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1  was evidenced from the electron transfer to methyl viologen.
2 d caffeyl-CoA-dependent oxidation of reduced methyl viologen.
3 persensitive to the oxidative stress reagent methyl viologen.
4 stress sensitivity of this E. coli mutant to methyl viologen.
5 achieved by using a surfactant derivative of methyl viologen.
6 xtreme sensitivity to the redox-active agent methyl viologen.
7  reduction of BSO by either NADPH or reduced methyl viologen.
8 nd the activity required Ti(III) citrate and methyl viologen.
9  as photocathodes in contact with an aqueous methyl viologen(2+/+) electrolyte, energy-conversion eff
10 en the enzyme was assayed in the presence of methyl viologen (4 mM) and inhibited by 70% when the enz
11 tiated electron transfer to generate reduced methyl viologen, a species that persists in the presence
12 ferent redox behavior was also observed when methyl viologen and benzyl viologen were used as reducta
13 nd Km values of 29 and 15 microM for reduced methyl viologen and biotin sulfoxide reductase, respecti
14  affinity for the heteroternary complex with methyl viologen and CB[8] (MVCB[8]) within a vast pool o
15 uced Fe(II) cores (Fe(II)-HoSF), prepared by methyl viologen and CO, also reduces M-HoSF and M-AvBF s
16 t all mutants were completely devoid of both methyl viologen and formate-linked thiosulfate reductase
17 ronmental stresses, including drought, salt, methyl viologen and H2O2 induced oxidative stress.
18  type, fib4 KD apples were more sensitive to methyl viologen and had higher superoxide levels during
19 ive protein after redox cycling with reduced methyl viologen and Me2SO.
20 e fraction of chloroplasts were increased by methyl viologen and ozone, but not by high-light treatme
21 lementation line C1 rescued the tolerance to methyl viologen and salinity and recovered the growth an
22 anced sensitivity to superoxide generated by methyl viologen and tellurite.
23 ing the photo-reduction of a redox mediator (methyl viologen) and light driven H2 generation.
24 ayed a soxS-dependent induction by paraquat (methyl viologen), and the fldB gene is preceded by two o
25               Ru(NH3)6(3+/2+), IrCl6(2-/3-), methyl viologen, and chlorpromazine all involve electron
26 Upon partial reduction with dithionite using methyl viologen as a mediator, a signal at g(ave) = 1.9
27 alyzed the reduction of NADP(+) with reduced methyl viologen as electron donor at a rate of 385 U/mg.
28 uction with Ti(III)-citrate as reductant and methyl viologen as mediator were similar to those obtain
29 2) evolved/mg at 80 degrees C) using reduced methyl viologen as the electron donor.
30  BSOR activity using either NADPH or reduced methyl viologen as the electron donor.
31 to the superoxide-generating agent paraquat (methyl viologen) as the inducer.
32 urthermore, a newly designed high-throughput methyl viologen-based photometric microtiter plate assay
33 e herbicides fosmidomycin, phosphonothrixin, methyl viologen, benzyl viologen, clomazone, 2-(dimethyl
34 ngsten-grown cells yielded decreased reduced methyl viologen:BSO reductase, NADPH:BSO reductase, and
35 rosative stress and the superoxide generator methyl viologen but remarkably resistant to hydrogen per
36 itive to an oxidative stress-inducing agent, methyl viologen, but the sarA sodA double mutant was mor
37 de or the reactive oxidative species inducer methyl viologen can induce macroautophagy in Arabidopsis
38 mical characterization of these Hg tips with methyl viologen, cobalt sepulchrate trichloride, and hex
39  SDS-PAGE for covalently bound haem, but the methyl-viologen-dependent nitrite reductase activities a
40                                         With methyl viologen dication (MV(2+)) added as a trap, Acr-(
41  uniquely different binding pocket wherein a methyl viologen dication is stabilized by interacting wi
42 (CN)6(3-/4-), Ru(NH3)6(3+/2+), IrCl6(2-/3-), methyl viologen, dopamine, ascorbic acid, Fe(3+/2+), and
43                                              Methyl viologen hexafluorophosphate (MV(2+).2PF6(-)) and
44 henol plus ascorbate as an electron donor to methyl viologen, however, was the same as observed in th
45 ent pi-radicals such as MV(+*) (MV refers to methyl viologen, i.e., N,N'-dimethyl-4,4'-bipyridinum) e
46                 F(A)- could be reoxidized by methyl viologen in F(B)-less PS I complexes, although at
47  from the artificial electron donor DCPIP to methyl viologen in thylakoid membranes.
48              The sodB- was very sensitive to methyl viologen, indicating a specific role for the FeSO
49                                              Methyl viologen is in turn a weaker pi-acceptor than ant
50 d with the WT, gr3 was sensitive to salt and methyl viologen; it showed inhibited growth, decreased m
51  hydA genes resulted in a loss of detectable methyl viologen-linked hydrogenase activity.
52 ond hydrogenase gene cluster, hyd, exhibited methyl viologen-linked hydrogenase enzymatic activity, b
53 e to transcribe nar and subsequently express methyl viologen-linked nitrate reductase activity under
54 und to catalyze the reduction of NO(2)(-) by methyl viologen monocation radical (MV(red)), displaying
55                Two BIPY(*+) radical cations, methyl viologen (MV(*+)) and a dibutynyl derivative (V(*
56 ers in the photoelectrochemical reduction of methyl viologen (MV(+2)).
57 of a 1:1 inclusion complex between the guest methyl viologen (MV(2+)) and the host cucurbit[7]uril (C
58 ometric reduction of nitrate to nitrite used methyl viologen (MV(2+)) as the electron transfer mediat
59                         Aqueous solutions of methyl viologen (MV(2+)) exhibit anomalous fluorescence
60 or the reaction of charged nanocrystals with methyl viologen (MV(2+)).
61 ivative, (DNP-BS(-)), and positively charged methyl viologen (MV(2+)).
62 der oxidative stress conditions generated by methyl viologen (MV) added during the early exponential
63 n to form 1:1:1 heteroternary complexes with methyl viologen (MV) and a second aromatic guest.
64                             When paired with methyl viologen (MV) as an anolyte, resulting FcNCl/MV a
65 es was measured by three electron acceptors, methyl viologen (MV), potassium ferricyanide, or dichlor
66 lasts resulted in an increased resistance to methyl viologen (MV)-induced oxidative stress, documente
67 re essential for superoxide stress response, methyl viologen (MV)-sensitive mutants of S. mutans were
68                                We discover a methyl viologen (MV)/bromide electrolyte that delivers a
69 n by a photosystem I (duraquinol [DQH(2)] to methyl viologen [MV]) proton pumping partial reaction wa
70 s (ruthenium bipyridine [Ru-(bipy)3(2+)] and methyl viologen [MV2+]) was quantified in a U-tube perme
71                                     By using methyl viologen (N,N'-dimethyl-4,4'-bipyridinium) to shu
72                        The protein possessed methyl viologen:NADP(+) oxidoreductase activity and cata
73 y was observed on recombinant CbR module and methyl viologen nitrate reduction by holo-NaR, suggestin
74 ties NADH:cytochrome c reductase and reduced methyl viologen:NR, closely paralleled the appearance an
75 ron-sulfur component oxidized CO and reduced methyl viologen or a ferredoxin isolated from M. thermop
76      Furthermore, the effects of exposure to methyl viologen or H2O2 on intracellular NADH and NAD(+)
77 lectron transport activity when treated with methyl viologen or norflurazon (NF).
78 n sulfoxide reductase activity using reduced methyl viologen or reduced benzyl viologen as artificial
79 re selectively sensitive to peroxide but not methyl viologen or Rose Bengal, and GPXs, APX, and MSRA2
80 sed to different oxidative stress conditions-methyl viologen, ozone, and high light-differences were
81 the antioxidant depletion in the presence of methyl viologen (paraquat), a known agent of oxidative s
82 ethal levels of the ROS-generating herbicide methyl viologen (paraquat), suggesting a common protecti
83                    Examples include enhanced methyl viologen (Paraquat)-induced oxidative stress tole
84 the redox-active superoxide-generating agent methyl viologen (paraquat).
85  1,1'-Dimethyl-4,4'-bipyridinium dichloride (methyl viologen; paraquat), an herbicide that causes dep
86 valuated using both aqueous (Fe(CN)(6)3-/4-, methyl viologen, Ru(NH3)(6)3+/2+, and IrCl(6)2-/3-) and
87 ccurs in the sarA background, can rescue the methyl viologen-sensitive phenotype observed in the abse
88  the enzyme-dependent reoxidation of reduced methyl viologen spectrophotometrically at 600 nm.
89          We show that AMC260 and AMC364 lack methyl viologen-supported nitrate reductase activity.
90 uests simultaneously and, in the presence of methyl viologen, to recognize N-terminal tryptophan over
91 on, with phosphatidylethanolamine increasing methyl viologen transport.
92 G18a transgenic plants are more sensitive to methyl viologen treatment than wild-type plants and accu
93 ogen and had higher superoxide levels during methyl viologen treatment.
94 n (MOP) 3 which bears 24 covalently attached methyl viologen units on its external surface, as eviden
95                                              Methyl viologen was allowed to absorb into the Nafion la
96 of Q8 to aromatic peptides in the absence of methyl viologen was studied by isothermal titration calo
97 g time as well as its resistance to H2O2 and methyl viologen were indistinguishable from those of the
98  with Mito-Bodipy-TOH in cells stressed with methyl viologen, whereas no enhancement was observed in
99 trary to 4,4'-dipyridinium (i.e., archetypal methyl viologen), which is reduced by two single-electro

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