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 Mechanistically, we find ABHD11 removes glutaryl adducts from lipoate-an essential fatty acid mo

3 N-glutarylspermidines can be derived from O-glutaryl-ADP-ribose.

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

5 Using succinyl, glutaryl and adipoyl phosphonates on the enzyme preparat

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

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

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

9 es of pyridine are joined with a molecule of glutaryl chloride to give the complete tetracyclic frame

10 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase inhibitors or statins a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 Glutaryl-CoA dehydrogenase also has intrinsic enoyl-CoA

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

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

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

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

41 2-Pentynoyl-CoA inactivates glutaryl-CoA dehydrogenase at a rate that considerably e

42 Glutaryl-CoA dehydrogenase catalyzes the oxidation and d

43 Glutaryl-CoA dehydrogenase catalyzes the oxidation of gl

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

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

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

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

48 Glutaryl-CoA dehydrogenase is also differentiated from o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 These glutaryl-CoA-derived metabolites are thought to originat

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

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

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

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

88 carboxylate of the physiological substrate, glutaryl-CoA.

89 naerobic reduction of the dehydrogenase with glutaryl-CoA.

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

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

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

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

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

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

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

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

98 terol biosynthesis called 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMGCR).

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

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

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

102 3-hydroxy-3-methyl glutaryl coenzyme A reductase inhibitors have been repor

103 SREBP2 and expression of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase, boosting intracellular ch

104 sis rate-limiting step enzyme, hydroxymethyl glutaryl coenzyme A reductase, show immunomodulatory act

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

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

107 of patients under regular 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor (stati

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

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

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

111 ogical phenotype caused by the deficiency of glutaryl-coenzyme A dehydrogenase (GCDH), the last enzym

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

113 rved suppressor of lin-12-like-hydroxymethyl glutaryl-coenzyme A reductase degradation 1 (SEL1L-HRD1)

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

115 diology (AHA/ACC) changed 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitor (statin) eligibi

116 guideline indications for 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitor (statin) therapy

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

118 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors (statins) exhib

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

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

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

122 k reversible inhibitor of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase, whose daily consumption c

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

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

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

126 DC(11) is chain-shortened in peroxisomes to glutaryl (DC(5))-CoA, which then gives rise to the GA1-l

127 -3'-methyl, followed by 3',3'-tetramethylene glutaryl derivatives (10 > 9 > 11 > 12, 18 > 17 > 19 > 2

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

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

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

131 es negatively charged malonyl, succinyl, and glutaryl groups from lysine residues and thereby regulat

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

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

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

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

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

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

138 oss of ABHD11 results in the accumulation of glutaryl-lipoyl adducts that drive an adaptive program,

139 oduced, in turn inhibiting GCDH function via glutaryl modification of GCDH lysine residues and can be

140 tes, but our understanding of these distinct glutaryl modifications is in its infancy.

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

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

143 mbranes of the oxidized lipid, 1-palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine (PGPC), and each of

144 rimary oxidation product being 1-palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine (PGPC).

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

146 iaminoethane motif in the ascending order of glutaryl-triethylene tetramine, succinyl-tetraethylene p