ライフサイエンスコーパス: 3-hydroxy-3-methylglutaryl-CoA reductase

1 ation of the cholesterol biosynthetic enzyme 3-hydroxy-3-methylglutaryl CoA reductase.

2 ccelerating sterol-stimulated degradation of 3-hydroxy-3-methylglutaryl CoA reductase.

3 ontrol point in cholesterol synthesis beyond 3-hydroxy-3-methylglutaryl-CoA reductase.

4 specific effect is through the inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase.

5 yme regulating the mevalonate (MVA) pathway, 3-Hydroxy-3-Methylglutaryl CoA Reductase 1 (HMGR1), inte

6 Dietary cholesterol suppressed hepatic 3-hydroxy-3-methylglutaryl CoA reductase activity, stimu

7 her reduced by 84% with empagliflozin, while 3-hydroxy-3-methylglutaryl-CoA reductase activity and to

8 ound ( approximately 20-fold) decrease in ER 3-hydroxy-3-methylglutaryl-CoA reductase activity in vit

9 as focused on the two rate-limiting enzymes: 3-hydroxy-3-methylglutaryl CoA reductase and squalene mo

10 cholesterol are associated with decreases in 3-hydroxy-3-methylglutaryl-CoA reductase and increases i

11 Both 3-Hydroxy-3-Methylglutaryl-CoA Reductase and Proprotein

12 is (3-hydroxy-3-methylglutaryl CoA synthase, 3-hydroxy-3-methylglutaryl CoA reductase), and fatty aci

13 imvastatin and pravastatin are inhibitors of 3-hydroxy-3-methylglutaryl CoA reductase, and are used a

14 e synthase, farnesyl-pyrophosphate synthase, 3-hydroxy-3-methylglutaryl-CoA reductase, and low densit

15 er, leptin treatment reduced the activity of 3-hydroxy-3-methylglutaryl-CoA reductase, but it did not

16 endoplasmic reticulum (ER)-localized enzyme 3-hydroxy-3-methylglutaryl CoA reductase catalyzes a rat

17 The endoplasmic reticulum (ER) enzyme, 3-hydroxy-3-methylglutaryl-CoA reductase, catalyzes the

18 with TCDD in the presence of simvastatin, a 3-Hydroxy-3-Methylglutaryl-CoA Reductase competitive inh

19 y mevalonic acid, a downstream metabolite of 3-hydroxy-3-methylglutaryl CoA reductase, confirming tha

20 th SREBP-1 and -2 increased on promoters for 3-hydroxy-3-methylglutaryl-CoA reductase, fatty-acid syn

21 f the sterol regulatory element (SRE) of the 3-hydroxy-3-methylglutaryl-CoA reductase gene.

22 Septic Shock Trial trial, we found that the 3-Hydroxy-3-Methylglutaryl-CoA Reductase genetic score,

23 rols accelerate degradation of the ER enzyme 3-hydroxy-3-methylglutaryl CoA reductase (HMG CoA reduct

24 on of the cholesterol synthesis pathway with 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reduct

25 rol-sensing domains in three other proteins: 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reduct

26 The degradation rate of 3-hydroxy-3-methylglutaryl CoA reductase (HMG-R), a key

27 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-R), a key

28 gulated endoplasmic reticulum degradation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-R).

29 MAD3 encodes 3-hydroxy-3-methylglutaryl CoA reductase (HMG1), which f

30 owever, the normal yeast ER membrane protein 3-hydroxy-3-methylglutaryl-CoA reductase (Hmg2p) undergo

31 es, including fatty acid synthase (FASN) and 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR).

32 Genetically proxied inhibition of 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR, targete

33 atoma cell lines, SUGP1 knockdown stimulated 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) alterna

34 egulation increases the protein abundance of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and ATP

35 s harboring deleterious mutations, including 3-Hydroxy-3-Methylglutaryl-CoA Reductase (HMGCR) and Uro

36 nti-signal recognition protein (SRP) or anti-3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) antibod

37 lone and in combination with variants in the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) gene.

38 iological studies report that utilization of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) inhibit

39 3-Hydroxy-3-methylglutaryl-CoA reductase (HMGCR) is the

40 ulatory element-binding protein 1 (Srebp1c), 3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr), and cy

41 The mRNA and expression levels of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), apolip

42 se in risk is a consequence of inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the in

43 he osmotic resistance, and the expression of 3-Hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the ra

44 latory element binding factor 2 (Srebf2) and 3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr).

45 The enzymes 3-hydroxy-3-methylglutaryl CoA reductase (HMGR) and C24-

46 cascade appears to control the expression of 3-hydroxy-3-methylglutaryl CoA reductase (HMGR) and l-ph

47 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) catalyze

48 The enzyme 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) catalyze

49 The 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) enzyme c

50 doplasmic reticulum (ER) and the activity of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) imbedded

51 with compromised proteasomal degradation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) or defic

52 Hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) protein

53 t, through feedback-regulated degradation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR).

54 biosynthesis of isoprenoids is catalysed by 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR).

55 We hypothesized that statins, inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase, inhibit cardia

56 organ cultured for 7 days with lovastatin, a 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, deve

57 n in an MMP-dependent manner and whether the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor atorv

58 e investigated the effects of simvastatin, a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, on h

59 Inhibition of isoprenoid synthesis with the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, simv

60 Furthermore, we show that the 3-hydroxy-3-methylglutaryl-CoA-reductase inhibitor mevas

61 , (cyclooxygenase-2 inhibitor), and statins (3-hydroxy-3-methylglutaryl CoA reductase inhibitors) inh

62 The statins, 3-hydroxy-3-methylglutaryl CoA reductase inhibitors, hav

63 ter overnight (or longer) treatment with the 3-hydroxy-3-methylglutaryl CoA reductase inhibitors, the

64 ation of Pyk2 in response to Ang II by using 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors and

65 nthesis and suggest a novel direct effect of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors on t

66 The use of statins, 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors that

67 In addition, our results indicate that 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, a c

68 ng drugs that selectively inhibit the enzyme 3-hydroxy-3-methylglutaryl CoA reductase, leading to dec

69 syl transferase (squalene synthase), but not 3-hydroxy-3-methylglutaryl-CoA reductase or farnesyl dip

70 The endoplasmic reticulum enzyme 3-hydroxy-3-methylglutaryl-CoA reductase produces mevalo

71 mmediate metabolic product of the acetyl CoA/3-hydroxy-3-methylglutaryl CoA reductase reaction.

72 ticulum-associated degradation of the enzyme 3-hydroxy-3-methylglutaryl-CoA reductase represents one

73 tein Convertase Subtilisin/Kexin type 9, and 3-Hydroxy-3-Methylglutaryl-CoA Reductase single nucleoti

74 Inhibitors of 3-hydroxy-3-methylglutaryl CoA reductase (statins) reduc

75 ins includes pharmacologic inhibitors of the 3-hydroxy-3-methylglutaryl-CoA reductase that are potent

76 Inhibition of 3-hydroxy-3-methylglutaryl CoA reductase, the rate-limit

77 ins; and the cholesterol biosynthetic enzyme 3-hydroxy-3-methylglutaryl CoA reductase, thus inducing