ライフサイエンスコーパス: sepiapterin

1 medium with a source of tetrahydrobiopterin (sepiapterin).

2 l(-1)) or the precursor for BH(4) synthesis sepiapterin (1 micromol l(-1)).

3 During incubation with sepiapterin (1 mumol/L) or MH4 (10 mumol/L), endothelium

4 , 3.1 x 10(5); isoxanthopterin, 2.8 x 10(5); sepiapterin, 1.3 x 10(5); folate, 1.3 x 10(5), xanthopte

5 absence of a tetrahydrobiopterin precursor, sepiapterin (10(-4) mol/L), and/or superoxide dismutase

6 Sepiapterin (2 mg/kg, stable tetrahydrobiopterin precurs

7 The addition of 100 microM sepiapterin (a BH4 precursor) or overexpression of GTP c

8 and proapoptotic effects were exacerbated by sepiapterin, a precursor of tetrahydrobiopterin, an esse

9 r liposome-entrapped superoxide dismutase or sepiapterin, a precursor to tetrahydrobiopterin, improve

10 Finally, we demonstrate that sepiapterin accumulation is a sensitive biomarker for SP

11 Sepiapterin also restored coronary FMD in DM patients.

12 hydrobiopterin, 7,8-dihydroxanthopterin, and sepiapterin, also prevent nitration of tyrosines caused

13 Sepiapterin and BH4 also enhanced the proliferation of S

14 Sepiapterin and MH4 did not affect vasodilatory response

15 data indicate that SPR-mediated reduction of sepiapterin and redox cycling occur by distinct mechanis

16 studied after incubation with L-arginine, L-sepiapterin, and liposome-entrapped superoxide dismutase

17 neurobehavioral tests following vehicle and sepiapterin (BH(4) analog) treatment of dams.

18 by medium supplementation with l-arginine or sepiapterin, but inhibition decreased with time of addit

19 tly or of its precursors dihydrobiopterin or sepiapterin, completely prevented the inhibition of NO-i

20 ffects were mediated by BH4 as inhibition of sepiapterin conversion to BH4 by a sepiapterin reductase

21 rast, BH(4) analogs 7,8-dihydrobiopterin and sepiapterin do not affect superoxide yields.

22 These sepiapterin effects were mediated by BH4 as inhibition o

23 trols (234 +/- 21 fmol (mg tissue)(-1)), and sepiapterin elevated flow-mediated vasodilatation in art

24 ere incubated with superoxide dismutase plus sepiapterin, endothelium-dependent relaxations to A23187

25 g chemicals inhibited sepiapterin reduction, sepiapterin had no effect on redox cycling.

26 pplementation prior to hypoxia-ischemia with sepiapterin increased BH(4) in all brain regions and esp

27 er control conditions, after incubation with sepiapterin (intracellularly converted to BH4) or synthe

28 Treatment of vessels with L-arginine, L-sepiapterin, liposome-entrapped SOD, or cis-vaccenic aci

29 Incubation with sepiapterin markedly increased intracellular tetrahydrob

30 inistration of MG132 or supplementation of l-sepiapterin normalized the impaired endothelium-dependen

31 tase (SOD), l-nitroarginine methyl ester, or sepiapterin not only reversed the effects of high glucos

32 ta indicate that exogenous administration of sepiapterin or MH4 restores the response to endothelium-

33 ation, which was restored in the presence of sepiapterin or MH4.

34 reatment with L-NIO (NO synthase inhibitor), sepiapterin (precursor of tetrahydrobiopterin), MitoTEMP

35 Sepiapterin reductase (SPR) catalyzes the last step in t

36 m of action, has recently been shown to be a sepiapterin reductase (SPR) inhibitor.

37 g activity in mouse lung epithelial cells as sepiapterin reductase (SPR), an enzyme important for the

38 at xanthurenic acid is a potent inhibitor of sepiapterin reductase (SPR), the final enzyme in de novo

39 o minimize risk of side effects, we targeted sepiapterin reductase (SPR), whose blockade allows minim

40 One candidate gene at this locus is sepiapterin reductase (SPR).

41 mes 6-pyruvoyl-tetrahydropterin synthase and sepiapterin reductase and decreased protein levels of th

42 Sepiapterin reductase catalyzes the final step in the bi

43 Sepiapterin reductase deficiency (SRD) is an under-recog

44 bition of sepiapterin conversion to BH4 by a sepiapterin reductase inhibitor, N-acetyl-serotonin, blo

45 in the tetrahydrobiopterin pathway involving sepiapterin reductase, and no abnormality in the gene en

46 or IFN-gamma did not affect the activity of sepiapterin reductase, the final enzyme in BH4 biosynthe

47 d by 6-pyruvoyltetrahydropterin synthase and sepiapterin reductase.

48 te-binding site (D257H) completely inhibited sepiapterin reduction but had minimal effects on redox c

49 henylquinone, were competitive inhibitors of sepiapterin reduction but noncompetitive redox cycling i

50 This activity, together with inhibition of sepiapterin reduction by redox-active chemicals and cons

51 Whereas redox cycling chemicals inhibited sepiapterin reduction, sepiapterin had no effect on redo

52 N-acetylserotonin, and indomethacin blocked sepiapterin reduction, with no effect on redox cycling.

53 c neurons, and addition of the BH4 precursor sepiapterin rescued catecholamine production in neurons

54 trahydrobiopterin (BH4) or the BH4 precursor sepiapterin resulted in a significant decrease in serum

55 Sepiapterin (Sep) also increased GTP-bound wild-type Ras

56 Sepiapterin (SEP) is a tetrahydrobiopterin precursor, an

57 In addition to reducing sepiapterin, SPR mediated chemical redox cycling of bipy

58 abolished coronary FMD, which was rescued by sepiapterin, the stable precursor of NO synthase (NOS) c

59 E. coli QueD can also convert PPH(4) and sepiapterin to CPH(4), allowing a mechanism to be propos

60 trations >10 microm or in PAECs treated with sepiapterin to increase intracellular BH(4).

61 Pretreatment of cells with sepiapterin to promote BH(4) biosynthesis or cell-permea

62 In sepiapterin-treated arteries, endothelium-dependent rela

63 Sepiapterin treatment also reduced incidence of severe m

64 Incubation with sepiapterin, which is converted enzymatically to BH4 wit