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1 n of catalytically active Haloferax volcanii 3-hydroxy-3-methylglutaryl coenzyme A (CoA) synthase (EC
4 increased levels of the ER membrane protein 3-hydroxy 3-methylglutaryl coenzyme A (HMG-CoA) reductas
5 ascularized patients derive benefit from the 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductas
6 raction, or left ventricular thrombus; using 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductas
7 excess, Insig-1 also binds to the ER enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductas
8 the cholesterol biosynthetic pathway enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductas
9 ave been made possible by the development of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductas
10 harmacologic concentrations of lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductas
11 nd blood lipids, saturation index, leukocyte 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductas
13 itted step in the pathway, the conversion of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) to meval
15 itavastatin (NK-104) is a novel inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
16 Certain pleiotropic activities reported for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
17 ed levels of the sterol biosynthetic enzyme, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
19 We examined the possible effects of a novel 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
22 s designed to assess the association between 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
23 functional protein predicted to possess both 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
24 equence analysis has revealed two classes of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
25 that mvaA, which encodes a putative class II 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
27 ell line (UT2 cells) that expresses only one 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
32 endoplasmic reticulum (ER) membrane protein, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
35 tched, to the cholesterol-sensing regions of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
36 holesterol biosynthetic pathway catalyzed by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
38 , and hepatic activities and mRNA levels for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
39 rs and angiotensin-receptor blockers (ARBs), 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
44 ic DNA to isolate the mvaS gene that encodes 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase
45 the proximal promoters of the genes encoding 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase
47 her the farnesyl diphosphate (FPP) synthase, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase
49 c loop, alanine 110 of Enterococcus faecalis 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase
50 ding mevalonate pyrophosphate decarboxylase, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase
51 ue to intramyofiber cascades downstream from 3-hydroxy-3-methylglutaryl-coenzyme A (HMG Co-A) reducta
52 lipoprotein deposition, we hypothesised that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG COA) reductas
59 endothelial and smooth muscle cells, such as 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
60 pathway, acetoacetyl-coenzyme A thiolase and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
63 in cholesterol and fatty acid biosyntheses, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
67 s (particularly, apolipoprotein E (ApoE) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
68 ter) and eubacterial (Pseudomonas mevalonii) 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
69 idylcholine, and cholesterol synthesis rate, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
70 endoplasmic reticulum (ER) membrane protein 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
71 -related genes (encoding 1,3-beta-glucanase, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
72 ng either the signal recognition particle or 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
73 his effect was mediated by inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
74 tion of angiogenesis, we studied the role of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
77 nstrated that systemic administration of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
78 sought to determine the effect of aggressive 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
80 th of these SNPs were in the gene coding for 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
81 inding of [1,2-(13)C]acetyl-CoA to wild-type 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) synthase
84 Statins are a class of drugs that inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMGcoA) reductase
86 h the studies of lipid modification with the 3-hydroxy-3-methylglutaryl coenzyme A inhibitors, or sta
88 suppressed squalestatin 1-mediated CYP2B and 3-hydroxy-3-methylglutaryl coenzyme A mRNA induction wit
89 elated protein kinase (SnRK1) phosphorylates 3-hydroxy-3-methylglutaryl-Coenzyme A, nitrate reductase
90 leucine in vibrios that is distinct from the 3-hydroxy-3-methylglutaryl-coenzyme A pathway seen in ps
93 Likewise several new autoantibodies (e.g. 3-hydroxy-3 methylglutaryl-coenzyme-A reductase and mela
94 ns, drugs that block the rate-limiting step (3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA
96 modified by homocysteine (Hcy) revealed that 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR)
97 cellar solubilisation of cholesterol, in the 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR)
99 bin receptor (Cf2r), hexosaminidase b(Hexb), 3-hydroxy-3-methylglutaryl coenzyme A reductase (Hmgcr),
100 anslated to mRNA leading to the formation of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR),
101 m membranes stimulates the ubiquitination of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR),
102 xtent to which specific genes for the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) a
103 ned to target histone deacetylase (HDAC) and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) b
104 solated two full-length cDNA clones encoding 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) f
106 ical studies have demonstrated that statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) i
109 e LDL receptor expression) and biosynthesis (3-hydroxy-3-methylglutaryl coenzyme A reductase activity
112 olesterol biosynthesis through inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase but has
113 r region of tomato (Lycopersicon esculentum) 3-hydroxy-3-methylglutaryl coenzyme A reductase gene 2 (
114 pathway and had the catalytic domain of the 3-hydroxy-3-methylglutaryl coenzyme A reductase gene int
115 reversed the effect, confirming the role of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibiti
116 ACE) inhibitors, proton-pump inhibitors, and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
120 Recent results indicate that 'statins', 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
122 secondary prevention benefit of therapy with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
123 Knowledge of long-term persistence with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
124 risk, and retrospective studies suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
125 w-density lipoprotein (LDL) cholesterol with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
129 ted is still controversial, as is the use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
134 ave shown that lipid-lowering therapy with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
135 of different beneficial effects of statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
142 and C evidence is available to suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
146 e, glycogen synthase kinase-3 inhibitors and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
152 as monotherapy and when co-administered with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
153 ulum retention upon Insig-1 binding, whereas 3-hydroxy-3-methylglutaryl coenzyme A reductase is ubiqu
154 Squalestatin 1 treatment increased CYP2B and 3-hydroxy-3-methylglutaryl coenzyme A reductase mRNA con
155 in skin associated with a marked increase in 3-hydroxy-3-methylglutaryl coenzyme A reductase protein.
157 e DNA site required for sterol regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase was show
158 t inhibiting the first step of this pathway (3-hydroxy-3-methylglutaryl coenzyme A reductase) reduces
160 biquitination and proteasomal degradation of 3-hydroxy-3-methylglutaryl coenzyme A reductase, a rate-
162 the cholesterol synthesis-regulating enzyme, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and the
165 reticulum (ER) allows for ubiquitination of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rat
166 evels in the body by specifically inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, which i
171 glioside production, proteoglycan synthesis, 3-hydroxy-3-methylglutaryl coenzyme-A reductase activity
173 ology to the sterol-sensing domains (SSD) of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-R)
174 imibe, either alone or in combination with a 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR)
177 y immunoprecipitation of in vitro-translated 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR)
178 genes in the mevalonate pathway, such as the 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR)
179 fic for signal recognition particle (SRP) or 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR).
180 ted variants in the genes encoding PCSK9 and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR;
181 d by a dose- and time-dependent elevation in 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR) a
182 the resident endoplasmic reticulum protein, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR),
183 t, through feedback-regulated degradation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR).
185 development, we identified a mutation in the 3-hydroxy-3-methylglutaryl-Coenzyme A reductase 1b (hmgc
186 ides) caused a significant decrease in their 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity
191 lesterol levels were noticeably resistant to 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibito
192 We have shown in mice that pravastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibito
195 sine-5'-triphosphate binding activity by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibito
196 ng recipients with pravastatin (Pravacol), a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibito
201 Sterol-accelerated degradation of the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase is one o
202 breast cancers were associated with elevated 3-hydroxy-3-methylglutaryl-coenzyme A reductase mRNA lev
203 one of three main synthetic products in the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway.
204 ERAD) of the cholesterol biosynthetic enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase results
205 nding protein (SREBP)-1a, SREBP-1c, SREBP-2, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, 3-hydro
206 ng two actions: 1) sterol-induced binding to 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an acti
207 -regulatory element-binding protein 2, human 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and hum
208 holesterol biosynthesis rate-limiting enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and inc
209 proteins (endoplasmic reticulum Ca2+-ATPase, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and pro
211 have previously reported that degradation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rat
212 ase in activity of its rate-limiting enzyme, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, under b
214 ements highly homologous to those present in 3-hydroxy-3-methylglutaryl-coenzyme A reductase; the CET
216 verse cell signaling pathways, inhibition of 3-hydroxy-3-methylglutaryl-coenzyme-A reductase may also
219 ed with and transactivate the genes encoding 3-HYDROXY-3-METHYLGLUTARYL-COENZYME A REDUCTASE1 (HMGR1)
220 mals manifested elevated levels of mRNAs for 3-hydroxy-3-methylglutaryl coenzyme A synthase and reduc
221 droxy-3-methylglutaryl-coenzyme A reductase, 3-hydroxy-3-methylglutaryl-coenzyme A synthase, and LDL
222 the up-regulation of lipogenic genes such as 3-hydroxy-3-methylglutaryl-coenzyme A synthase, fatty ac
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