コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
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
12 nhibitors and angiotensin receptor blockers, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductas
13 endoplasmic reticulum (ER) membrane protein 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductas
15 itted step in the pathway, the conversion of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) to meval
18 itavastatin (NK-104) is a novel inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
19 Certain pleiotropic activities reported for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
20 ed levels of the sterol biosynthetic enzyme, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
22 We examined the possible effects of a novel 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
25 s designed to assess the association between 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
26 functional protein predicted to possess both 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
27 equence analysis has revealed two classes of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
28 that mvaA, which encodes a putative class II 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
30 ell line (UT2 cells) that expresses only one 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
35 endoplasmic reticulum (ER) membrane protein, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
38 tched, to the cholesterol-sensing regions of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
39 holesterol biosynthetic pathway catalyzed by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
40 , and hepatic activities and mRNA levels for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
41 studies suggest that statins, which inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
43 rs and angiotensin-receptor blockers (ARBs), 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductas
47 ic DNA to isolate the mvaS gene that encodes 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase
48 the proximal promoters of the genes encoding 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase
50 her the farnesyl diphosphate (FPP) synthase, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase
52 c loop, alanine 110 of Enterococcus faecalis 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase
53 ding mevalonate pyrophosphate decarboxylase, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase
54 ue to intramyofiber cascades downstream from 3-hydroxy-3-methylglutaryl-coenzyme A (HMG Co-A) reducta
55 lipoprotein deposition, we hypothesised that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG COA) reductas
59 th of these SNPs were in the gene coding for 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
62 endothelial and smooth muscle cells, such as 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
63 pathway, acetoacetyl-coenzyme A thiolase and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
66 in cholesterol and fatty acid biosyntheses, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
70 ter) and eubacterial (Pseudomonas mevalonii) 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
71 idylcholine, and cholesterol synthesis rate, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
72 endoplasmic reticulum (ER) membrane protein 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
73 -related genes (encoding 1,3-beta-glucanase, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
74 s (particularly, apolipoprotein E (ApoE) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
75 ng either the signal recognition particle or 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
76 his effect was mediated by inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
77 tion of angiogenesis, we studied the role of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
81 nstrated that systemic administration of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
82 sought to determine the effect of aggressive 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductas
85 inding of [1,2-(13)C]acetyl-CoA to wild-type 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) synthase
88 Statins are a class of drugs that inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMGcoA) reductase
90 h the studies of lipid modification with the 3-hydroxy-3-methylglutaryl coenzyme A inhibitors, or sta
92 suppressed squalestatin 1-mediated CYP2B and 3-hydroxy-3-methylglutaryl coenzyme A mRNA induction wit
93 elated protein kinase (SnRK1) phosphorylates 3-hydroxy-3-methylglutaryl-Coenzyme A, nitrate reductase
94 leucine in vibrios that is distinct from the 3-hydroxy-3-methylglutaryl-coenzyme A pathway seen in ps
97 Likewise several new autoantibodies (e.g. 3-hydroxy-3 methylglutaryl-coenzyme-A reductase and mela
98 ns, drugs that block the rate-limiting step (3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA
100 modified by homocysteine (Hcy) revealed that 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR)
103 cellar solubilisation of cholesterol, in the 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR)
105 m membranes stimulates the ubiquitination of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR),
106 bin receptor (Cf2r), hexosaminidase b(Hexb), 3-hydroxy-3-methylglutaryl coenzyme A reductase (Hmgcr),
107 endoplasmic reticulum (ER)-localized enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR),
108 anslated to mRNA leading to the formation of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR),
109 the expression of the statin target enzyme, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR).
110 xtent to which specific genes for the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) a
111 ned to target histone deacetylase (HDAC) and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) b
112 solated two full-length cDNA clones encoding 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) f
114 ical studies have demonstrated that statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) i
117 e LDL receptor expression) and biosynthesis (3-hydroxy-3-methylglutaryl coenzyme A reductase activity
120 olesterol biosynthesis through inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase but has
121 r region of tomato (Lycopersicon esculentum) 3-hydroxy-3-methylglutaryl coenzyme A reductase gene 2 (
122 pathway and had the catalytic domain of the 3-hydroxy-3-methylglutaryl coenzyme A reductase gene int
123 reversed the effect, confirming the role of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibiti
124 on to their cholesterol-lowering properties, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
127 as monotherapy and when co-administered with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
129 ACE) inhibitors, proton-pump inhibitors, and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
133 Recent results indicate that 'statins', 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
136 secondary prevention benefit of therapy with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
137 Knowledge of long-term persistence with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
138 risk, and retrospective studies suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
139 w-density lipoprotein (LDL) cholesterol with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
143 ted is still controversial, as is the use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
147 ave shown that lipid-lowering therapy with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
148 Interventions were treatment with statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
149 s for seven statins, a group of FDA-approved 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
151 of different beneficial effects of statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
156 and C evidence is available to suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
160 e, glycogen synthase kinase-3 inhibitors and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibito
164 ulum retention upon Insig-1 binding, whereas 3-hydroxy-3-methylglutaryl coenzyme A reductase is ubiqu
165 Squalestatin 1 treatment increased CYP2B and 3-hydroxy-3-methylglutaryl coenzyme A reductase mRNA con
166 in skin associated with a marked increase in 3-hydroxy-3-methylglutaryl coenzyme A reductase protein.
168 e DNA site required for sterol regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase was show
169 t inhibiting the first step of this pathway (3-hydroxy-3-methylglutaryl coenzyme A reductase) reduces
171 biquitination and proteasomal degradation of 3-hydroxy-3-methylglutaryl coenzyme A reductase, a rate-
173 the cholesterol synthesis-regulating enzyme, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and the
176 reticulum (ER) allows for ubiquitination of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rat
177 evels in the body by specifically inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, which i
183 glioside production, proteoglycan synthesis, 3-hydroxy-3-methylglutaryl coenzyme-A reductase activity
185 ology to the sterol-sensing domains (SSD) of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-R)
186 imibe, either alone or in combination with a 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR)
187 hed genetic instruments to mimic statins via 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR)
188 extracted single-nucleotide polymorphisms in 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR)
191 y immunoprecipitation of in vitro-translated 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR)
192 genes in the mevalonate pathway, such as the 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR)
193 r 1, transcriptional corepressor (TLE1), and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR))
194 cholesterol-biosynthesis pathway upstream of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR),
195 s and compare those to genetic inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR).
196 fic for signal recognition particle (SRP) or 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR).
197 ted variants in the genes encoding PCSK9 and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR;
198 d by a dose- and time-dependent elevation in 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR) a
199 the resident endoplasmic reticulum protein, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR),
200 t, through feedback-regulated degradation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR).
202 development, we identified a mutation in the 3-hydroxy-3-methylglutaryl-Coenzyme A reductase 1b (hmgc
203 ides) caused a significant decrease in their 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity
208 lesterol levels were noticeably resistant to 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibito
209 We have shown in mice that pravastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibito
212 sine-5'-triphosphate binding activity by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibito
213 ng recipients with pravastatin (Pravacol), a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibito
216 duct an in silico drug screen and identified 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibito
220 Sterol-accelerated degradation of the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase is one o
221 breast cancers were associated with elevated 3-hydroxy-3-methylglutaryl-coenzyme A reductase mRNA lev
222 or minimize its severity, inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway
223 one of three main synthetic products in the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway.
224 ERAD) of the cholesterol biosynthetic enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase results
225 lead to discontinuation or non-initiation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase therapy
226 nding protein (SREBP)-1a, SREBP-1c, SREBP-2, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, 3-hydro
227 ng two actions: 1) sterol-induced binding to 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an acti
228 -regulatory element-binding protein 2, human 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and hum
229 holesterol biosynthesis rate-limiting enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and inc
230 proteins (endoplasmic reticulum Ca2+-ATPase, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and pro
232 hich reduce LDL-cholesterol by inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, are amo
233 have previously reported that degradation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rat
234 d to treat hypercholesterolemia, inhibit the 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rat
235 ase in activity of its rate-limiting enzyme, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, under b
237 ements highly homologous to those present in 3-hydroxy-3-methylglutaryl-coenzyme A reductase; the CET
239 verse cell signaling pathways, inhibition of 3-hydroxy-3-methylglutaryl-coenzyme-A reductase may also
242 ed with and transactivate the genes encoding 3-HYDROXY-3-METHYLGLUTARYL-COENZYME A REDUCTASE1 (HMGR1)
243 mals manifested elevated levels of mRNAs for 3-hydroxy-3-methylglutaryl coenzyme A synthase and reduc
245 droxy-3-methylglutaryl-coenzyme A reductase, 3-hydroxy-3-methylglutaryl-coenzyme A synthase, and LDL
246 the up-regulation of lipogenic genes such as 3-hydroxy-3-methylglutaryl-coenzyme A synthase, fatty ac