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1 kers (Glutathione peroxidase, and superoxide dismutase).
2 , with a rate constant similar to superoxide dismutase.
3 uperoxide to hydrogen peroxide by superoxide dismutase.
4 hich is crucial for NPs' function as nitrite dismutase.
5 o-STAT3 and loss of extracellular superoxide dismutase.
6 whereas it enhances expression of superoxide dismutase.
7 strongly donating thiolates in Ni superoxide dismutase.
8 her Tar DNA-binding protein 43 or superoxide dismutase.
9 tionally redundant SoxR-regulated superoxide dismutase.
10 e G985R and G93A mutated forms of superoxide dismutase 1 (linked to familial amyotrophic lateral scle
13 by expression of a mutant form of superoxide dismutase 1 (SOD1 G93A) that causes astrocyte dysfunctio
16 We administered fenofibrate to superoxide dismutase 1 (SOD1(G93A)) mice daily prior to any detecta
17 se model of ALS expressing mutant superoxide dismutase 1 (SOD1(G93A)), we show that motor neurons for
18 s such as ALS, where mutations of superoxide dismutase 1 (SOD1) account for about 20% of the inherite
19 ndrial dysfunction, and disturbed superoxide dismutase 1 (SOD1) and Keap1/Nrf2 antioxidant responses
20 activity of antioxidant enzymes, superoxide dismutase 1 (SOD1) and peroxiredoxin-4 (PRDX4) during hy
21 Mutations in the gene encoding superoxide dismutase 1 (SOD1) are the second most common cause of f
22 Non-natively folded variants of superoxide dismutase 1 (SOD1) are thought to contribute to the path
28 ic mouse models expressing mutant superoxide dismutase 1 (SOD1) have been critical in furthering our
29 the sequence of the gene encoding superoxide dismutase 1 (SOD1) have been linked to toxic protein agg
30 ty and release of a model enzyme, superoxide dismutase 1 (SOD1) immobilized by polyion coupling on di
31 ALS-associated mutations in Cu/Zn superoxide dismutase 1 (SOD1) impair axonal transport of mitochondr
33 ins amyloid-beta (Abeta), tau and superoxide dismutase 1 (SOD1) in the cerebrospinal fluid of healthy
34 injection of oligomers of mutant superoxide dismutase 1 (SOD1) into the cytoplasm of invertebrate ne
35 ne (E40K) residue substitution in superoxide dismutase 1 (SOD1) is associated with canine degenerativ
37 that mediates the degradation of superoxide dismutase 1 (SOD1) messenger RNA to reduce SOD1 protein
38 creasing metabolism in the mutant superoxide dismutase 1 (SOD1) mouse model of ALS (G93A SOD1) would
39 re we show that, in vitro, mutant superoxide dismutase 1 (SOD1) mouse oligodendrocytes induce WT moto
40 ateral sclerosis (ALS)-associated superoxide dismutase 1 (SOD1) mutant protein induces changes in HSP
41 nd neutralize misfolded and toxic superoxide dismutase 1 (SOD1) mutant proteins may find application
44 al sclerosis-associated cytosolic superoxide dismutase 1 (SOD1) protein between motor neurons could b
45 erosis (ALS)-causing mutations in superoxide dismutase 1 (SOD1) provokes noncell autonomous paralytic
46 G85R is a mutant version of Cu/Zn superoxide dismutase 1 (SOD1) that is unable to reach native form a
47 examined potential inhibitors of superoxide dismutase 1 (SOD1) using ThT-fluorescence including the
48 nd mutations in the gene encoding superoxide dismutase 1 (SOD1) were treated with a single intratheca
49 eral sclerosis (ALS) mouse model, superoxide dismutase 1 (SOD1)(G93A), revealed that these EVs contai
51 ence lacking cytoplasmic protein, superoxide dismutase 1 (SOD1), and its mutant form linked to amyotr
52 y oligomers of mutant human Cu/Zn superoxide dismutase 1 (SOD1), which are associated with motor neur
54 ently during aggregation of human superoxide dismutase 1 (SOD1), which is known to form misfolded agg
55 erosis-associated protein variant superoxide dismutase 1 (SOD1)-A4V, whereas HSPA1L enhanced its aggr
62 tures from a mutant form of human superoxide dismutase 1 (SOD1G93A) mouse model of ALS allow the dete
63 Co-expression of wild-type human superoxide dismutase 1 (WT-hSOD1) with ALS mutant hSOD1 accelerates
64 cetin increased the expression of superoxide dismutase 1 and 2, and reduced the levels of oxidative s
65 ression of free radical scavenger superoxide dismutase 1 and aldehyde dehydrogenase 2 was reduced, wh
66 ownstream of Nrf2, levels of oPMN superoxide dismutase 1 and catalase were decreased in severe CP, de
67 lation of the antioxidant enzymes superoxide dismutase 1 and catalase, and activation of the pro-oxid
68 and translation of antioxidants, superoxide dismutase 1 and glutathione peroxidase-1, were significa
69 ochondrial dysfunction, disturbed superoxide dismutase 1 and Keap1/Nrf2 antioxidant responses, over-p
71 ant FUS (Fused in sarcoma), SOD1 (superoxide dismutase 1), TDP43 (TAR DNA-binding protein 43), and ta
72 ocytes isolated from mutant human superoxide dismutase 1-overexpressing mice as well as human post-mo
73 hich astrocytes expressing mutant superoxide dismutase-1 (mutSOD1) kill wild-type motor neurons (MNs)
75 icle investigates how the rate of superoxide dismutase-1 (SOD1) fibrillization is affected by 12 diff
76 e acylation of lysine residues in superoxide dismutase-1 (SOD1) has been previously shown to decrease
79 setup and use the specificity of superoxide dismutase-1 (SOD1) to show, for the first time, that H2O
80 ice expressing the ALS-associated superoxide dismutase-1 (SOD1)(G93A) mutant decreased spinal motoneu
81 nced the association of DJ-1 with superoxide dismutase-1 (SOD1), paralleled by significant increases
82 of familial ALS expressing mutant superoxide dismutase-1 (SOD1), TAR DNA-binding protein 43 (TDP-43),
85 ce with high numbers of the Cu/Zn superoxide dismutase-1 G93A transgene (SOD1(G93A) G1H) have become
88 n messenger RNA of shared targets superoxide dismutase 2 (P <= 0.001) and heme oxygenase 1 (P <= 0.00
89 of Sirt1 increased mitochondrial superoxide dismutase 2 (Sod2) acetylation of lysine residue 68, the
92 rms of stress, or enzymes such as superoxide dismutase 2 (SOD2) and catalase, which directly detoxify
94 ased acetylation of mitochondrial superoxide dismutase 2 (SOD2) and isocitrate dehydrogenase 2 (IDH2)
95 ed that inhibitory acetylation of superoxide dismutase 2 (SOD2) at K122 was increased in WT (but not
97 d induced a rapid upregulation of superoxide dismutase 2 (SOD2) expression and a delayed upregulation
98 protein 70 (hsp70) interacts with superoxide dismutase 2 (SOD2) in the cytosol after synthesis to tra
102 ology, elevated protein levels of superoxide dismutase 2 (SOD2), and increased levels of peroxisome p
103 and increased antioxidant enzymes superoxide dismutase 2 (SOD2), catalase, glutathione peroxidase 1 (
106 oxides, had reduced activities of superoxide dismutase 2 and catalase, and were hypersensitive to hyd
107 aused significant upregulation of superoxide dismutase 2 and heme oxygenase 1 protein following hypox
108 the levels of peroxiredoxin 3 and superoxide dismutase 2 in adipose tissue, indicating increased mito
109 ylation of the antioxidant enzyme superoxide dismutase 2 in muscle but not the liver of MCD(-/-) mice
110 tive damage markers, and of SOD2 (superoxide dismutase 2), PGC1alpha [peroxisome proliferator-activat
112 ms were discovered in relation to superoxide dismutase 2, ATP binding cassette subfamily A member 1,
113 A) isocitrate dehydrogenase 2 and superoxide dismutase 2, concomitant with increases in citrate synth
117 et genes (including mitochondrial superoxide dismutase), (2) enhanced phagocytic activity toward red
119 al and vascular oxidative stress (superoxide dismutase-2), neuroinflammation (astroglial and microgli
120 d enhanced lung concentrations of superoxide dismutase-2, thereby reducing lung tissue reactive oxida
122 dy, we investigated the effect of superoxide dismutase 3 (SOD3) on LL-37- or KLK-5-induced skin infla
123 lysis with higher MMP-2 and lower superoxide dismutase 3 gene expression, independent of age and aort
124 P-2), MMP-14, endoglin (ENG), and superoxide dismutase 3 in ascending aorta samples from 50 tricuspid
125 .6% of normoxic control), reduced superoxide dismutase (60.7 +/- 6.3%), increased phosphodiesterase t
126 omolecules, e.g., of enzyme Cu/Zn-superoxide dismutase, abnormal aggregation of which is linked to am
127 further increases in catalase and superoxide dismutase activities, which led to a significant reducti
129 ype levels of manganese-dependent superoxide dismutase activity in the presence of calprotectin.
133 ctivity of the antioxidant enzyme superoxide dismutase and a different regulation of the glutathione
136 restored NO production, increased superoxide dismutase and catalase, and suppressed NADPH oxidase and
137 including one of three copies of superoxide dismutase and five novel members of its regulon that cou
138 h A lowered DON-induced catalase, superoxide dismutase and glutathione peroxidase antioxidant enzyme
139 ynamin related protein, manganese superoxide dismutase and Lon protease, respectively, were generated
140 higher activities of antioxidant (superoxide dismutase and peroxidase) and defense enzymes (polypheno
141 itochondrial manganese-containing superoxide dismutase and peroxiredoxin 5 were only upregulated by P
144 ion, oxidative stress protection (superoxide dismutases) and iron and nitrogen metabolism varied amon
145 omoted antioxidant enzymes (i.e., superoxide dismutase, and catalase), strong DPPH-scavenging activit
146 including glutathione peroxidase, superoxide dismutase, and catalase, were evaluated in each of the i
147 ldehyde (MDA), nitric oxide (NO), superoxide dismutase, and glutathione peroxidase (GPX) levels in se
149 ultaneously possessing catalase-, superoxide dismutase-, and glutathione peroxidase-mimicking enzyme
150 aracterized by higher activity of superoxide dismutase, ascorbate peroxidase and phenylalanine ammoni
151 ) is produced, via superoxide and superoxide dismutase, by electron transport in chloroplasts and mit
153 mol L(-1) treatment showed higher superoxide dismutase, catalase and ascorbate peroxidase activities
154 and S.EPS significantly improved superoxide dismutase, catalase and glutathione peroxidase activitie
155 TNF-alpha) and oxidative stress (superoxide dismutase, catalase, glutathione peroxidase, lipidic and
158 mutations in Copper Chaperone for Superoxide Dismutase (CCSD) resulted in enhanced susceptibility.
160 for miR398 in an isoform of Cu/Zn superoxide dismutase (CSD1) is eliminated by alternative splicing t
161 genesis (RNA-binding protein FUS, superoxide dismutase Cu-Zn and neurofilaments light polypeptide) al
162 droxy-2'-deoxyguanosine (8-OHdG), superoxide dismutase (Cu-Zn SOD), and thiobarbituric acid reactive
165 reduction using PTR, homodimeric superoxide dismutase/CuZn (31.4 kDa) was subjected to PTR in order
166 Ras-related nuclear, p53, PEPCK1, superoxide dismutase, cyclophilin D, and Hsp10, and analyzed the de
167 meric beta-lactoglobulin, dimeric superoxide dismutase, dimeric and tetrameric concanavalin A, and he
169 7 is able to induce extracellular superoxide dismutase during differentiation of monocytes but not in
170 extracellular antioxidant enzyme superoxide dismutase (EC-SOD) as a novel substrate of CatA, which d
171 x-binding domain of extracellular superoxide dismutase (EC-SOD), with arginine to glycine substitutio
172 h varying levels of extracellular superoxide dismutase (ecSOD) activity, we have recently shown that
173 e training enhances extracellular superoxide dismutase (EcSOD) expression in skeletal muscle and elic
174 ssing lung-specific extracellular superoxide dismutase (ecSOD) were exposed to HEPA-filtered air or t
178 activated catalase and manganese superoxide dismutase expression, indicating that this pathway is co
180 linking of mutations in the Cu,Zn superoxide dismutase gene (sod1) to amyotrophic lateral sclerosis (
181 es and demonstrated that multiple superoxide dismutase genes contribute to miR398b-regulated rice imm
182 1(+)) mouse with the mutant human superoxide dismutase glycine to alanine point mutation at amino aci
184 gers of superoxide radical anion (superoxide dismutase), hydrogen peroxide (catalase), hydroxyl radic
185 bility of the ALS related protein superoxide dismutase I (SOD1) in mammalian cells, we show that quin
186 substrate (tryparedoxin) and iron superoxide dismutase in COL and SYL (versus TCC) trypomastigotes.
187 OD1) is the principal cytoplasmic superoxide dismutase in humans and plays a major role in redox pote
188 an functionally replace cytosolic superoxide dismutase in yeast, indicating that the pool of Mn displ
189 F-alpha), CXCL10, CCL5, IL-6, and superoxide dismutase, in human macrophages infected with 3 ATCC and
190 t mice with SOD1(G85R) mice, which express a dismutase-inactive mutant of SOD1 and are considered a m
191 tion are similar, suggesting that superoxide dismutase is calibrated so the oxygen- and superoxide-se
192 e-related pine genes such as SOD (superoxide dismutase), LOX (lipoxygenase), PAL (phenylalanine ammon
193 reatment with the small-molecule, superoxide dismutase mimetic (GC4419; 0.25 mumol/L) significantly m
194 Coadministration of tempol, a superoxide dismutase mimetic, ameliorated the exaggerated inflammat
195 because treatment with Tempol, an superoxide dismutase mimetic, rescued kidney injury in knockout mic
196 efficacy and safety of GC4419, a superoxide dismutase mimetic, with placebo to reduce the duration,
197 partially inhibited by Tempol (a superoxide dismutase-mimetic agent) and by glyburide (an inhibitor
198 on of 4-hydroxy-TEMPO (TEMPOL), a superoxide dismutase mimic that reacts with superoxide, rescued the
199 r stress proteins (e.g. manganese superoxide dismutase, mitochondrial KATP channels and peroxisome pr
200 part, by deacetylating manganese superoxide dismutase (MnSOD) and mitochondrial 8-oxoguanine DNA gly
205 dant enzyme, manganese-containing superoxide dismutase (MnSOD), has dual roles in early- and late-car
208 l antioxidant defenses [manganese superoxide dismutase (MnSOD)P< 0.05; copper/zinc superoxide dismuta
210 stable monomeric variant of Cu/Zn superoxide dismutase (mSOD1), an enzyme responsible for the convers
212 ellular antioxidants (sulfhydryl, superoxide dismutase) of zebrafish brain were assessed after recove
214 anine aminotransferase, catalase, superoxide dismutase, ornithine decarboxylase, glutamate receptor,
215 y high abundance of extracellular superoxide dismutase produced by Synechococcus and a dynamic secret
216 istidine-containing peptides, and superoxide dismutase (SOD) activity have been detected in the raw a
217 ulation, which result from higher superoxide dismutase (SOD) activity, associated with lower catalase
219 delivery of antioxidant enzymes - superoxide dismutase (SOD) and catalase (CAT), encapsulated in biod
220 f antioxidants (i.e., copper/zinc superoxide dismutase (SOD) and extracellular SOD only in oxidative
222 catalase (CAT), peroxidase (POD), superoxide dismutase (SOD) and glutathione reductase (GR) activitie
223 peroxidase (APX), catalase (CAT), superoxide dismutase (SOD) and peroxidase (POD) in roots and shoots
224 ic or mitochondrial ROS scavenger superoxide dismutase (SOD) caused a significant increase in segrega
225 dase (PPO), peroxidase (POX), and superoxide dismutase (SOD) enzymes activities were measured during
226 toma cells the beneficial role of superoxide dismutase (SOD) enzymes against paraquat-induced toxicit
227 n eukaryotes the bimetallic Cu/Zn superoxide dismutase (SOD) enzymes play important roles in the biol
228 The ubiquitous iron/manganese superoxide dismutase (SOD) family exemplifies this deficit, as the
229 ered expression of CSDs and other superoxide dismutase (SOD) family members, leading to increased tot
234 ences in antioxidant capacity and superoxide dismutase (SOD) levels between phenotypes may allow for
235 racellular superoxide by specific superoxide dismutase (SOD) showed the applicability for selective i
236 (glutathione-S-transferase (GST), superoxide dismutase (SOD)), and fish health (condition factor (K),
238 ehyde (MDA) and activity of total superoxide dismutase (SOD), and its mitochondrial (Mn-SOD) and cyst
240 ldehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), matrix metalloproteinas
242 V-A also inhibits the activity of superoxide dismutase (SOD), magnifying the imbalance of redox statu
246 ant strains lacking mitochondrial superoxide dismutase (sod-2) showed oxidative stress for two FeOx a
252 t the activity of the copper/zinc superoxide dismutase Sod1 and that loss of Sod1 activity contribute
254 ae) Cu chaperone for Cu-zinc (Zn) superoxide dismutase (SOD1) activates by directly promoting both Cu
255 sis by repressing a Cu-containing superoxide dismutase (SOD1) and inducing Mn-containing SOD3 as a no
256 between homodimeric mutant Cu, Zn superoxide dismutase (SOD1) and wild-type (WT) SOD1 is suspected to
257 1) activates immature copper-zinc superoxide dismutase (Sod1) by delivering copper and facilitating t
258 an inhibit the amyloidogenesis of superoxide dismutase (SOD1) by increasing the intrinsic net negativ
259 lation (nanozyme) for copper/Zinc superoxide dismutase (SOD1) by polyion condensation with a conventi
262 examine the trajectory that Cu/Zn superoxide dismutase (SOD1) dimers take over the unfolding and diss
266 ously, we found that human Cu, Zn-superoxide dismutase (SOD1) is S-acylated (palmitoylated) in vitro
269 uitous expression of mutant Cu/Zn-superoxide dismutase (SOD1) selectively affects motor neurons in th
270 into the ALS-linked protein Cu,Zn superoxide dismutase (SOD1) upon translation promotes protein misfo
276 ctivated by the UPR(mt), we suggest that the dismutases SOD2 and SOD1 may play key roles in the estab
278 tivator PGC-1alpha, mitochondrial superoxide dismutase (SOD2), and chemical antioxidants alpha-tocoph
279 upregulation of the antioxidants superoxide dismutase (SOD2), catalase, methionine sulfoxide reducta
280 hyperacetylation of mitochondrial superoxide dismutase (SOD2), increases HIF1alpha (hypoxia-inducible
282 on of ROS-producing extracellular superoxide dismutase (SOD3) in thyroid cancer cell lines although a
283 antioxidant enzyme extracellular superoxide dismutase (SOD3) protects against hypoxia-induced PH.
290 in catalase, guaiacol peroxidase, superoxide dismutase, soluble protein, lignin, chlorophyll, and ele
291 tems, including a nascent form of superoxide dismutase that is implicated in neurodegenerative diseas
292 organisms employ a separate enzyme, chlorite dismutase, to prevent accumulation of the destructive Cl
293 atalase, ascorbate peroxidase and superoxide dismutase together with xanthophyll cycle and non-photoc
295 NADP-dependent glyceraldehyde and superoxide dismutase were found significantly upregulated in infect
296 , and mRNA levels of catalase and superoxide dismutase were increased, whereas those of nitric oxide
297 component, biotin carboxylase and superoxide dismutase were related to energy and carbon metabolism,
298 s, and activities of catalase and superoxide dismutase were significantly deteriorated in the CSD gro
299 alase, glutathione peroxidase and superoxide dismutase were significantly lower in PSE-induced sample