戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ication of protein cysteine residues to form S-nitrosocysteine.
2 5-HT whereas the BJR responses elicited by L-S-nitrosocysteine (10 micromol/kg, i.v.) were similar be
3                             In this setting, S-nitrosocysteine (10 muM) effectively blocked the Trx-m
4  responses elicited by the S-nitrosothiol, L-S-nitrosocysteine (5 micromol/kg, i.v.), were not attenu
5 cular smooth muscle cells, both the NO donor S-nitrosocysteine and atrial natriuretic peptide induced
6                        We observed that both S-nitrosocysteine and cytokine-activated NOS2 inhibited
7  aortic smooth muscle cells upon exposure to S-nitrosocysteine and propylamine propylamine NONOate.
8 peared to be due to both competition between S-nitrosocysteine and Prx1 for the Trx system and direct
9 e system and in cells, NO/SNO donors such as S-nitrosocysteine and S-nitrosoglutathione readily induc
10 cond order rate constants of 76,900 M-1 s-1 (S-nitrosocysteine) and 12,800 M-1 s-1 (S-nitrosoglutathi
11 f nitrosothiols (i.e., S-nitrosoglutathione, S-nitrosocysteine, and S-nitrosoalbumin) and amperometri
12 with other cellular thiols, the formation of S-nitrosocysteine at Cys-145 was found to lead to the ra
13 es similar to those seen with injection of L-S-nitrosocysteine, blockade of excitatory amino acid rec
14 of cystine and nitric oxide, two products of S-nitrosocysteine breakdown, produced no significant res
15 ar weight RSNOs (i.e., S-nitrosoglutathione, S-nitrosocysteine) by tuning the irradiation exposure.
16           This strategy identified 20 unique S-nitrosocysteine-containing peptides belonging to 18 pr
17                     Sequence analysis of the S-nitrosocysteine-containing peptides revealed the prese
18 ted in primary aortic smooth muscle cells by S-nitrosocysteine (CSNO), an S-nitrosylating agent, in h
19 r effects of S-nitrosothiols is specific for S-nitrosocysteine (CSNO), is stereoselective, and requir
20           In the present study, we show that S-nitrosocysteine (CSNO), S-nitrosoglutathione (GSNO), a
21 ls and human erythroid progenitor cells with S-nitrosocysteine (CysNO), an NO donor, and found simila
22 y the reaction of cysteine with GSNO to form S-nitrosocysteine (CysNO), mixed disulfides, and nitrosy
23 an be poly-S-nitrosylated by the NO carrier, S-nitrosocysteine (CysNO).
24 O from the biologically occurring substrate, S-nitrosocysteine (CysNO).
25 henanthroline were related to suppression of S-nitrosocysteine decay by cysteine-mediated reduction o
26                   Comparison of the rates of S-nitrosocysteine decay in different subcellular fractio
27 used a concentration-dependent inhibition of S-nitrosocysteine decay, whereas deferoxamine (100 micro
28         In the presence of o-phenanthroline, S-nitrosocysteine decomposition followed saturable kinet
29                                  The rate of S-nitrosocysteine degradation by aortic homogenates in t
30 try as well as nitrosation experiments using S-nitrosocysteine demonstrate that GSNO binding does not
31 molecular mass cell-permeable S-nitrosothiol S-nitrosocysteine ethyl ester (SNCEE).
32             In HepG2 cells, we observed that S-nitrosocysteine ethyl ester impedes the activity of ca
33 res that underlie the specificity of protein S-nitrosocysteine formation in these cells remain unknow
34                                     The free S-nitrosocysteine generated in the reaction with GSNO br
35 eterolytic decomposition of the S-NO bond of S-nitrosocysteine in a process involving redox cycling o
36     We recently reported that degradation of S-nitrosocysteine in homogenates of porcine aorta increa
37 ular effects elicited by microinjection of L-S-nitrosocysteine in the nucleus tractus solitarii (NTS)
38 , we established that Trx1 protects GC1 from S-nitrosocysteine-induced desensitization.
39                  The study demonstrates that S-nitrosocysteine is biologically active in the NTS.
40 ion of cysteine residues in proteins to form S-nitrosocysteine, is a major emerging mechanism by whic
41 ication of protein cysteine residues to form S-nitrosocysteine, is one of the molecular mechanisms by
42 he reaction at low initial concentrations of S-nitrosocysteine (< or = 15 microM) and inhibited the r
43 within the ER molecule by immunodetection of S-nitrosocysteine moieties in ER.
44  for the Trx system and direct modulation by S-nitrosocysteine of Trx reductase activity.
45                               With regard to S-nitrosocysteine or cysteine oxide formation, no eviden
46 eact with cysteine sulfhydryl groups to form S-nitrosocysteine or cysteine oxides such as cysteinesul
47                                Incubation of S-nitrosocysteine or S-nitrosoglutathione (5-100 M) in t
48 when exposed to S-nitrosoglutathione (GSNO), S-nitrosocysteine, or S-nitrosoacteylpenicillamine, resu
49                                            L-S-nitrosocysteine produced dose-related decreases of art
50 ing chemiluminescence revealed that L- and D-S-nitrosocysteine released identical amounts of nitric o
51 lity plot indicated that the distribution of S-nitrosocysteine residues was skewed toward larger surf
52                               In contrast, D-S-nitrosocysteine, S-nitrosoglutathione, glyceryl trinit
53                                              S-nitrosocysteine (SNC) and, to a more modest extent, S-
54 s of the endothelium-derived relaxing factor S-nitrosocysteine (SNC) may not be simply due to its dec
55  in clusters and are indirectly activated by S-nitrosocysteine (SNC), an NO donor.
56 SNAP, 5 to 10 nmol/L or 100 to 800 mumol/L), S-nitrosocysteine (SNC, 100 mumol/L or 1 mmol/L), and S-
57                                              S-Nitrosocysteine (SNC, an NO donor) and 8-bromo-cGMP (8
58 esponse directed against proteins containing S-nitrosocysteine (SNO-cysteine) and showed that anti-NO
59 ctal neuron processes bathed in the NO donor S-nitrosocysteine (SNOC) and in RGC growth cones to whic
60               Among the NO-donors used, only S-nitrosocysteine (SNOC) was found to be capable of mode
61  prevents formation from either *NO donor or S-nitrosocysteine, the latter treatment resulting in 100
62            At non-limiting concentrations of S-nitrosocysteine, the rate of degradation in the cytoso
63              This reaction converts unstable S-nitrosocysteines to dehydroalanine derivatives under v
64                   A reductive elimination of S-nitrosocysteines using phosphine substrates has been d
65                               Responses to L-S-nitrosocysteine were not affected by local injection o

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。