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1                                              DNIC formation requires free *NO, because addition of ox
2                                              DNICs were triggered either by immersion of the hindpaw
3 (CO)Fe(NO)(2) (2), a reduced {Fe(NO)(2)}(10) DNIC.
4 ompound affords the isolable {Fe(NO)(2)}(10) DNIC.
5 f {Fe(NO)2}(9) and diamagnetic {Fe(NO)2}(10) DNICs (Enemark-Feltham notation).
6 pecies, a new type of neutral {Fe(NO)(2)}(9) DNIC was prepared containing a beta-diketiminate ligand.
7 ent a rare example of structurally analogous DNIC redox partners.
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
10 ransferase P1-1 (GST P1-1) was shown to bind DNICs as dinitrosyl-diglutathionyl iron complexes.
11                                         Both DNIC and RSNO are also increased during overproduction o
12                         While the IlvD-bound DNIC and other protein-bound DNICs are stable in cells u
13 at a large number of different protein-bound DNICs are formed by NO.
14  the IlvD-bound DNIC and other protein-bound DNICs are stable in cells under anaerobic growth conditi
15  EPR-active, neutral dinitrosyliron complex (DNIC) (IMes)Fe(SPh)(NO)(2) (3, {Fe(NO)(2)}(9)).
16 -bound {Fe(NO)2}(9) dinitrosyl iron complex (DNIC) [(HS)2Fe(NO)2](-) (1) into [(NO)2Fe(mu-S)]2(2-) (R
17 n of the IlvD-bound dinitrosyl iron complex (DNIC).
18  the appearance of dinitrosyliron complexes (DNIC) are key determinants.
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
21                    Dinitrosyliron complexes (DNICs) are organometallic-like compounds of biological s
22  of {Fe(NO)(2)}(9) dinitrosyliron complexes (DNICs).
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
26  and formation of dinitrosyl iron complexes (DNICs).
27 uster to generate dinitrosyl iron complexes (DNICs).
28  is a hallmark of dinitrosyl iron complexes, DNIC's.
29                        Under our conditions, DNIC formation, like RSNO formation, is inhibited by app
30 menon of diffuse noxious inhibitory control (DNIC).
31 respect diffuse noxious inhibitory controls (DNIC) are a unique form of endogenous descending inhibit
32 induced diffuse noxious inhibitory controls (DNICs).
33                                          Cys-DNIC and Cys-RSE interconvert, and the rates of this pro
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
37                                The dinuclear DNIC Fe2(mu-CysS)2(NO)4, a Roussin's red salt ester (Cys
38 on of GST P1-1 and ability of MRP1 to efflux DNICs are vital in protection against NO cytotoxicity.
39 4 equiv of (Et4N)(SPh) to yield the expected DNIC.
40  Gstp1, suggesting GSTP1 was responsible for DNIC binding/storage.
41 SIH added during the *NO treatment "freezes" DNIC levels, showing that the complexes are formed from
42 rmed from free *NO via transnitrosation from DNIC derived from the CIP.
43 e transformation of RRS into DNIC 1 (RRS --> DNIC 1) in the presence of H2S was demonstrated.
44        Furthermore, Mrp1 silencing increased DNIC accumulation in macrophages, indicating a role for
45 ne shows quantitative conversion of CIP into DNIC by *NO.
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
48                              The mononuclear DNIC Fe(NO)2(CysS)2(-) (Cys-DNIC) is produced from the s
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
53 modulation (CPM) is the human counterpart of DNIC and requires a descending control also.
54 eceptors, influences the final expression of DNIC also.
55               In some cases the formation of DNICs from such cluster systems can lead to activation o
56 ordinately regulate storage and transport of DNICs as long lived NO intermediates.
57 charge (Zeff) of the iron center and prevent DNIC 1 from dimerization in an organic solvent (MeCN).
58                    SIH pretreatment prevents DNIC formation from *NO, and SIH added during the *NO tr
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
61 ce of thiolate-to-iron ratios in stabilizing DNICs.
62 pinal pharmacology of pathways that subserve DNIC are complicated; in the normal situation these desc
63       Here we report the first evidence that DNICs also form in the reaction of NO with Rieske-type [
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
67                                    Thus, the DNIC storage function of GST P1-1 and ability of MRP1 to
68      Isolation and characterization of these DNICs, including the new compound, (Et(4)N)[(N(2)CHPh)Fe
69 lfide redox processes, which when coupled to DNICs may lead to intricate redox processes involving ir
70 , indicating a role for MRP1 in transporting DNICs out of cells.
71 ain significantly greater levels of a unique DNIC signal.
72 (NBD = nitrobenzofurazan), was observed when DNIC 1 was dissolved in water at ambient temperature.

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