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1 ould be reversed by treating the enzyme with methionine sulfoxide reductase.
2 and the oxidized protein was incubated with methionine sulfoxide reductase.
3 ribonucleotide reductase, peroxiredoxin, and methionine sulfoxide reductase.
4 it is reversed by coexpression with peptide methionine sulfoxide reductase.
5 ion mediated by a ubiquitous enzyme, peptide methionine sulfoxide reductase.
6 he action of stereospecific enzymes known as methionine sulfoxide reductases.
7 so observed that are catalyzed by endogenous methionine sulfoxide reductases.
8 thione peroxidase, ascorbate peroxidase, and methionine sulfoxide reductase 2) are slightly up-regula
9 cardial CaMKII inhibition, overexpression of methionine sulfoxide reductase A (an enzyme that reduces
16 that a mutant form of M. genitalium lacking methionine sulfoxide reductase A (MsrA), an antioxidant
18 n that can be reversed through the action of methionine sulfoxide reductase A (MsrA), which is implic
19 n-like domain (NT domain) is fused to tandem methionine sulfoxide reductase A and B domains (MsrA/B).
20 r, we demonstrate almost absent catalase and methionine sulfoxide reductase A and B protein expressio
21 horesis (CE) method for the determination of methionine sulfoxide reductase A and methionine sulfoxid
25 have unraveled the redox relay mechanisms of methionine sulfoxide reductase A of the pathogen Coryneb
26 quinone reductase, glutathione reductase and methionine sulfoxide reductase A proteins were significa
27 xpressions of only glutathione reductase and methionine sulfoxide reductase A proteins were significa
28 ecies signaling by targeting the antioxidant methionine sulfoxide reductase A to modulate liposarcoma
29 dium-restricted transgenic overexpression of methionine sulfoxide reductase A, an enzyme that reduces
30 dants superoxide dismutase (SOD2), catalase, methionine sulfoxide reductase A, and the 20S proteasome
31 ysine residues of diverse targets, including methionine sulfoxide reductase A, myosin light chain kin
32 whereas over-expression of a repair enzyme, methionine sulfoxide reductase A, rendered them resistan
34 (MetO) residues in proteins is catalyzed by methionine sulfoxide reductases A (MSRA) and B (MSRB), w
36 S) can be repaired in the human epidermis by methionine sulfoxide reductases A and B, respectively.
39 ained by uniform selenium deficiency because methionine sulfoxide reductase activities were similar i
44 tion of methionine sulfoxide reductase A and methionine sulfoxide reductase B activities in mouse liv
47 activity of plastidial thiol peroxidases and methionine sulfoxide reductases employing a single cyste
49 ossesses significant homology to the peptide methionine sulfoxide reductase family of enzymes, specif
50 these genes are fused to form a bifunctional methionine sulfoxide reductase (i.e., MsrBA) enzyme.
51 s of apoA-I and oxidized apoA-I treated with methionine sulfoxide reductase implicate oxidation of sp
53 ding or the repair of oxidized calmodulin by methionine sulfoxide reductase induces comparable change
55 e pK(a) of the active site cysteine of mouse methionine sulfoxide reductase is 7.2 even in the absenc
56 of oxidized methionine residues performed by methionine sulfoxide reductase is important for the gast
57 enerally accepted, primarily from studies on methionine sulfoxide reductase (Msr) A, that the biologi
61 Met5 of alphaS are excellent substrates for methionine sulfoxide reductase (Msr), thereby providing
63 nt study on the reducing requirement for the methionine sulfoxide reductases (Msr), we have shown tha
67 teins or repair oxidized residues, including methionine sulfoxide reductases MsrA and MsrB, which red
73 ty with the carboxyl terminus of the peptide-methionine sulfoxide reductase (MsrA), a repair enzyme,
75 ted by an unrelated protein known as peptide methionine sulfoxide reductase (MsrA), an antioxidant re
76 an mutants in cytochrome c peroxidase (ccp), methionine sulfoxide reductase (msrA), or the metal-bind
77 oxidized alpha/beta-type SASP with peptidyl methionine sulfoxide reductase (MsrA), which can reduce
85 s damage is reversible through the action of methionine sulfoxide reductases (MSRs), which play key r
88 revisiae as a model, we show that of the two methionine sulfoxide reductases (MXR1, MXR2), deletion o
91 ild-type plants and a mutant lacking peptide methionine sulfoxide reductase (pmsr2-1) showed increase
92 sporadically evolved Sec-containing forms of methionine sulfoxide reductases reflect catalytic advant
94 rx2) and the intracellular and extracellular methionine sulfoxide reductases (SpMsrAB1 and SpMsrAB2,
96 hesin (one UGA) of Mycoplasma pneumoniae and methionine sulfoxide reductase (two UGAs) of Mycoplasma
97 ine in proteins involving the enzyme peptide methionine sulfoxide reductase type A (MSRA) is postulat
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