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1 ADPH to glutathione reductase or thioredoxin reductase.
2 but via conversion of nitrite by the nitrate reductase.
3 t likely caused by S-nitrosylation of aldose reductase.
4 e reductase, and one had nitrate and nitrite reductase.
5 DPH-dependent CDP-3-C-methyl-6-deoxyhexose 4-reductase.
6 he subunit b of the menaquinone:cytochrome c reductase.
7 ty but not the activity of NADH-ferricyanide reductase.
8 calized 3-hydroxy-3-methylglutaryl (HMG) CoA reductase.
9 d by the FMN domain of NADPH-cytochrome P450 reductase.
10 oyltetrahydropterin synthase and sepiapterin reductase.
11 been hampered by the lack of an Ngb-specific reductase.
12 pression of the p53-inducible ribonucleotide reductase.
13 choconstriction, S-nitrosoglutathione (GSNO) reductase.
14 how encodes an EDEM2/3-associated disulphide reductase.
15 phosphoenolpyruvate carboxylase and nitrate reductase.
16 osystem 1 complex, itself also an NADPH oxio-reductase.
17 d reoxidation to N(tz) ADP(+) by glutathione reductase.
18 doxins (Trxs) via a ferredoxin-dependent Trx reductase.
19 losis is a short-chain alcohol dehydrogenase/reductase.
20 s involving non-proton-pumping plastoquinone reductases.
21 pha-bromoesters using flavin-dependent 'ene'-reductases.
22 ng the mechanism of flavodiiron nitric oxide reductases.
23 ghts regarding the mechanism of nitric oxide reductases.
24 ymes, such as respiratory heme-copper oxygen reductases.
25 ght other short-chain alcohol dehydrogenases/reductases.
27 rolled predominantly by S-nitrosoglutathione reductase 1 (GSNOR1) which turns over the natural NO don
32 ed peptide derived from human fatty acyl-CoA reductase 1 in complex with heme exhibited a significant
33 statistics identified a higher prostaglandin reductase 2 expression at early reperfusion with RIPC th
34 wo subunits of NADPH-dependent dehydrogenase reductase 3 (DHRS3), which catalyzes the reduction of re
35 -sGC-cGMP signaling and reveal cytochrome b5 reductase 3 as the first identified physiological sGC he
36 Mechanistically, we show that cytochrome b5 reductase 3 directly reduces oxidized sGC required for N
37 mooth muscle cells reveal that cytochrome b5 reductase 3 expression and activity is critical for NO-s
38 tein-protein complexes between cytochrome b5 reductase 3, also known as methemoglobin reductase, and
39 lications of SD may be contributed by 5alpha-reductase (5alphaR), the rate-limiting enzyme in the con
41 63, heme oxygenase-1 (HMOX1), and biliverdin reductase A (BLVRA) showed robust changes following trau
43 rgeting the antioxidant methionine sulfoxide reductase A to modulate liposarcoma cell survival and AS
44 utase (SOD2), catalase, methionine sulfoxide reductase A, and the 20S proteasome subunits PSMB5 and a
48 blast cells showed deficient ferredoxin NADP reductase activity and mitochondrial dysfunction evidenc
52 d that LND inhibits the succinate-ubiquinone reductase activity of respiratory complex II without ful
53 ss-link caused a >/=95% loss of cytochrome c reductase activity that was reversible with DTT treatmen
54 es a rhodanase-like protein that shows As(V) reductase activity when expressed in Escherichia coli.
55 transcript levels, as well as ferric chelate reductase activity, and is causal for a portion of the o
58 ropionate-CoA ligase (PrpE) and acryloyl-CoA reductase (AcuI) as the key enzymes involved and through
59 In many bacteria, a dedicated peroxiredoxin reductase, alkyl hydroperoxide reductase subunit F (AhpF
60 l gene, nirS (encoding cytchrome-cd1 nitrite reductase), along the salinity gradient of San Francisco
61 methanogens is mediated by methyl-coenzyme M reductase, an enzyme that is also responsible for the ut
62 The effector proteins, alkyl hydroperoxide reductase and acetyl-CoA acetyltransferase, recognizing
64 increase in ROS production and augmented GSH reductase and antioxidant regulator NRF2 activity, but d
66 n catalyzed by the drug target dihydrofolate reductase and established that protonation at N5 of H2F
67 ulates the expression of the plastid nitrite reductase and genes involved in the subsequent incorpora
68 idine residues in the key proteins in aldose reductase and heat-shock protein-70 within living cancer
69 ting in protein unfolding, inhibition of PDI reductase and isomerase activity in vitro and in vivo, a
70 Recombinant Chlamydomonas GPD2 showed both reductase and phosphatase activities in vitro and it can
72 holesterol, resist GGpp-induced release from reductase and remain sequestered in the ER to block redu
74 ctures of the Vitis vinifera dihydroflavonol reductase and SbCCR1, residues threonine-154 and tyrosin
75 tor of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase and the N-bisphosphonate zoledronic acid monoh
77 delivers nitrate to the respiratory nitrate reductase and transfers the product, nitrite, to the per
78 ntified genes encoding the subsequent 4-HPAA reductase and tyrosol:UDP-glucose 8-O-glucosyltransferas
79 cally characterized three leucoanthocyanidin reductases and two anthocyanidin reductases from P. nigr
80 oid isomerase, the SH3 domain, dihydrofolate reductase, and cytochrome c, where the transparent windo
81 milar to that in hemerythrin, ribonucleotide reductase, and methane monooxygenase, all of which can b
82 ined genes for both nitrate and nitric oxide reductase, and one had nitrate and nitrite reductase.
84 NADPH-cytochrome P450 reductase, biliverdin reductase, and thioredoxin reductase, resulting in a con
87 hway key enzyme, adenosine 5'-phosphosulfate reductase (APR, EC 1.8.99.2), was significantly higher i
89 nt and variants in the gene encoding HMG-CoA reductase are associated with reductions in both the con
90 the bacterium synthesizes succinate:quinone reductase as part of its respiratory chain, whereas unde
91 hat two isolates held genes encoding nitrate reductase as the only dissimilatory N-oxide reductase, o
93 Tfu-FNO is likely to act in vivo as an F420 reductase at the expense of NADPH, similar to its counte
97 glutathione reductase, NADPH-cytochrome P450 reductase, biliverdin reductase, and thioredoxin reducta
103 t, ascorbic acid and the enzymes glutathione reductase, catalase, ascorbate peroxidase and superoxide
107 L3 was shown to interact with geranylgeranyl reductase (CHLP), an enzyme of terpene biosynthesis that
108 on, mutations in genes encoding the chlorate reductase clrABC, predicted molybdopterin cofactor chape
111 f the Bacillus C-methyltransferase and the 4-reductase confirmed their involvement in the formation o
112 s supported the hypothesis that each N-oxide reductase could provide a selectable benefit on its own,
113 separately co-expressed with cytochrome P450 reductase (CPR) in insect Spodoptera frugiperda (Sf9) ce
116 cades with other enzymes, including carbonyl reductases (CREDs), hydrolases and monoamine oxidases (M
117 in 3-dioxygenase (F3H) and dihydroflavonol-4-reductase (DFR) in leaves, whereas a bHLH transcription
119 he functional importance of dehydroascorbate reductases (DHARs) in interactions between ascorbate and
122 iated by Plasmodium falciparum dihydrofolate reductase (DHFR) to two related inhibitors-pyrimethamine
123 P)-tagged bacterial-chromosome dihydrofolate reductase (DHFR) transgene can be visualized in a living
124 hymidylate synthase (TYMS) and dihydrofolate reductase (DHFR), as well as the components of the DNA r
128 ytic cycle of Escherichia coli dihydrofolate reductase (ecDHFR) is whether the Met(20) loop is dynami
129 mutations in KDSR (3-ketodihydrosphingosine reductase), encoding an enzyme in the ceramide synthesis
130 ive feedback between dATP and ribonucleotide reductase ensures tight control of dNTP concentration.
131 igher levels of malondialdehyde, glutathione reductase enzyme activity, and calcium levels, which wer
134 establish UBIAD1 as a central player in the reductase ERAD pathway and regulation of isoprenoid synt
135 o-Golgi transport enables UBIAD1 to modulate reductase ERAD such that synthesis of nonsterol isopreno
136 indicate that UBIAD1-mediated inhibition of reductase ERAD underlies cholesterol accumulation associ
137 , an SCD-associated UBIAD1 variant inhibited reductase ERAD, thereby stabilizing the enzyme and contr
140 ized by different ferredoxin-dependent bilin reductases (FDBRs): PPhiB is synthesized by HY2, whereas
142 genases, ferredoxins, and ferredoxin-NADP(+) reductases (FNR) are redox proteins that mediate electro
146 In addition, we identify the E. coli flavin reductase Fre, which is related to the dehydrogenase dom
147 archaeal strain to produce methyl-coenzyme M reductase from unculturable anaerobic methanotrophs for
148 thocyanidin reductases and two anthocyanidin reductases from P. nigra involved in catalyzing the last
149 m and substrate specificity of cinnamoyl-CoA reductases from sorghum (Sorghum bicolor), a strategic p
150 Nevertheless, the widespread quinone oxido-reductases from the cytochrome bc family limit the amoun
151 thioredoxins (Trxs), and an Fd-dependent Trx reductase (FTR), the Fd-FTR-Trxs system, which links red
153 nd GDP-4-keto-6-deoxymannose 3,5-epimerase-4-reductase (FX or tissue specific transplantation antigen
154 nd GDP-4-keto-6-deoxymannose 3,5-epimerase-4-reductase (FX or tissue specific transplantation antigen
155 e characterized the diversity of the nitrite reductase gene (aniA), the factor H-binding protein gene
156 tion, we generated a knockout in the nitrate reductase gene (NR-KO) of the model pennate diatom Phaeo
157 the upstream promoter region of the nitrate reductase gene, NIA1, and physically interact under cont
158 ition, DnrF induced the expression of the NO reductase genes (norCB), which promote NO consumption.
159 arise between the presence of known N-oxide reductase genes and phenotypic features, bacteria able t
161 AD(P)H dehydrogenase, quinone 1, glutathione reductase, glutamate-cysteine ligase catalytic subunit,
163 te that the gene for guanosine monophosphate reductase (GMPR) is a direct MITF target, and that the p
164 Here, we establish that S-nitrosoglutathione reductase (GSNOR), a major protein denitrosylase, provid
165 NO-metabolizing enzyme, S-nitrosoglutathione reductase (GSNOR), which exhibit enhanced S-nitrosylatio
166 nations of gene knockout, including arsenate reductase (HAC1), gamma-glutamyl-cysteine synthetase (ga
168 (SRP) or anti-3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) antibodies (Abs), and the titer of the
170 avastatin, hydroxymethylglutarate coenzyme-A reductase (HMGCR), was found to be over-expressed in all
176 first identified physiological sGC heme iron reductase in vascular smooth muscle cells, serving as a
177 ed gene ahpC, encoding an alkylhydroperoxide reductase, independently of H2O2 A conserved cysteine re
181 ity of mature gametocytes to the glutathione reductase inhibitor and redox cycler drug methylene blue
184 ([S]-LIP), that are loaded with the HMG-CoA reductase inhibitor simvastatin [S], were evaluated in t
186 thesis inhibitor) and auranofin (thioredoxin reductase inhibitor) induces oxidative burst, mitochondr
187 nfluence of hydroxymethylglutaryl-coenzyme A reductase inhibitors (also known as statins) on colorect
188 ydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have been the main therap
189 Hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins are well tolerated, but
191 atins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are an important group of hypolipi
192 atins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors), commonly prescribed in the primar
193 CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors, are drugs with multiple properties
195 ,e]azepines has highlighted the use of imine reductase (IRED) and omega-transaminase (omega-TA) bioca
197 ess, suggesting that the alkyl hydroperoxide reductase is an important regulator of redox homeostasis
198 the catalytic cycle of E. coli dihydrofolate reductase is tetrahydrofolate (THF) product release, whi
200 ing enzyme of dNTP synthesis, ribonucleotide reductase, is inhibited by endogenous levels of deoxyATP
204 n of the unsaturated lactone; and the ferric-reductase-like enzyme RbtH, which regioselectively reduc
210 h effects on 1-CM, methylenetetrahydrofolate reductase (MTHFR) 677C>T, rs1801133, and phosphatidyleth
211 1298A > C, of the methylene-tetrahydrofolate reductase (MTHFR) gene, an enzyme essential in DNA synth
216 orm of the Cu4S active site of nitrous oxide reductase (N2OR) that is observed in single turnover of
217 atalase, glutathione synthetase, glutathione reductase, NADPH-cytochrome P450 reductase, biliverdin r
218 s electrons through the mycothiol/mycothione reductase/NADPH pathway to activate TP053, preferentiall
219 port that DnrF selectively repressed nitrate reductase (nap) genes, preventing further NO formation.
220 ning subunit NarI of the respiratory nitrate reductase NarGHI as proteins that interact with HemW.
221 with the highly similar respiratory nitrate reductase NarGHI, which has a relatively much lower affi
224 monia monooxygenase (amoA) and nitrous oxide reductase (nosZ) genes, mediating oxidation of ammonia a
226 jor mechanism of NO synthesis is via NITRATE REDUCTASE (NR), an enzyme of nitrogen assimilation [5].
227 undance of ribosomal proteins and nucleotide reductase NrdEF was observed in post-infection samples c
228 tly, a plastid-localized NADPH-dependent Trx reductase (NTR) with a joint Trx domain, termed NTRC, wa
232 reductase as the only dissimilatory N-oxide reductase, one contained genes for both nitrate and nitr
233 lerated, ER-associated degradation (ERAD) of reductase, one of several mechanisms for feedback contro
239 symporter NasA from the assimilatory nitrate reductase pathway, support that NarK1 functions as a nit
241 ER membranes triggers release of UBIAD1 from reductase, permitting its maximal ERAD and ER-to-Golgi t
242 uster genes, we determined that the putative reductase PfmaG and the PKS are sufficient for the synth
243 rent energetic niches, express nitrous oxide reductase, potentially acting as a global sink for the g
244 system in conjunction with the dihydrofolate reductase protein-fragment complementation assay in Sacc
246 chia coli Complex II homolog quinol:fumarate reductase (QFR, FrdABCD) catalyzes the interconversion o
247 hytochrome photoreceptor, and ribonucleotide reductase R2 illustrate the power and versatility of thi
249 membrane-associated flavoprotein ferrodoxin reductase required for electron transport from NADPH to
250 eme-depleted, catalytically inactive nitrate reductase, restoring its nitrate-reducing enzyme activit
251 ctase, biliverdin reductase, and thioredoxin reductase, resulting in a concomitant reduction of intra
252 a highly active ferredoxin/flavodoxin-NAD(+) reductase (Rnf) that catalyzes the irreversible reductio
253 ective rate-limiting enzymes, ribonucleotide reductase (RNR) and deoxycytidine kinase (dCK), via dist
254 ression of genes encoding the ribonucleotide reductase (RNR) and proteins that facilitate the use of
255 during activation of class I ribonucleotide reductase (RNR) beta subunits, which self-assemble dimet
262 discovery in the chemistry of ribonucleotide reductases (RNRs) has been the identification of a diman
264 We recently found that the ribonucleotide reductase (RR) subunit M2 is potentially regulated by th
266 ly, mycobacterial short chain dehydrogenases/reductases (SDRs) within family TIGR03971 contain an ins
267 lines under-expressing monodehydroascorbate reductase showed a slight decrease in degradation produc
268 hydride transfer step in human dihydrofolate reductase shows that both the participation of the prote
270 peroxiredoxin reductase, alkyl hydroperoxide reductase subunit F (AhpF), catalyzes the rapid reductio
271 Q is a newly identified methionine sulfoxide reductase system found in bacteria, which appears to be
272 I nitroreductase (TbNTR) or cytochrome P450 reductase (TbCPR) dependent prodrugs that, following act
274 e bo3 is a respiratory proton-pumping oxygen reductase that is a member of the heme-copper superfamil
276 variant known to mimic inhibition of HMG-CoA reductase (the intended drug target) with the same lipid
277 -12 nrf operon encodes a periplasmic nitrite reductase, the expression of which is driven from a sing
278 holesterol, causing upregulation of HMG Co-A reductase, the rate-limiting enzyme in cholesterol synth
279 tins lower cholesterol by inhibiting HMG-CoA reductase, the rate-limiting enzyme of the metabolic pat
280 the superfamily of short chain dehydrogenase-reductases, the epimerase-active KR(0) domains from poly
281 lete study of a plant DHFR-TS (dihydrofolate reductase-thymidylate synthase) gene family that impleme
283 chrome bd-II oxidase synergized with nitrate reductases to drive luminal expansion, and both were req
284 the Escherichia coli trimethylamine N-oxide reductase (TorA) signal peptide in TatBC receptor bindin
285 by increased catalytic efficiency of aldose reductase toward hemithioacetal (product of glutathione
287 llular H2O2 levels by inhibiting thioredoxin reductase (TrxR) in cells expressing CRBN, causing accum
288 d NO sensitivity because the Trx/thioredoxin reductase (TrxR) system maintains thiol redox homeostasi
291 tudy in vitro to suppress expression of GSNO reductase, was decreased in hyperoxia-exposed pups.
292 efficient hydrogen-dependent carbon dioxide reductase when gaseous CO2 and H2 are placed under press
293 enhanced level of the encoded glutamyl-tRNA reductase, which catalyzes one of the rate-limiting step
294 , chloroplasts harbor an NADPH-dependent Trx reductase, which has a joint Trx domain at the carboxyl
295 biting 3-hydroxy-3-methylglutaryl coenzyme A reductase, which is a rate-limiting enzyme for cholester
296 In the presence of FMN, NADH, and flavin reductase, which reduces FMN to FMNH2 using NADH as the
297 that Rv2466c is a novel mycothiol-dependent reductase, which represents a mycoredoxin cluster of enz
300 hat co-occurrence of cld and a chloroxyanion reductase within a single organism is not necessary and
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