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1 w that glutathione acts as the main cellular redox buffer.
2 oxidative perturbation of the ER glutathione redox buffer.
3 ithout any added oxidized PDI or glutathione redox buffer.
4 y similar to when hydroquinone was used as a redox buffer.
5 e presence of 0.5 M guanidine and a suitable redox buffer.
6 n the reducing capacity of the extracellular redox buffer.
7 tored by circular dichroism in a glutathione redox buffer.
8 ation, even in the presence of a glutathione redox buffer.
9 essive copper entry, which is deleterious to redox buffers.
10 n be followed in the presence of glutathione redox buffers.
11 ore versatile than classical aliphatic thiol redox buffers.
12 th the disulfide-scrambled state in the same redox buffers.
13 binds to melanin and cooperatively increases redox buffering.
14 in thiol redox signaling and acts as a major redox buffer against reactive oxygen species, helping to
15 l-glycine, GSH) has vital functions as thiol redox buffer and cofactor of antioxidant and detoxificat
16 M may preserve Fe(II) by functioning both as redox buffer and complexant, which may help explain the
17 omises production of glutathione, a critical redox buffer and enzymatic cofactor.
18 lized by the covalent attachment of a cobalt redox buffer and used as a new solid contact for ion-sel
19 zed and reduced species of a redox couple as redox buffer and used them to make SC-ISEs that exhibite
20 h and survival, fuels key pathways including redox buffering and coenzyme production.
21       The metabolites that function in thiol redox buffering and homeostasis in Bacillus are not well
22 y GSH as a fulcrum in the liver's balance of redox buffering and triglyceride production.
23 logens accelerate the redox equilibration of redox buffers and [Fe(4)S(4)](B) during catalysis.
24 ature, as evidenced by precursor behavior in redox buffers and by thermodynamic calculations.
25 og units above the fayalite-magnetite-quartz redox buffer) and sulfur-rich.
26 scanning Raman spectroscopy, turbidimetry in redox buffers, and free thiol quantitation.
27 ridyl, which makes it possible to extend the redox buffer approach to ionophore-based ISEs.
28 s surface-attached CIM-ph-Tpy-Co(III/II)-Tpy redox buffer as a solid contact were tested as K(+) sens
29  emerged as key species involved in cellular redox buffering as well as RSS generation, translocation
30 is not only an important intracellular thiol redox buffer but also a cofactor for several redox activ
31 med that cysteine is the major intracellular redox buffer by showing that T. vaginalis contains high
32 V) dissolution at S/Fe = 0.112 is due to the redox buffer capacity of FeS, which is evidenced by the
33 rations in this pathway could compromise the redox buffering capacity of cells, which may in turn be
34 ll size, limited hydraulic conductivity, and redox buffering capacity.
35 es its contribution to glutathione-dependent redox-buffering capacity under ex vivo conditions in bra
36 , and that the rate of electron flux through redox buffering circuits is directly linked to changes i
37 s-induced JH(2)O(2) production to NNT-linked redox buffering circuits provides a potential means of i
38  is reduced to H(2)O by electrons drawn from redox buffering circuits supplied by NADPH, and that the
39 lus pharmacological or genetic inhibition of redox buffering circuits.
40 ized PVC membranes, along with a hydrophilic redox buffer composed of ferrocyanide and ferricyanide t
41 s intermediate layer based on the lipophilic redox buffer consisting of the Co(III) and Co(II) comple
42 HCY regulate spare respiratory capacity, the redox buffer cystathionine, lipid and amino acid metabol
43 cs and lipidomics revealed elevations in the redox buffers cystathionine, hexosylceramides, and gluco
44 ioxidants (e.g., ascorbic acid) and cellular redox buffers (e.g., glutathione), and the Abeta-Cu(I) c
45 ivity and was positively associated with the redox-buffering efficiency of tannins.
46 environment without reducing agents and in a redox-buffered environment by adding redox mediator 9,10
47                   To create a more efficient redox buffer for the in vitro folding of disulfide conta
48                          This application of redox buffers for controlled doping provides a new metho
49 wever, the effects of the composition of the redox buffer, GSSG and GSH, on folding has not been exte
50                                         This redox buffer has also been successfully applied to sodiu
51 e disulphide (GSSG) forms the most important redox buffer in organisms responsible for detoxification
52 he host is cysteine, which acts as the major redox buffer in the blood by transitioning between reduc
53                                A glutathione redox buffer increases the kcat for single-cysteine muta
54                              Due to the high redox buffer intensity of heterogeneous mixed valent iro
55 inhibit isomerization and oxidize PDI when a redox buffer is not present to maintain the PDI redox st
56      In cyanobacteria, the glutathione (GSH) redox buffer majorly controls intracellular redox potent
57 chronic oxidative stress condition through a redox-buffering mechanism.
58 e-containing proteins is slow and involves a redox buffer of glutathione and glutathione disulfide.
59 r study reveals that spermine metabolism via redox buffering of the ER underpins appressorial adhesio
60        In this study we tested the effect of redox buffer on platelet aggregation and the effect of r
61             Kinetic studies suggest that the redox buffer participates as the nucleophile and/or the
62 lecting compensatory increases in alterative redox-buffering pathways.
63                Here we report on an improved redox buffer platform based on equimolar amounts of the
64 ded proteins in the ER depends on an optimum redox buffer ratio.
65                                 The relevant redox buffering reactions, however, remain poorly constr
66                                           In redox buffers, rLIN-12.1 forms only one disulfide isomer
67 ase in the ratio of the reduced and oxidized redox buffer species.
68 cohols to afford benzyl ethers, enabled by a redox-buffering strategy that maintains the activity of
69      Glutathione and GSSG form the principle redox buffering system in the cell, with the endoplasmic
70 added back to alkali-treated microsomes in a redox buffer that reflected conditions found in the lume
71             In the absence of either QSOX or redox buffer, the fastest refolding of RfBP is accomplis
72                          In the absence of a redox buffer, these steady-state reduction-oxidation cyc
73 w rate and the addition of hydroquinone as a redox buffer to the spray solvent were found to decrease
74 recursors to both guanidine denaturation and redox buffer unfolding are similar, as are in vitro fold
75       The refolding performed in glutathione redox buffer was quenched at different time points by ad
76 h agents manipulate the cellular glutathione redox buffer, we conclude that the observed effects of E
77               By reacting at this electrode, redox buffers were able to maintain electrode potentials
78                                      Several redox buffers were introduced for controlling electroche
79                                 Two types of redox buffers were used.
80 cult-to-handle modifications to the cellular redox buffer which can impair proper cellular function.
81            Melanin is a fungal extracellular redox buffer which, in principle, can neutralize antimic
82            Many of these reactions include a redox buffer, which is a mixture of a thiol (RSH) and th
83 t catalyzes protein disulfide formation in a redox buffer with an initial velocity that is 30-fold fa