ライフサイエンスコーパス: sepiapterin

1 medium with a source of tetrahydrobiopterin (sepiapterin).

2 sment of blood Phe concentration response to sepiapterin.

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

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

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

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

7 Sepiapterin (2 mg/kg, stable tetrahydrobiopterin precurs

8 of blood Phe concentration after 6 weeks of sepiapterin (-63%, SD 20) compared with placebo (1%, 29;

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

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

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

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

13 Interestingly, sepiapterin also increased inflammatory cytokine levels

14 Sepiapterin also restored coronary FMD in DM patients.

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

16 in 33 (59%) of 56 participants who received sepiapterin and 18 (33%) of 54 participants who received

17 Sepiapterin and BH4 also enhanced the proliferation of S

18 Sepiapterin and MH4 did not affect vasodilatory response

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

20 ts (11 [20%] of 56 participants who received sepiapterin and ten [19%] of 54 participants who receive

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

22 were treated with the stable BH(4) precursor sepiapterin at the onset of hypoxia and their retinas as

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

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

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

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

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

28 These sepiapterin effects were mediated by BH4 as inhibition o

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

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

31 ermuted block size of 2 and 4) to 6 weeks of sepiapterin (forced-dose escalation: 20, 40, and 60 mg/k

32 pants (49 in the placebo group and 49 in the sepiapterin group) were in the primary analysis set.

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

34 BH(4) supplementation by sepiapterin improved both redox state and neuronal survi

35 and safety of orally administered synthetic sepiapterin in children and adults with phenylketonuria.

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

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

38 Sepiapterin is a promising oral therapy for individuals

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

40 Incubation with sepiapterin markedly increased intracellular tetrahydrob

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

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

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

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

45 levant interactions and binding modes in the sepiapterin pocket.

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

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

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

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

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

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

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

53 y regions near genes associated with pterin [sepiapterin reductase (SPR)] and carotenoid [beta-carote

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

55 in chronic low back pain patients identified sepiapterin reductase as a high interest target for deve

56 Sepiapterin reductase catalyzes the final step in the bi

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

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

59 enzymes, such as soluble epoxide hydrolase, sepiapterin reductase, and MAGL/FAAH, have also been tar

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

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

62 d by 6-pyruvoyltetrahydropterin synthase and sepiapterin reductase.

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

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

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

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

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

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

69 ssessed or evaluated, of whom 114 (73%) were sepiapterin-responsive (ie, >=15% reduction in blood Phe

70 In part 2, sepiapterin-responsive participants were randomly assign

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

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

73 Sepiapterin (SEP) is a tetrahydrobiopterin precursor, an

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

75 lysis confirmed elevated BH(4) levels in all sepiapterin supplemented groups and increased NOS activi

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

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

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

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

80 In sepiapterin-treated arteries, endothelium-dependent rela

81 Sepiapterin treatment also reduced incidence of severe m

82 Sepiapterin treatment caused a significant decrease in n

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