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1 DNIC formation requires free *NO, because addition of ox
2 DNICs were triggered either by immersion of the hindpaw
6 pecies, a new type of neutral {Fe(NO)(2)}(9) DNIC was prepared containing a beta-diketiminate ligand.
8 dicate that GST P1-1 acts to sequester NO as DNICs, reducing their transport out of the cell by MRP1.
9 ck and forward translational studies between DNIC and CPM, gauged between bench and bedside, are key
14 the IlvD-bound DNIC and other protein-bound DNICs are stable in cells under anaerobic growth conditi
16 -bound {Fe(NO)2}(9) dinitrosyl iron complex (DNIC) [(HS)2Fe(NO)2](-) (1) into [(NO)2Fe(mu-S)]2(2-) (R
19 the iron for these dinitrosyliron complexes (DNIC), and its relationship to cellular iron homeostasis
20 ion of thiols with dinitrosyliron complexes (DNIC), which are formed in cells from the reaction of *N
23 onic {Fe(NO)2}(9) dinitrosyl iron complexes (DNICs) [((R)DDB)Fe(NO)2](+) (R = Me, Et, Iso; (R)DDB = N
24 ers NO as dinitrosyl-dithiol iron complexes (DNICs) and inhibits NO-mediated iron release from cells
25 the formation of dinitrosyl iron complexes (DNICs) now viewed as playing important roles in the mamm
31 respect diffuse noxious inhibitory controls (DNIC) are a unique form of endogenous descending inhibit
34 The mononuclear DNIC Fe(NO)2(CysS)2(-) (Cys-DNIC) is produced from the same three components at pH 1
35 cs studies suggest that both Cys-RSE and Cys-DNIC are formed via a common intermediate Fe(NO)(CysS)2(
36 otolysis of the mononuclear-DNIC species Cys-DNIC formed from Fe(II)/NO/cysteine mixtures in anaerobi
38 on of GST P1-1 and ability of MRP1 to efflux DNICs are vital in protection against NO cytotoxicity.
41 SIH added during the *NO treatment "freezes" DNIC levels, showing that the complexes are formed from
46 The reversible transformation of RRS into DNIC 1 (RRS --> DNIC 1) in the presence of H2S was demon
47 nverted to paramagnetic large molecular mass DNIC from exposure to free *NO but not from cellular nit
49 that dinuclear RRE species, not mononuclear DNICs, may be the primary iron dinitrosyl species respon
50 ed ester (RRE) formula, and that mononuclear DNICs account for only a minor fraction of nitrosylated
51 In contrast, photolysis of the mononuclear-DNIC species Cys-DNIC formed from Fe(II)/NO/cysteine mix
52 ergic primary afferents in the activation of DNIC by noxious heat and mechanical stimulations, substa
57 charge (Zeff) of the iron center and prevent DNIC 1 from dimerization in an organic solvent (MeCN).
59 CH2)2-o-C6H4) cleanly affords the respective DNIC, [Fe(NO)2(SR)2](-), with concomitant reductive elim
60 use of an N-heterocyclic carbene-stabilized DNIC, (NHC)(RS)Fe(NO)2, we have explored the DNIC-promot
62 pinal pharmacology of pathways that subserve DNIC are complicated; in the normal situation these desc
64 pinal MOPR and DOPR similarly attenuates the DNIC and neurokinin type 1 receptor internalization indu
65 DNIC, (NHC)(RS)Fe(NO)2, we have explored the DNIC-promoted RS(-)/RS* oxidation in the presence of add
66 icated reaction dynamics interconnecting the DNIC species and offer a mechanistic model for the key s
69 lfide redox processes, which when coupled to DNICs may lead to intricate redox processes involving ir
72 (NBD = nitrobenzofurazan), was observed when DNIC 1 was dissolved in water at ambient temperature.
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