ライフサイエンスコーパス: glutaryl-CoA

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

2 carboxylate of the physiological substrate, glutaryl-CoA.

3 naerobic reduction of the dehydrogenase with glutaryl-CoA.

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

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

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

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

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

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

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

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

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

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

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

15 Glutaryl-CoA dehydrogenase also has intrinsic enoyl-CoA

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

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

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

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

20 2-Pentynoyl-CoA inactivates glutaryl-CoA dehydrogenase at a rate that considerably e

21 Glutaryl-CoA dehydrogenase catalyzes the oxidation and d

22 Glutaryl-CoA dehydrogenase catalyzes the oxidation of gl

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

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

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

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

27 Glutaryl-CoA dehydrogenase is also differentiated from o

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

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

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

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

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

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

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

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

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

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

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

39 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase inhibitors or statins a

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

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

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

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

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

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

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

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

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

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

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

51 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors may operate through a

52 3-Hydroxy-3-methyl-glutaryl-CoA reductase inhibitors, endothelin receptor a

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

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

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

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

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

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

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

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

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

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(