ライフサイエンスコーパス: glutaryl

1 Saccharopine dehydrogenase [N6-(glutaryl-2)-L-lysine:NAD oxidoreductase (L-lysine formin

2 hibit cleavage of the fluorogenic peptide, N-glutaryl-alanylalanylphenylalanyl-3-methoxynaphthylamide

3 Succinyl and 3'-substituted glutaryl betulin derivatives showed stronger anti-HIV ac

4 -Arg104, where XL represents the succinyl or glutaryl bridging span moiety.

5 creased short-chain dicarboxylacylcarnitines glutaryl carnitine, octenedioyl carnitine, and adipoyl c

6 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase inhibitors or statins a

7 ood disorder caused by defective activity of glutaryl CoA dehydrogenase (GCDH) which disturb lysine (

8 d by pretreatment with the 3-hydroxymethyl-3-glutaryl CoA reductase inhibitor pravastatin and was res

9 small interfering RNA and 3-hydroxy-3-methyl-glutaryl CoA reductase inhibitor simvastatin (statin) af

10 poptosis was induced using the hydroxymethyl glutaryl CoA reductase inhibitor, lovastatin, and was ev

11 onsive genes (LDL receptor and hydroxymethyl glutaryl CoA reductase) also showed evidence of altered

12 and CREB, to the promoter for hydroxymethyl glutaryl CoA reductase, another key gene of intracellula

13 lpha-glucosidase, lipase and hydroxyl methyl glutaryl CoA reductase.

14 correlated with elevated 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase activity and mRNA level

15 Three-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors (statins) re

16 wering drugs that inhibit 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase, the rate-limiting enzy

17 It is also possible that Arg-94 may orient glutaryl-CoA and 3-thiaglutaryl-CoA for abstraction of a

18 ting from abstraction of the alpha-proton of glutaryl-CoA and 3-thiaglutaryl-CoA, both of which conta

19 constants of glutaryl-CoA dehydrogenase with glutaryl-CoA and the alternative substrates, pentanoyl-C

20 Arg-94 does not make a major contribution to glutaryl-CoA binding.

21 Of nine known ACDs, glutaryl-CoA dehydrogenase (GCD) is unique: in addition

22 were already present at that time: ancestral glutaryl-CoA dehydrogenase (GCD), isovaleryl-CoA dehydro

23 an disease, glutaric aciduria type I (GA-1), glutaryl-CoA dehydrogenase (GCDH) deficiency disrupts th

24 id metabolism resulting from a deficiency of glutaryl-CoA dehydrogenase (GCDH).

25 We demonstrated glutaconyl-CoA bound to glutaryl-CoA dehydrogenase after anaerobic reduction of

26 Glutaryl-CoA dehydrogenase also has intrinsic enoyl-CoA

27 tion of a spectral species between wild type glutaryl-CoA dehydrogenase and a E370D mutant are consis

28 sm via beta-oxidation, a non-decarboxylating glutaryl-CoA dehydrogenase and a subsequent glutaconyl-C

29 tic pathway catalyzed by the E370D mutant of glutaryl-CoA dehydrogenase and compared them with those

30 Thus short-chain, medium-chain, and glutaryl-CoA dehydrogenase are rapidly inactivated by 2-

31 2-Pentynoyl-CoA inactivates glutaryl-CoA dehydrogenase at a rate that considerably e

32 Glutaryl-CoA dehydrogenase catalyzes the oxidation and d

33 Glutaryl-CoA dehydrogenase catalyzes the oxidation of gl

34 nsistent with the idea that this distance in glutaryl-CoA dehydrogenase contributes to the enhanced r

35 y diagnosis, one-third of Amish infants with glutaryl-CoA dehydrogenase deficiency (GA1) develop stri

36 Glu370Asp and Glu370Gln mutants of glutaryl-CoA dehydrogenase exhibit 7% and 0.04% residual

37 eening the conditions for crystallization of glutaryl-CoA dehydrogenase from Burkholderia pseudomalle

38 Glutaryl-CoA dehydrogenase is also differentiated from o

39 This distance for wild type glutaryl-CoA dehydrogenase is not known.

40 Glutaryl-CoA dehydrogenase is the only member of the acy

41 dehydrogenation reaction catalyzed by human glutaryl-CoA dehydrogenase was investigated using a seri

42 llowing decarboxylation of glutaconyl-CoA by glutaryl-CoA dehydrogenase was investigated.

43 The involvement of water in catalysis by glutaryl-CoA dehydrogenase was previously unrecognized a

44 parison of steady-state kinetic constants of glutaryl-CoA dehydrogenase with glutaryl-CoA and the alt

45 medium chain acyl-CoA dehydrogenase and the glutaryl-CoA dehydrogenase.

46 the active site in these binary complexes of glutaryl-CoA dehydrogenase.

47 f a proton at C-4, this is not the case with glutaryl-CoA dehydrogenase.

48 ylation of glutaryl-CoA that is catalyzed by glutaryl-CoA dehydrogenase.

49 ces (e.g., in short-chain, medium-chain, and glutaryl-CoA dehydrogenases) or on the G helix (long-cha

50 K(m) of these mutant dehydrogenases for glutaryl-CoA increases 10- to 16-fold.

51 d multiple members of the 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitor drug class (referred to

52 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors may operate through a

53 3-Hydroxy-3-methyl-glutaryl-CoA reductase inhibitors, endothelin receptor a

54 emonstrated in vivo using 3-hydroxy-3-methyl-glutaryl-CoA reductase siRNA as an active payload result

55 Simvastatin inhibited 3-hydroxy-3-methyl-glutaryl-CoA reductase, which in turn activated PI3K-kin

56 uggesting production in a 3-hydroxy-3-methyl-glutaryl-CoA reductase-dependent manner.

57 A, suggests that the gamma-carboxyl group of glutaryl-CoA stabilizes the enzyme-substrate complex by

58 rmediate in the oxidative decarboxylation of glutaryl-CoA that is catalyzed by glutaryl-CoA dehydroge

59 CoA dehydrogenase catalyzes the oxidation of glutaryl-CoA to crotonyl-CoA and CO(2) in the mitochondr

60 talyzes the oxidation and decarboxylation of glutaryl-CoA to crotonyl-CoA and CO(2).

61 o all ACDs, GCD catalyzes decarboxylation of glutaryl-CoA to produce CO(2) and crotonyl-CoA.

62 tial downstream metabolites pimeloyl-CoA and glutaryl-CoA was proved in cell free extracts, yielding

63 h a k(cat) that is less than 2% of that with glutaryl-CoA when ferrocenium hexafluorophosphate (FcPF(

64 e elevated, suggesting impaired formation of glutaryl-CoA.

65 carboxylate of the physiological substrate, glutaryl-CoA.

66 naerobic reduction of the dehydrogenase with glutaryl-CoA.

67 bonding distance of the gamma-carboxylate of glutaryl-CoA.

68 r activations, acute phase response pathway, glutaryl-CoA/tryptophan degradations and EIF2/AMPK/mTOR

69 nd sterol composition, hepatic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase activity, and lo

70 The 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors are w

71 vating protein (SCAP) and 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase.

72 The structure of the human glutaryl coenzyme A dehydrogenase (GCD) gene was determi

73 re powerful inhibitors of 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMG-CoA reductase), the k

74 pyrophosphate through the 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (Hmgcr) pathway is critica

75 ction by interfering with 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMGR) activity, a key pla

76 we report the ability of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitor (statin), which

77 us, we tested the effects of 3 hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins), simv

78 3-hydroxy-3-methyl glutaryl coenzyme A reductase inhibitors have been repor

79 competitive inhibitor of 3-hydroxy-2-methyl-glutaryl coenzyme A reductase.

80 competitive inhibitor of 3-hydroxy-2-methyl-glutaryl coenzyme A reductase.

81 We demonstrate that the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors atorv

82 Hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors or st

83 In glutaric aciduria type 1, glutaryl-coenzyme A and its derivatives are produced fro

84 l as the transcription of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase and acyl-coenzyme A:choles

85 Hydroxymethyl glutaryl-coenzyme A reductase degradation protein 1 (Hrd

86 time after transplantation, 3-hydroxy-methyl-glutaryl-coenzyme A reductase inhibitor use and prior cy

87 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors (statins) exhib

88 e immunomodulatory effects of hydroxy methyl glutaryl-coenzyme A reductase inhibitors have been incre

89 Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors have been shown

90 he intermediate following 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase) but upstream of cholester

91 ns for the development of anti-hydroxymethyl glutaryl-coenzyme A reductase-positive statin-induced my

92 nomuconate to 2-ketoadipate and, ultimately, glutaryl-coenzyme A.

93 For various 3'-substituted glutaryl compounds, the order of anti-HIV effects, from

94 -3'-methyl, followed by 3',3'-tetramethylene glutaryl derivatives (10 > 9 > 11 > 12, 18 > 17 > 19 > 2

95 With 3',3'-tetramethylene glutaryl derivatives, triacyl 29 showed stronger inhibit

96 idosides, rutinosides and 3-hydroxy-3-methyl glutaryl derivatives.

97 cytotoxic peptide conjugates containing 14-O-glutaryl esters of doxorubicin (DOX) or 2-pyrrolino-DOX

98 ed to single and multiple 3-hydroxy-3-methyl-glutaryl (HMG) substitutions.

99 d increased expression of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase (Hmg1) under iron starvatio

100 Inhibitors of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase (the statins) reduce levels

101 vastatin, an inhibitor of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase and the N-bisphosphonate zo

102 Lovastatin is an inhibitor of hydroxymethyl glutaryl (HMG)-CoA reductase, the rate-limiting enzyme i

103 From these studies we selected Glutaryl-Hyp-Ala-Ser-Chg-Gln-Ser-Leu-Dox, 27, as the pep

104 nordihydroguaiaretic acid (NDGA), catechol, glutaryl probucol, and N-acetylcysteine increased eNOS e

105 phosphocholine (m/z 594.3) and 1-palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine (m/z 610.2).

106 n-glycero-3-phosphocholine and 1-palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine inhibited TLR2 sign