SOD was found in the intermembrane space and Mn-SOD in the matrix and also on the inner membrane.

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

44 nhibited complex resembles that of the azide-Mn-SOD complex, suggesting that the inhibited complex ha

45 Unlike planktonic bacteria, Mn-SOD was constitutive in the lasI and lasR mutant biof

46 The promoter for the bacterial Mn-SOD, as well as both 5'-untranslated and transcriptio

47 although in iron-limited wild-type biofilms Mn-SOD was detected within the initial 24 h of biofilm e

48 In wild-type biofilms, Mn-SOD was not detected until after 6 days, although in

49 These findings indicate that both Mn-SOD and O2 may regulate the levels of a cellular oxid

50 activity, and that this repression was both Mn-SOD promoter and AP-2-specific.

51 nduced PC-12 apoptosis that is attenuated by Mn-SOD overexpression and is independent of cellular GSH

52 duced activation of NF-kappaB was blocked by Mn-SOD, indicating a common pathway of activation.

53 for the zero-order phase in the catalysis by Mn-SOD of superoxide dismutation can be reached through

54 t not GSH, indicating that cytoprotection by Mn-SOD overexpression is related to mitochondrial ROS el

55 the matrix (where it is converted to H2O2 by Mn-SOD) but not into the intermembrane space.

56 ty to stromal cells, the activation of HQ by Mn-SOD did not contribute to the induction of DNA strand

57 acid, H2O2, and taxol was also inhibited by Mn-SOD but not that induced by vincristine, vinblastine,

58 a heterologously expressed Escherichia coli Mn-SOD, but not a highly homologous Fe-SOD.

59 Studies comparing Mn-SOD activity in P. aeruginosa biofilms and planktonic

60 OD; while the mitochondrial matrix contained Mn-SOD.

61 were given recombinant adenovirus containing Mn-SOD (Ad.SOD2) or beta-galactosidase (Ad.lacZ) and the

62 underlying regulatory mechanisms controlling Mn-SOD expression, we utilized DNase I-hypersensitive (H

63 uperoxide dismutase (CuZn-SOD) (sod1 delta), Mn-SOD (sod2 delta), or both SODs, throughout their grow

64 (Cu/Zn SOD), manganese superoxide dismutase (Mn SOD), catalase, and glutathione peroxidase (GSPx).

65 oduction, increased Mn superoxide dismutase (Mn-SOD) activity, increased call viability, decreased LD

66 dant enzymes manganese superoxide dismutase (Mn-SOD) and copper-zinc superoxide dismutase (CuZn-SOD)

67 Increased manganese superoxide dismutase (Mn-SOD) and decreased catalase activities were also appa

68 antioxidant manganese superoxide dismutase (Mn-SOD) as a potential end effector in mediating this pr

69 tramer human manganese superoxide dismutase (Mn-SOD) form a hydrogen bond across the dimer interface

70 Manganese superoxide dismutase (Mn-SOD) immunoreactivity was present in the vehicle and

71 (c-IAP2) and manganese superoxide dismutase (Mn-SOD) in breast cancer cells.

72 xpression of manganese superoxide dismutase (Mn-SOD) in human breast cancer MCF-7 cells completely ab

73 Manganese superoxide dismutase (Mn-SOD) is a primary antioxidant enzyme whose expression

74 Manganese superoxide dismutase (Mn-SOD) is an enzyme that preserves mitochondria, a key

75 idant enzyme manganese superoxide dismutase (Mn-SOD) is crucial in maintaining cellular and organisma

76 Manganese superoxide dismutase (Mn-SOD) is one of many genes, but only antioxidant enzym

77 itochondrial manganese superoxide dismutase (Mn-SOD) is the primary cellular defense against damaging

78 ls contain a manganese-superoxide dismutase (Mn-SOD) plasmid.

79 antioxidant manganese superoxide dismutase (Mn-SOD) plays a critical cytoprotective role against oxi

80 ve Escherichia coli Mn-superoxide dismutase (Mn-SOD) promoter, we have developed a vector system that

81 tochondrial isoform of superoxide dismutase (Mn-SOD) via recombinant adenovirus would reduce alcohol-

82 or manganese-dependent superoxide dismutase (Mn-SOD), a marker of oxidative stress, was positively co

83 Manganous superoxide dismutase (Mn-SOD), a tumor necrosis factor (TNF)-inducible gene pr

84 tatus (TAS), manganese superoxide dismutase (Mn-SOD), aconitase, glutathione peroxidase (GPx), heat s

85 ), manganese-dependent superoxide dismutase (Mn-SOD), and glutathione peroxidase in basal ganglia of

86 enzymes Mn-containing superoxide dismutase (Mn-SOD), catalase, and glutathione peroxidase (GPX), inc

87 antioxidant manganese superoxide dismutase (Mn-SOD).

88 itochondrial manganese superoxide dismutase (Mn-SOD).

89 e (KatG) and manganese superoxide dismutase (Mn-SOD).

90 d manganese-containing superoxide dismutase (Mn-SOD).

91 Manganese superoxide dismutase (Mn-SOD; SOD2), a primary mitochondrial antioxidant enzym

92 g manganese-cofactored superoxide dismutase [Mn-SOD]) and Mn-SOD were used as a reporter gene and end

93 operon containing the sodA gene that encodes Mn-SOD.

94 The expression of sodA (encoding Mn-SOD) was particularly dependent on PAI-1, whereas the

95 troduction of additional transgenes encoding Mn-SOD or thioredoxin reductase in the same genetic back

96 t inducible interactions with the endogenous Mn-SOD enhancer, and also opposite effects on Mn-SOD tra

97 These data suggest that the enhanced Mn-SOD activity during ischemia-reperfusion injury, whic

98 EBP beta/LAP* served as a true activator for Mn-SOD, whereas LAP, LIP, and C/EBP delta functioned as

99 the same treatment, hearts were assayed for Mn-SOD content and activity.

100 Immunocytochemistry for Mn-SOD and Cu/Zn-SOD and ultracytochemical localization

101 rmed fibroblasts and suggest a mechanism for Mn-SOD down-regulation in cancer.

102 erize the transcription factors required for Mn-SOD enhancer function, a yeast one-hybrid assay was u

103 lear factor (NF)-kappaB p65 are required for Mn-SOD induction by TNF.

104 hich is inside intron 2, are responsible for Mn-SOD expression.

105 n-poor environment, the opposite is true for Mn-SODs of organisms such as Escherichia coli and bakers

106 However, Mn-SOD activity was completely suppressed in the wild-ty

107 In contrast, however, Mn-SOD expression is dramatically regulated in a variety

108 cted AP-2-deficient HepG2 cells with a human Mn-SOD promoter-reporter construct and expression vector

109 st the vector, both native and mutated human Mn-SOD cDNAs were cloned and expressed, respectively.

110 erated an active site mutant (H30N) of human Mn-SOD, which exhibits significantly reduced product inh

111 o wild-type bacteria produced an increase in Mn-SOD activity and a decrease in total catalase activit

112 Our findings suggest that the increase in Mn-SOD expression in ovarian cancer is a cellular respon

113 nimals with EAE showed an 8-fold increase in Mn-SOD immunogold in astroglial cells and a 13-fold incr

114 Increases in Mn-SOD activity in astroglial cells and microglial/phago

115 Increases in Mn-SOD immunogold were contiguous to H2O2-derived reacti

116 proteins appeared to play distinct roles in Mn-SOD gene regulation.

117 , VWR reduced eNOS and EC SOD, but increased Mn SOD in kidney.

118 m of FKHRL1 (TMFKHRL1) resulted in increased Mn-SOD expression, suggesting that the negative effect o

119 t pyochelin biosynthesis, produced increased Mn-SOD activity.

120 ransient transfection assays, VEGF increased Mn-SOD promoter activity, an effect that was dependent o

121 cherichia coli Mn- and Fe-SODs and mammalian Mn-SOD, whereas Fe-SODB was exceptionally resistant to o

122 Manganese (Mn) SOD is preferentially induced in terminally differen

123 scularly administered CuZn-SOD or manganese (Mn)-SOD.

124 in the cytosol (Cu,Zn-SOD) and mitochondria (Mn-SOD), where they locally scavenge O2 (-) leading to p

125 import into mitochondria, and mitochondrial Mn-SOD.

126 suggest an important role for mitochondrial Mn-SOD as a potential end effector of this protection.

127 grafts, possibly by increasing mitochondrial Mn-SOD, thus protecting against free radical production

128 tracellular CuZn (IC)-SOD and mitochondrial (Mn)-SOD.

129 in cytosolic (Cu,Zn-SOD) and mitochondrial (Mn-SOD) forms in multiple tissues, including brain.

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

131 is a novel transcription factor of the mouse Mn-SOD gene and plays a crucial role as a neuroprotectan

132 r and upregulates transcription of the mouse Mn-SOD gene in the normal brain.

133 ition, transcriptional activity of the mouse Mn-SOD gene was significantly reduced by STAT3 inhibitio

134 TAT3) as a transcription factor of the mouse Mn-SOD gene, and elucidated the mechanism of O(2)(*-) ov

135 ed STAT3 is usually recruited into the mouse Mn-SOD promoter and upregulates transcription of the mou

136 In the aged cohort, hippocampal GFAP mRNA, Mn-SOD mRNA, and beta APP emerged as predictors of behav

137 sitivity assays were performed on the murine Mn-SOD gene.

138 induced a significant increase in myocardial Mn-SOD content and activity compared with the control co

139 n environment similar to that of the native (Mn)SOD protein.

140 SOD activity, but not Mn-SOD or Cu,Zn-SOD protein, was lower in asthmatic seru

141 lutathione peroxidase-1 or catalase, but not Mn-SOD or Cu,Zn-SOD, significantly reduced both NF kappa

142 revisae cannot readily support activation of Mn-SOD molecules.

143 ttent anoxia exhibited decreased activity of Mn-SOD and increased O2- production 24 hours later.

144 roethidine, reflecting decreased activity of Mn-SOD.

145 The amount of Mn-SOD cellular staining was concentration-dependently i

146 In all cases of Mn-SOD overexpression, IL-1alpha protein and mRNA levels

147 oscopy showed a perivascular distribution of Mn-SOD-positive cells in the optic nerves of animals wit

148 The effect of Mn-SOD overexpression on IL-1alpha expression can be ove

149 has long been recognized, the expression of Mn-SOD in cancer and its role in cancer development rema

150 was shown previously to induce expression of Mn-SOD in endothelial cells by a NADPH oxidase-dependent

151 utes to the constitutively low expression of Mn-SOD in SV40-transformed fibroblasts and suggest a mec

152 Elevated expression of Mn-SOD therefore provides a potent cytoprotective advant

153 ressing plasmids, enhanced the expression of Mn-SOD.

154 al O(2)(-) production induced an increase of Mn-SOD expression.

155 gin as there is a differential inducement of Mn-SOD gene, and are causal to cold-induced cell injury

156 d the importance of LAP* in the induction of Mn-SOD and emphasized the crucial role of this isoform.

157 Induction of Mn-SOD gene expression by the proinflammatory cytokine I

158 In contrast, VEGF-mediated induction of Mn-SOD was enhanced by the phosphatidylinositol 3-kinase

159 from injury in EAE, whereas the low level of Mn-SOD in oligodendroglial cells and axons may increase

160 e glaucoma group (p = 0.003); serum level of Mn-SOD was significantly lower in glaucoma patients (p =

161 pase-3 activation, and the elevated level of Mn-SOD.

162 Levels of Mn-SOD mRNA were increased in the nucleus accumbens (P<0

163 Significantly higher levels of Mn-SOD protein expression were detected in the malignant

164 Longer anoxia resulted in loss of Mn-SOD activity in anoxic controls 24 hours later, where

165 However, the regulatory mechanism of Mn-SOD expression during cerebral ischemia and reperfusi

166 Accordingly, the stable overexpression of Mn-SOD attenuated TBH-induced mitochondrial ROS generati

167 We report that overexpression of Mn-SOD enhances tyrosine phosphorylation of TCR-associat

168 acetylation during the induction process of Mn-SOD in response to TNF.

169 Repression of Mn-SOD by AP-2 was dependent on DNA binding, and express

170 only was sufficient for full restoration of Mn-SOD activity.

171 y active IkappaB blocked VEGF stimulation of Mn-SOD.

172 In experimental systems, suppression of Mn-SOD expression by small interfering RNA caused a 70%

173 regions contributes to the transcription of Mn-SOD, quantitative reverse transcription-PCR, chromati

174 To examine the functional role of AP-2 on Mn-SOD promoter transactivation we cotransfected AP-2-de

175 nslocation of NF-kappaB and had no effect on Mn-SOD expression.

176 n-SOD enhancer, and also opposite effects on Mn-SOD transcription.

177 e of DNA binding, relieved the repression on Mn-SOD promoter and reactivated Mn-SOD expression in the

178 that activation of HQ by either Cu/Zn-SOD or Mn-SOD results in cytotoxicity to primary bone marrow st

179 ection by superoxide dismutase (Cu,Zn-SOD or Mn-SOD) or catalase indicates mediation of the toxicity

180 wild-type mice receiving either CuZn-SOD or Mn-SOD.

181 ot altered by overexpression of Cu/Zn-SOD or Mn-SOD.

182 to TNF, we have constitutively overexpressed Mn-SOD in a human fibrosarcoma cell line and asked what

183 ty of the SOD1 polypeptide, we overexpressed Mn-SOD from Bacillus stearothermophilus in the cytoplasm

184 P)H oxidase subunits (gp91phox and P67phox), Mn SOD, inducible NOS (iNOS), endothelial NOS (eNOS), an

185 status of antioxidant enzymes, particularly Mn-SOD, in patients with Parkinson's disease and their r

186 Postischemic Mn-SOD content and activity in the HSP72-transfected hea

187 ve protein-DNA binding sites in the proximal Mn-SOD promoter as well as two stimulus-specific enhance

188 ence antisense to the initiation site of rat Mn-SOD mRNA.

189 epression on Mn-SOD promoter and reactivated Mn-SOD expression in the AP-2 abundant SV40-transformed

190 vity induced neuronal cell death by reducing Mn-SOD expression.

191 we hypothesized that AP-2 may down-regulate Mn-SOD expression.

192 icated that AP-2 could significantly repress Mn-SOD promoter activity, and that this repression was b

193 The manganese-containing SOD (Mn-SOD) has been suggested to have tumor suppressor func

194 mes such as CuZn-superoxide dismutase (SOD), Mn-SOD, and catalase has previously been reported to ext

195 ant enzymes [superoxide dismutase (CuZn SOD, Mn SOD), catalase, glutathione peroxidase (GPX)], nitric

196 In the cortex, KA induced Cu/Zn SOD, Mn SOD and catalase activity, but there was no significa

197 key antioxidant enzymes, such as Cu/Zn-SOD, Mn-SOD, CAT, GR, and guaiacol peroxidase, were also dete

198 n to BQ, which was accelerated by Cu/Zn-SOD, Mn-SOD, or Fe-SOD with similar efficiency.

199 es, whereas expressions of COX-2, Cu/Zn-SOD, Mn-SOD, xanthine oxidase, and the NAD(P)H oxidase subuni

200 ression of two superoxide dismutases (SODs), Mn-SOD and Fe-SOD, and the major catalase, KatA.

201 date the basis for the inactivity of Fe-sub-(Mn)SOD, despite its apparent similarity to Fe-SOD.

202 ubstituted (Mn)superoxide dismutase [Fe-sub-(Mn)SOD] and Fe-SOD to elucidate the basis for the inacti

203 The active site of (reduced) Fe2+-sub-(Mn)SOD is qualitatively similar to that of native Fe2+-S

204 lectrostatics, and consistent with Fe2+-sub-(Mn)SOD's retention of ability to reduce O2*-.

205 The non-native pKs observed in Fe3+-sub-(Mn)SOD and the differences in the Fe3+ coordination indi

206 Although Fe3+-sub-(Mn)SOD binds the small anions N3- and F-, the KD for N3-

207 The active site of (oxidized) Fe3+-sub-(Mn)SOD differs from that of Fe3+-SOD with respect to the

208 he EPR spectra are consistent with Fe3+-sub-(Mn)SOD's inability to oxidize O2*- and suggest that its

209 )](i), whereas mitochondrial matrix-targeted Mn-SOD (SOD-II) augmented [Ca(2+)](i).

210 We found that Mn-SOD expression is significantly reduced by reperfusio

211 + heterozygous knock-out mice, we found that Mn-SOD is a direct target of STAT3 in reperfusion-induce

212 We hypothesized that Mn-SOD would play a role in HSP72-mediated cardioprotect

213 Our initial observations revealed that Mn-SOD expression was inversely correlated with expressi

214 impairment, but immunoblotting revealed that Mn-SOD protein was depressed in the aged hippocampus com

215 These data suggest that Mn-SOD blocks cytosolic release of cytochrome c and coul

216 The Mn-SOD associated with the inner membrane was solubilize

217 In co-transfection assays, the Mn-SOD promoter was transactivated by TMFKHRL1.

218 downregulated, and its recruitment into the Mn-SOD promoter was completely blocked.

219 g overall homology with other members of the Mn-SOD family, but computer-assisted modeling revealed s

220 type mice and heterozygous knock-outs of the Mn-SOD gene (Sod2 -/+) after permanent FCI, in which apo

221 gh all three AP-2 proteins could repress the Mn-SOD promoter, AP-2alpha and AP-2gamma were more activ

222 s of the nigrostriatal pathway, and that the Mn-SOD gene appears to be inducible in rat basal ganglia

223 Electron microscopy showed that the Mn-SOD immunogold was confined exclusively to mitochondr

224 gene product is 74 and 70% identical to the Mn-SODs of Haemophilus influenzae and E. coli, respectiv

225 than that of Fe3+-SOD, suggesting that the (Mn)SOD protein favors anion binding more than does the (

226 binding mode for N3- in Thermus thermophilus Mn-SOD than Fe-SOD.

227 These Mn-SODs still capture manganese in an iron-rich cell, an

228 ata suggest that VEGF is uniquely coupled to Mn-SOD expression through growth factor-specific reactiv

229 pha (IL-1alpha) was modulated in response to Mn-SOD overexpression.

230 Whereas transient Mn-SOD expression similarly prevented PC-12 apoptosis, t

231 n cells grown in Trypticase soy broth (TSB), Mn-SOD was found in wild-type stationary-phase planktoni

232 That is, His30 and Tyr166 in wild-type Mn-SOD act to prolong the lifetime of the inhibited comp

233 Compared with wild-type Mn-SOD, the site-specific mutants H30N, Y166F, and the c

234 However, unlike Mn-SODs, the H ducreyi SodA protein was inhibited by hyd

235 ic forms of superoxide dismutase (SOD) (viz. Mn-SOD or CuZn-SOD, respectively).

236 Comparisons with Mn(SOD) and Fe(SOD) reveal that although different strat

237 arly seen with the Cu,Zn-SOD but barely with Mn-SOD because the former retains full activity from pH

238 ely suppressed by transfection of cells with Mn-SOD.

239 teraction of HQ with Cu/Zn-SOD, but not with Mn-SOD, resulted in the significant formation of POBN-CH

240 apparent but not to the degree observed with Mn-SOD.

241 Myocytes treated with Mn-SOD during short, intermittent anoxia exhibited decre

242 2) and NaCN, characteristics associated with Mn-SODs.

243 the wild-type compared with the mutant Y34F Mn-SOD.