ライフサイエンスコーパス: DNIC

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 en process), the hs-Fe(II)/{Fe(NO)(2)}(9/10) DNICs obtained from 2-X show unexpected reactivity and p

7 pecies, a new type of neutral {Fe(NO)(2)}(9) DNIC was prepared containing a beta-diketiminate ligand.

8 f O(2(g)) and one-electron-reduced DNIC 1, a DNIC featuring an electronically localized {Fe(NO)(2)}(9

9 ent a rare example of structurally analogous DNIC redox partners.

10 dicate that GST P1-1 acts to sequester NO as DNICs, reducing their transport out of the cell by MRP1.

11 ck and forward translational studies between DNIC and CPM, gauged between bench and bedside, are key

12 ransferase P1-1 (GST P1-1) was shown to bind DNICs as dinitrosyl-diglutathionyl iron complexes.

13 Both DNIC and RSNO are also increased during overproduction o

14 While the IlvD-bound DNIC and other protein-bound DNICs are stable in cells u

15 at a large number of different protein-bound DNICs are formed by NO.

16 the IlvD-bound DNIC and other protein-bound DNICs are stable in cells under anaerobic growth conditi

17 protein post-translational modifications by DNICs.

18 EPR-active, neutral dinitrosyliron complex (DNIC) (IMes)Fe(SPh)(NO)(2) (3, {Fe(NO)(2)}(9)).

19 iron atom forming a dinitrosyliron complex (DNIC) and preventing cosubstrates from binding.

20 -bound {Fe(NO)2}(9) dinitrosyl iron complex (DNIC) [(HS)2Fe(NO)2](-) (1) into [(NO)2Fe(mu-S)]2(2-) (R

21 coupling of NO in a dinitrosyl iron complex (DNIC) induced by hydrogen bond donors in the secondary c

22 n of the IlvD-bound dinitrosyl iron complex (DNIC).

23 the appearance of dinitrosyliron complexes (DNIC) are key determinants.

24 the iron for these dinitrosyliron complexes (DNIC), and its relationship to cellular iron homeostasis

25 ion of thiols with dinitrosyliron complexes (DNIC), which are formed in cells from the reaction of *N

26 Dinitrosyliron complexes (DNICs) are organometallic-like compounds of biological s

27 of {Fe(NO)(2)}(9) dinitrosyliron complexes (DNICs).

28 onic {Fe(NO)2}(9) dinitrosyl iron complexes (DNICs) [((R)DDB)Fe(NO)2](+) (R = Me, Et, Iso; (R)DDB = N

29 ers NO as dinitrosyl-dithiol iron complexes (DNICs) and inhibits NO-mediated iron release from cells

30 nitrosothiols and dinitrosyl iron complexes (DNICs) can serve as an alternative vehicle for NO storag

31 the formation of dinitrosyl iron complexes (DNICs) now viewed as playing important roles in the mamm

32 ght/protein-bound dinitrosyl iron complexes (DNICs) was discovered as a metallocofactor assembled und

33 ways produced the dinitrosyl iron complexes (DNICs), [Fe(E(5))(NO)(2)](1-) (E = S, Se), and binuclear

34 ionate by forming dinitrosyl iron complexes (DNICs), but the mechanism of this reaction is not unders

35 and formation of dinitrosyl iron complexes (DNICs).

36 uster to generate dinitrosyl iron complexes (DNICs).

37 {Fe(NO)(2)}(9/10) dinitrosyl iron complexes (DNICs).

38 is a hallmark of dinitrosyl iron complexes, DNIC's.

39 Under our conditions, DNIC formation, like RSNO formation, is inhibited by app

40 icacy of diffuse noxious inhibitory control (DNIC) endogenous pain control pathways and lumber norepi

41 menon of diffuse noxious inhibitory control (DNIC).

42 respect diffuse noxious inhibitory controls (DNIC) are a unique form of endogenous descending inhibit

43 induced diffuse noxious inhibitory controls (DNICs).

44 Cys-DNIC and Cys-RSE interconvert, and the rates of this pro

45 The mononuclear DNIC Fe(NO)2(CysS)2(-) (Cys-DNIC) is produced from the same three components at pH 1

46 cs studies suggest that both Cys-RSE and Cys-DNIC are formed via a common intermediate Fe(NO)(CysS)2(

47 otolysis of the mononuclear-DNIC species Cys-DNIC formed from Fe(II)/NO/cysteine mixtures in anaerobi

48 the supporting/bridging ligands in dinuclear DNIC 1/3 (or 1-red/3-red) control the selective monooxyg

49 The dinuclear DNIC Fe2(mu-CysS)2(NO)4, a Roussin's red salt ester (Cys

50 on of GST P1-1 and ability of MRP1 to efflux DNICs are vital in protection against NO cytotoxicity.

51 4 equiv of (Et4N)(SPh) to yield the expected DNIC.

52 Gstp1, suggesting GSTP1 was responsible for DNIC binding/storage.

53 SIH added during the *NO treatment "freezes" DNIC levels, showing that the complexes are formed from

54 rmed from free *NO via transnitrosation from DNIC derived from the CIP.

55 e transformation of RRS into DNIC 1 (RRS --> DNIC 1) in the presence of H2S was demonstrated.

56 Furthermore, Mrp1 silencing increased DNIC accumulation in macrophages, indicating a role for

57 superoxide-induced conversion of DNIC 1 into DNIC [(K-18-crown-6-ether)(2)(NO(2))][Fe(mu-(Me)Pyr)(4)(

58 ne shows quantitative conversion of CIP into DNIC by *NO.

59 The reversible transformation of RRS into DNIC 1 (RRS --> DNIC 1) in the presence of H2S was demon

60 nverted to paramagnetic large molecular mass DNIC from exposure to free *NO but not from cellular nit

61 In naive mice, DNIC was mediated through alpha2 adrenoceptors, but sens

62 The mononuclear DNIC Fe(NO)2(CysS)2(-) (Cys-DNIC) is produced from the s

63 that dinuclear RRE species, not mononuclear DNICs, may be the primary iron dinitrosyl species respon

64 ed ester (RRE) formula, and that mononuclear DNICs account for only a minor fraction of nitrosylated

65 Even though mononuclear DNICs are stable and do not show N-N coupling (since it

66 In contrast, photolysis of the mononuclear-DNIC species Cys-DNIC formed from Fe(II)/NO/cysteine mix

67 ergic primary afferents in the activation of DNIC by noxious heat and mechanical stimulations, substa

68 DNIC 1-red leads to the similar assembly of DNIC 2-K-crown, of which the electronic structure is bes

69 During the superoxide-induced conversion of DNIC 1 into DNIC [(K-18-crown-6-ether)(2)(NO(2))][Fe(mu-

70 modulation (CPM) is the human counterpart of DNIC and requires a descending control also.

71 eceptors, influences the final expression of DNIC also.

72 injection of ondansetron showed that loss of DNIC was not due to excess serotonergic signaling throug

73 Oxygenation of DNIC 1-red leads to the similar assembly of DNIC 2-K-cro

74 N-O stretching band vanishes, but no sign of DNIC or N(2) O formation is observed.

75 In some cases the formation of DNICs from such cluster systems can lead to activation o

76 the reactivity toward O(2)(-) by a series of DNICs [(NO)(2)Fe(mu-(Me)Pyr)(2)Fe(NO)(2)] (1) and [(NO)(

77 ordinately regulate storage and transport of DNICs as long lived NO intermediates.

78 charge (Zeff) of the iron center and prevent DNIC 1 from dimerization in an organic solvent (MeCN).

79 SIH pretreatment prevents DNIC formation from *NO, and SIH added during the *NO tr

80 In contrast to DNICs 1 and 1-red, DNICs 3 and [K-18-crown-6-ether][(NO)(2)Fe(mu-SEt)(2)Fe(

81 reaction of O(2(g)) and one-electron-reduced DNIC 1, a DNIC featuring an electronically localized {Fe

82 CH2)2-o-C6H4) cleanly affords the respective DNIC, [Fe(NO)2(SR)2](-), with concomitant reductive elim

83 after TBI, and reboxetine failed to restore DNIC in these mice.

84 bitor escitalopram both effectively restored DNIC after TBI in both male and female mice.

85 use of an N-heterocyclic carbene-stabilized DNIC, (NHC)(RS)Fe(NO)2, we have explored the DNIC-promot

86 ce of thiolate-to-iron ratios in stabilizing DNICs.

87 pinal pharmacology of pathways that subserve DNIC are complicated; in the normal situation these desc

88 We observed that DNIC is strongly reduced in both male and female mice af

89 Here we report the first evidence that DNICs also form in the reaction of NO with Rieske-type [

90 pinal MOPR and DOPR similarly attenuates the DNIC and neurokinin type 1 receptor internalization indu

91 DNIC, (NHC)(RS)Fe(NO)2, we have explored the DNIC-promoted RS(-)/RS* oxidation in the presence of add

92 icated reaction dynamics interconnecting the DNIC species and offer a mechanistic model for the key s

93 Thus, the DNIC storage function of GST P1-1 and ability of MRP1 to

94 Isolation and characterization of these DNICs, including the new compound, (Et(4)N)[(N(2)CHPh)Fe

95 In contrast to DNICs 1 and 1-red, DNICs 3 and [K-18-crown-6-ether][(NO)

96 lfide redox processes, which when coupled to DNICs may lead to intricate redox processes involving ir

97 , indicating a role for MRP1 in transporting DNICs out of cells.

98 ain significantly greater levels of a unique DNIC signal.

99 (NBD = nitrobenzofurazan), was observed when DNIC 1 was dissolved in water at ambient temperature.