ライフサイエンスコーパス: glutaryl-CoA

1 stence of an alternative enzymatic source of glutaryl-CoA.

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

3 carboxylate of the physiological substrate, glutaryl-CoA.

4 naerobic reduction of the dehydrogenase with glutaryl-CoA.

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

6 harge of free C-carboxyl group of the primer glutaryl-CoA.

7 ation that can be nonenzymatically driven by glutaryl-CoA.

8 ven pimelate carbon atoms being derived from glutaryl-CoA, an intermediate in lysine degradation.

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

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

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

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

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

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

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

16 ation on the lysine oxidation pathway enzyme glutaryl-CoA dehydrogenase (GCDH) and show increased GCD

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

18 l-coenzyme A (crotonyl-CoA)-producing enzyme glutaryl-CoA dehydrogenase (GCDH) with downregulation of

19 nd to and stabilize the mitochondrial enzyme glutaryl-CoA dehydrogenase (GCDH), the computational sit

20 transferase (SUGCT) and become substrate for glutaryl-CoA dehydrogenase (GCDH), the enzyme that is de

21 anoma addiction to the mitochondrial protein glutaryl-CoA dehydrogenase (GCDH), which functions in ly

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

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

24 Glutaryl-CoA dehydrogenase also has intrinsic enoyl-CoA

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

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

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

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

29 2-Pentynoyl-CoA inactivates glutaryl-CoA dehydrogenase at a rate that considerably e

30 Glutaryl-CoA dehydrogenase catalyzes the oxidation and d

31 Glutaryl-CoA dehydrogenase catalyzes the oxidation of gl

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

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

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

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

36 Glutaryl-CoA dehydrogenase is also differentiated from o

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

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

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

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

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

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

43 DHTKD1, an enzyme upstream of the defective glutaryl-CoA dehydrogenase, has been investigated as a p

44 Here, we show that loss of DHTKD1 in glutaryl-CoA dehydrogenase-deficient HEK-293 cells leads

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 These glutaryl-CoA-derived metabolites are thought to originat

51 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase inhibitors or statins a

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

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

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

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

56 lysine/tryptophan oxidation pathway in which glutaryl-CoA is produced, in turn inhibiting GCDH functi

57 ates that BioZ catalyzes the condensation of glutaryl-CoA (or ACP) with malonyl-ACP to give 5'-keto-p

58 oduction and a significantly reduced rate of glutaryl-CoA production by dihydrolipoamide succinyl-tra

59 ) and show increased GCDH glutarylation when glutaryl-CoA production is stimulated by lysine cataboli

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

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

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

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

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

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

66 esterol synthesis enzymes 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR) and acetyl-coenzyme A cho

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

68 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors may operate through a

69 3-Hydroxy-3-methyl-glutaryl-CoA reductase inhibitors, endothelin receptor a

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

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

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

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

74 A1, may exacerbate disease by increasing the glutaryl-CoA substrate load in mitochondria.

75 re strains defective in CaiB which catalyzes glutaryl-CoA synthesis from glutarate and succinyl-CoA.

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

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

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

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

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

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

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