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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
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
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.
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
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
25 henanthroline were related to suppression of S-nitrosocysteine decay by cysteine-mediated reduction o
27 used a concentration-dependent inhibition of S-nitrosocysteine decay, whereas deferoxamine (100 micro
30 try as well as nitrosation experiments using S-nitrosocysteine demonstrate that GSNO binding does not
33 res that underlie the specificity of protein S-nitrosocysteine formation in these cells remain unknow
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)
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
46 eact with cysteine sulfhydryl groups to form S-nitrosocysteine or cysteine oxides such as cysteinesul
48 when exposed to S-nitrosoglutathione (GSNO), S-nitrosocysteine, or S-nitrosoacteylpenicillamine, resu
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
54 s of the endothelium-derived relaxing factor S-nitrosocysteine (SNC) may not be simply due to its dec
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-
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
61 prevents formation from either *NO donor or S-nitrosocysteine, the latter treatment resulting in 100
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