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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 specific effect is through the inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase.
4 ontrol point in cholesterol synthesis beyond 3-hydroxy-3-methylglutaryl-CoA reductase.
5 yme regulating the mevalonate (MVA) pathway, 3-Hydroxy-3-Methylglutaryl CoA Reductase 1 (HMGR1), inte
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 cholesterol are associated with decreases in 3-hydroxy-3-methylglutaryl-CoA reductase and increases i
10 is (3-hydroxy-3-methylglutaryl CoA synthase, 3-hydroxy-3-methylglutaryl CoA reductase), and fatty aci
11 imvastatin and pravastatin are inhibitors of 3-hydroxy-3-methylglutaryl CoA reductase, and are used a
12 e synthase, farnesyl-pyrophosphate synthase, 3-hydroxy-3-methylglutaryl-CoA reductase, and low densit
13 er, leptin treatment reduced the activity of 3-hydroxy-3-methylglutaryl-CoA reductase, but it did not
14 endoplasmic reticulum (ER)-localized enzyme 3-hydroxy-3-methylglutaryl CoA reductase catalyzes a rat
16 y mevalonic acid, a downstream metabolite of 3-hydroxy-3-methylglutaryl CoA reductase, confirming tha
17 th SREBP-1 and -2 increased on promoters for 3-hydroxy-3-methylglutaryl-CoA reductase, fatty-acid syn
19 rols accelerate degradation of the ER enzyme 3-hydroxy-3-methylglutaryl CoA reductase (HMG CoA reduct
20 on of the cholesterol synthesis pathway with 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reduct
21 rol-sensing domains in three other proteins: 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reduct
26 owever, the normal yeast ER membrane protein 3-hydroxy-3-methylglutaryl-CoA reductase (Hmg2p) undergo
28 atoma cell lines, SUGP1 knockdown stimulated 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) alterna
29 nti-signal recognition protein (SRP) or anti-3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) antibod
30 lone and in combination with variants in the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) gene.
31 iological studies report that utilization of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) inhibit
33 se in risk is a consequence of inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the in
36 cascade appears to control the expression of 3-hydroxy-3-methylglutaryl CoA reductase (HMGR) and l-ph
40 doplasmic reticulum (ER) and the activity of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) imbedded
41 with compromised proteasomal degradation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) or defic
45 We hypothesized that statins, inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase, inhibit cardia
46 organ cultured for 7 days with lovastatin, a 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, deve
47 n in an MMP-dependent manner and whether the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor atorv
48 e investigated the effects of simvastatin, a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, on h
49 Inhibition of isoprenoid synthesis with the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, simv
51 , (cyclooxygenase-2 inhibitor), and statins (3-hydroxy-3-methylglutaryl CoA reductase inhibitors) inh
53 ter overnight (or longer) treatment with the 3-hydroxy-3-methylglutaryl CoA reductase inhibitors, the
54 ation of Pyk2 in response to Ang II by using 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors and
55 nthesis and suggest a novel direct effect of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors on t
58 ng drugs that selectively inhibit the enzyme 3-hydroxy-3-methylglutaryl CoA reductase, leading to dec
59 syl transferase (squalene synthase), but not 3-hydroxy-3-methylglutaryl-CoA reductase or farnesyl dip
62 ticulum-associated degradation of the enzyme 3-hydroxy-3-methylglutaryl-CoA reductase represents one
64 ins includes pharmacologic inhibitors of the 3-hydroxy-3-methylglutaryl-CoA reductase that are potent
66 ins; and the cholesterol biosynthetic enzyme 3-hydroxy-3-methylglutaryl CoA reductase, thus inducing
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