ライフサイエンスコーパス: S-nitrosohemoglobin

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1 ion in the respiratory cycle is dependent on S-nitrosohemoglobin.

2 nitric oxide (NO) to cysteinebeta93, forming S-nitrosohemoglobin.

3 iminates superoxide, increasing the yield of S-nitrosohemoglobin and nitrosylated hemes.

4 S-nitrosohemoglobin and plasma S-nitrosothiols did not c

5 he relative roles of adenosine triphosphate, S-nitrosohemoglobin, and nitrite as effectors.

6 terial vs. venous differences in nitrite and S-nitrosohemoglobin are diminished in sepsis and associa

7 Systemic nitrite and S-nitrosohemoglobin consumption can be assessed by compa

8 S-nitrosohemoglobin contracts blood vessels and decrease

9 terial vs. venous red blood cell nitrite and S-nitrosohemoglobin differences were absent.

10 groups is a rapidly reversible process, and S-nitrosohemoglobin formation is probably not a primary

11 No S-nitrosohemoglobin forms during these reactions.

12 s accompanied by an allosteric transition in S-nitrosohemoglobin [from the R (oxygenated) to the T (d

13 issue oxygenation and is proportional to RBC S-nitrosohemoglobin (HbSNO) content (but not nitrosylhem

14 of hypotheses concerning the role played by S-nitrosohemoglobin in vivo.

15 sting systemic nitrite consumption), whereas S-nitrosohemoglobin levels are higher in venous vs. arte

16 S-nitrosohemoglobin levels were in the nanomolar range,

17 ologic paradigms contend that nitrite and/or S-nitrosohemoglobin mediate intravascular delivery of ni

18 nous vs. arterial blood (suggesting systemic S-nitrosohemoglobin production).

19 d relaxations during hypoxia correlated with S-nitrosohemoglobin (SNO-Hb) (R2=0.88) but not iron nitr

20 In erythrocytes, S-nitrosohemoglobin (SNO-Hb) arises from S-nitrosylation

21 We report that S-nitrosohemoglobin (SNO-Hb) concentrations declined rap

22 O-liganded Hb could support the chemistry of S-nitrosohemoglobin (SNO-Hb) formation.

23 S-Nitrosohemoglobin (SNO-Hb) is a vasodilator whose acti

24 s results run counter to the hypothesis that S-nitrosohemoglobin (SNO-Hb) serves as an in vivo reserv

25 sial, with separate roles for nitrite () and S-nitrosohemoglobin (SNO-Hb) widely contested given thei

26 itrosation of cysteine beta93 in hemoglobin (S-nitrosohemoglobin (SNO-Hb)) occurs in vivo, and transn

27 , RBC-dependent vasoregulatory function, and S-nitrosohemoglobin (SNO-Hb), through which hemoglobin (

28 Banked blood shows reduced levels of S-nitrosohemoglobin (SNO-Hb), which in turn impairs the

29 the blood is bound to thiols of Hb, forming S-nitrosohemoglobin (SNO-Hb), which releases the NO grou

30 ally, for S-nitrosation of betaCys93 to form S-nitrosohemoglobin (SNO-Hb).

31 ol, yielding a deficiency in the vasodilator S-nitrosohemoglobin (SNO-Hb).

32 nitrite, LMW-SNOs and HMW-SNOs, and red cell S-nitrosohemoglobin (SNO-Hb).

33 ation, and in transfer of the NO moiety from S-nitrosohemoglobin (SNO-HbS) to the RBC membrane.

34 The mechanisms by which S-nitrosohemoglobin (SNOHb) stimulates vasodilation are

35 NO adducts were found in the RBCs, including S-nitrosohemoglobin (SNOHb).

36 the minority deoxyheme to subsequently form S-nitrosohemoglobin (SNOHb).

37 Maintenance of S-nitrosohemoglobin was associated with improvements in

38 In contrast, S-nitrosohemoglobin was higher in venous compared to art

39 ing nitric oxide bioactivity (in the form of S-nitrosohemoglobin) was markedly diminished 10 hours af

40 te S-nitrosothiol content (reflecting mainly S-nitrosohemoglobin) was significantly higher for blood

41 Nitrite and S-nitrosohemoglobin were measured using tri-iodide-based

42 93 cysteine S-nitrosylated hemoglobin [SNOHb:S-nitrosohemoglobin], which has been shown to induce vas

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