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2 rom clinical trials suggest that 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitors may help
3 nism for this putative effect of 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitors, and whe
4 ed by compactin, an inhibitor of 3-hydroxy-3-methylglutaryl CoA (HMG CoA) reductase that inhibits cho
5 c reticulum (ER)-resident enzyme 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase catalyzes the rat
8 bolic pathway by the hydrophobic 3-hydroxy-3-methylglutaryl CoA (HMGCoA) reductase inhibitors, simvas
9 ate degradation of the ER enzyme 3-hydroxy-3-methylglutaryl CoA reductase (HMG CoA reductase), which
10 olesterol synthesis pathway with 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reductase) inhibit
14 ars to control the expression of 3-hydroxy-3-methylglutaryl CoA reductase (HMGR) and l-phenylalanine
15 -2 (COX-2) inhibitors and statins [hydroxy-3-methylglutaryl CoA reductase (HMGR) inhibitors] inhibit
17 ng the mevalonate (MVA) pathway, 3-Hydroxy-3-Methylglutaryl CoA Reductase 1 (HMGR1), interacts with D
18 reticulum (ER)-localized enzyme 3-hydroxy-3-methylglutaryl CoA reductase catalyzes a rate-limiting s
19 enase-2 inhibitor), and statins (3-hydroxy-3-methylglutaryl CoA reductase inhibitors) inhibit colon c
21 t (or longer) treatment with the 3-hydroxy-3-methylglutaryl CoA reductase inhibitors, the statins.
23 y-3-methylglutaryl CoA synthase, 3-hydroxy-3-methylglutaryl CoA reductase), and fatty acid synthase.
24 nd pravastatin are inhibitors of 3-hydroxy-3-methylglutaryl CoA reductase, and are used as antihyperc
25 acid, a downstream metabolite of 3-hydroxy-3-methylglutaryl CoA reductase, confirming that simvastati
26 t selectively inhibit the enzyme 3-hydroxy-3-methylglutaryl CoA reductase, leading to decreased chole
28 cholesterol biosynthetic enzyme 3-hydroxy-3-methylglutaryl CoA reductase, thus inducing the ubiquiti
33 uired for cholesterol synthesis (3-hydroxy-3-methylglutaryl CoA synthase, 3-hydroxy-3-methylglutaryl
37 PC1L1) inhibitor (ezetimibe) and 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors (stati
40 ays between the OleA homologues, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase and the fatty acid
44 s expression of ketogenic enzyme 3-hydroxy-3-methylglutaryl-CoA lyase and promotes the formation of t
46 unction with a partial defect in 3-hydroxy-3-methylglutaryl-CoA lyase, and accumulation of oxidative
48 normal yeast ER membrane protein 3-hydroxy-3-methylglutaryl-CoA reductase (Hmg2p) undergoes ERAD that
49 ines, SUGP1 knockdown stimulated 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) alternative splicin
50 ecognition protein (SRP) or anti-3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) antibodies (Abs), a
52 udies report that utilization of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) inhibitors called s
54 s a consequence of inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the intended drug
58 ticulum (ER) and the activity of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) imbedded therein res
59 mised proteasomal degradation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) or deficient in ubiq
63 by 84% with empagliflozin, while 3-hydroxy-3-methylglutaryl-CoA reductase activity and total choleste
65 are associated with decreases in 3-hydroxy-3-methylglutaryl-CoA reductase and increases in ATP-bindin
66 dependent manner and whether the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor atorvastatin can
67 ed the effects of simvastatin, a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, on hippocampal A
68 of isoprenoid synthesis with the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, simvastatin (Sim
69 2 in response to Ang II by using 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors and isoprenoid i
71 cent reports suggest that statins (hydroxy-3-methylglutaryl-CoA reductase inhibitors) exhibit potenti
72 ition, our results indicate that 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, a class of chol
73 ase (squalene synthase), but not 3-hydroxy-3-methylglutaryl-CoA reductase or farnesyl diphosphate syn
74 The endoplasmic reticulum enzyme 3-hydroxy-3-methylglutaryl-CoA reductase produces mevalonate, which
75 ciated degradation of the enzyme 3-hydroxy-3-methylglutaryl-CoA reductase represents one mechanism by
76 pharmacologic inhibitors of the 3-hydroxy-3-methylglutaryl-CoA reductase that are potent regulators
77 farnesyl-pyrophosphate synthase, 3-hydroxy-3-methylglutaryl-CoA reductase, and low density lipoprotei
78 reatment reduced the activity of 3-hydroxy-3-methylglutaryl-CoA reductase, but it did not change acti
79 doplasmic reticulum (ER) enzyme, 3-hydroxy-3-methylglutaryl-CoA reductase, catalyzes the production o
80 nd -2 increased on promoters for 3-hydroxy-3-methylglutaryl-CoA reductase, fatty-acid synthase, and s
81 ized that statins, inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase, inhibit cardiac hypertroph
85 ect repression of sterol enzymes 3-hydroxy-3-methylglutaryl-CoA synthase 1 and methylsterol monooxyge
87 etabolism pathway, mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2), as a major down-
88 hain acyl-CoA dehydrogenase, and 3-hydroxy-3-methylglutaryl-CoA synthase 2, and enhances fat metaboli
89 of VMH ketone production with a 3-hydroxy-3-methylglutaryl-CoA synthase inhibitor reversed the 3- to
91 o the hydrophobic active site of 3-hydroxy-3-methylglutaryl-CoA synthase, site-directed mutagenesis w
92 synthases, polyketide synthases, 3-hydroxy-3-methylglutaryl-CoA synthases, and biosynthetic thiolases
93 Furthermore, we show that the 3-hydroxy-3-methylglutaryl-CoA-reductase inhibitor mevastatin, which
95 signal recognition particle and 3-hydroxy-3-methylglutaryl-coenzime A reductase (HMG-CoA) reductase.
96 ically active Haloferax volcanii 3-hydroxy-3-methylglutaryl coenzyme A (CoA) synthase (EC 2.3.310).
98 alcohol dehydrogenase, elongation factor-TU, methylglutaryl coenzyme A (CoA), acyl CoA synthetase, ox
100 e possible by the development of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors
101 n-2 receptor blockers, and beta-hydroxy-beta-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors
102 ig-1 also binds to the ER enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, facilitat
104 rotein predicted to possess both 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and acetyl
105 o assess the association between 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition
106 patients derive benefit from the 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor
107 the possible effects of a novel 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor,
111 n randomized, controlled trials, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors
112 iotropic activities reported for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors
114 re, cholesterol-lowering agents, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors
115 left ventricular thrombus; using 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors
117 ical trials have shown that the 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors
118 tensin-receptor blockers (ARBs), 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors
120 the sterol biosynthetic enzyme, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase isozyme, H
122 2 cells) that expresses only one 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase protein wh
123 hich encodes a putative class II 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, is essent
124 atins, a class of inhibitors for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, significa
125 (NK-104) is a novel inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-
126 n is a specific inhibitor of three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, used comm
127 ed efferocytosis in vitro in an 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase-dependent
131 ine 110 of Enterococcus faecalis 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase was mutated
134 promoters of the genes encoding 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase, farnesyl d
135 ate pyrophosphate decarboxylase, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase, HMG-CoA re
136 olate the mvaS gene that encodes 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase, the second
141 at block the rate-limiting step (3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase))
143 ilisation of cholesterol, in the 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) activity, an
145 homocysteine (Hcy) revealed that 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) was upregula
146 mRNA leading to the formation of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), a main regu
147 stimulates the ubiquitination of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), which catal
148 t histone deacetylase (HDAC) and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) by having a h
150 have demonstrated that statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) inhibitors, a
152 or expression) and biosynthesis (3-hydroxy-3-methylglutaryl coenzyme A reductase activity) are regula
154 , not only statins targeting the 3-hydroxy-3-methylglutaryl coenzyme A reductase but also inhibitors
155 osynthesis through inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase but has no effect on
156 had the catalytic domain of the 3-hydroxy-3-methylglutaryl coenzyme A reductase gene integrated into
157 e effect, confirming the role of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibition and sugge
158 poprotein (LDL) cholesterol with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor ("statin")
159 ge of long-term persistence with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) t
161 vational studies have shown that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) u
163 pleiotropic effects of statins, 3-hydroxy-3 methylglutaryl coenzyme A reductase inhibitor, have been
166 nce is available to suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)
169 py and when co-administered with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)
170 ors, proton-pump inhibitors, and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)
173 Cardiovascular risk reduction by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)
175 evention benefit of therapy with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)
176 trospective studies suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)
178 controversial, as is the use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)
182 The hepatotoxic potential of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in patien
188 t beneficial effects of statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) on renal
191 he debate whether statins, 3-hydroxymethyl-3-methylglutaryl coenzyme A reductase inhibitors, are safe
193 results indicate that 'statins', 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, which ar
195 on upon Insig-1 binding, whereas 3-hydroxy-3-methylglutaryl coenzyme A reductase is ubiquitinated and
198 the first step of this pathway (3-hydroxy-3-methylglutaryl coenzyme A reductase) reduces the growth
200 y acid synthase, squalene epoxidase, hydroxy-methylglutaryl coenzyme A reductase), while genes involv
201 l-regulated ubiquitination marks 3-hydroxy-3-methylglutaryl coenzyme A reductase, a rate-determining
202 n and proteasomal degradation of 3-hydroxy-3-methylglutaryl coenzyme A reductase, a rate-limiting enz
203 rol synthesis-regulating enzyme, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and the cholesterol
204 -1 (SREBP-1), fatty acid synthase, hydroxy-3-methylglutaryl coenzyme A reductase, farnesyl pyrophosph
207 ER) allows for ubiquitination of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting e
208 tatins as dependent on inhibition of hydroxy-methylglutaryl coenzyme A reductase, we treated C57Bl/6
209 body by specifically inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, which is a rate-lim
210 or the continued proteolysis of 3-hydroxyl-3-methylglutaryl coenzyme A reductase, which may undermine
214 duction, proteoglycan synthesis, 3-hydroxy-3-methylglutaryl coenzyme-A reductase activity, and cell w
215 yofiber cascades downstream from 3-hydroxy-3-methylglutaryl-coenzyme A (HMG Co-A) reductase inhibitio
216 deposition, we hypothesised that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG COA) reductase inhibitors
219 rly, apolipoprotein E (ApoE) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (HMGR)) ha
220 ogenesis, we studied the role of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and alphaP
221 as mediated by inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and subseq
223 t systemic administration of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor
224 termine the effect of aggressive 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor
226 This study evaluated whether 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors
228 and smooth muscle cells, such as 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors
230 indings support further study of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors
232 Mevastatin is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the rate-
233 SNPs were in the gene coding for 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the targe
237 ,2-(13)C]acetyl-CoA to wild-type 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) synthase is characte
238 re a class of drugs that inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMGcoA) reductase, a critical
239 ibrios that is distinct from the 3-hydroxy-3-methylglutaryl-coenzyme A pathway seen in pseudomonads.
241 sterol-sensing domains (SSD) of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-R) and sterol r
245 r alone or in combination with a 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) inhibitor (s
246 ipitation of in vitro-translated 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) protein.
248 in the genes encoding PCSK9 and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR; the target o
249 and time-dependent elevation in 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR) activity, enh
250 t endoplasmic reticulum protein, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR), is regulated
253 we identified a mutation in the 3-hydroxy-3-methylglutaryl-Coenzyme A reductase 1b (hmgcr1b) gene th
255 cleation was also induced by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor lovastatin
256 hosphate binding activity by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor simvastati
257 hown in mice that pravastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, prevents
267 erated degradation of the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase is one of several me
268 rs were associated with elevated 3-hydroxy-3-methylglutaryl-coenzyme A reductase mRNA levels and anti
270 cholesterol biosynthetic enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase results from its ste
271 n (SREBP)-1a, SREBP-1c, SREBP-2, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, 3-hydroxy-3-methylg
272 ns: 1) sterol-induced binding to 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an action that lead
273 element-binding protein 2, human 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and human low-densi
274 iosynthesis rate-limiting enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and increased plasm
277 transactivate the genes encoding 3-HYDROXY-3-METHYLGLUTARYL-COENZYME A REDUCTASE1 (HMGR1) and MAKIBIS
278 ylglutaryl-coenzyme A reductase, 3-hydroxy-3-methylglutaryl-coenzyme A synthase, and LDL receptor mRN
279 ation of lipogenic genes such as 3-hydroxy-3-methylglutaryl-coenzyme A synthase, fatty acid synthase,
282 in kinase (SnRK1) phosphorylates 3-hydroxy-3-methylglutaryl-Coenzyme A, nitrate reductase and sucrose
283 several new autoantibodies (e.g. 3-hydroxy-3 methylglutaryl-coenzyme-A reductase and melanoma differe
285 ignaling pathways, inhibition of 3-hydroxy-3-methylglutaryl-coenzyme-A reductase may also result in p
286 mponents include a halogenase, a 3-hydroxy-3-methylglutaryl enzyme cassette for polyketide beta-branc
287 uercetin-3-O-hexoside, quercetin 3-hydroxy-3-methylglutaryl-glycoside), an O-triglycosyl flavanone (n
288 4'-methyl ether and scoparin), a 3-hydroxy-3-methylglutaryl glycosyl flavonol (3-hydroxy-3-methylglut
289 ethylglutaryl glycosyl flavonol (3-hydroxy-3-methylglutaryl glycosyl quercetin) and a flavone O-glyco
291 etermine whether atorvastatin, a 3-hydroxy-3-methylglutaryl (HMG)-co-enzyme A (CoA) reductase inhibit
296 reased expression of SREBP-2 and 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase, which results in inc
297 iquely among condensing enzymes, 3-hydroxy-3-methylglutaryl (HMG)-CoA synthase (HMGS) catalyzes the f
298 posure to beta-cyclodextrins and 3-hydroxy-3-methylglutaryl (HMG)-coenzyme A reductase inhibitors (st
299 a gamma-chlorination step on (S)-3-hydroxy-3-methylglutaryl mediated by Cur halogenase, a non-haem Fe
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