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1 ration of (E)-3-methylglutaconyl-CoA to (3S)-hydroxymethylglutaryl-CoA.
2 f acetyl-CoA, acetoacetyl-CoA, succinyl-CoA, hydroxymethylglutaryl-CoA, and malonyl-CoA confirmed tha
3 In this study, the comparative effects of hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors
6 acetoacetyl-CoA, succinyl-CoA, malonyl-CoA, hydroxymethylglutaryl-CoA (HMG-CoA), and acetyl-CoA in I
8 iNOS expression, and NF-kappaB activation by hydroxymethylglutaryl-CoA, mevalonate, and farnesyl pyro
10 d that "high-risk" patients are treated with hydroxymethylglutaryl CoA reductase inhibitors to reduce
11 nhibited by both lovastatin, an inhibitor of hydroxymethylglutaryl CoA reductase, and alendronate.
12 REBP binding to three specific target genes: hydroxymethylglutaryl-CoA reductase (Red), fatty acid sy
13 (AMPK), phosphorylates and regulates in vivo hydroxymethylglutaryl-CoA reductase and acetyl-CoA carbo
15 protein pathway and increases expression of hydroxymethylglutaryl-CoA reductase and low density lipo
16 ed in the regulated degradation of wild-type hydroxymethylglutaryl-CoA reductase in the ER membrane.
17 or the hepatic uptake of this liver-specific hydroxymethylglutaryl-CoA reductase inhibitor in rat and
18 hamster ovary cell lines with lovastatin (a hydroxymethylglutaryl-CoA reductase inhibitor) and meval
19 sulfate, and thyroid hormone, as well as the hydroxymethylglutaryl-CoA reductase inhibitor, pravastat
20 dence suggests that long term treatment with hydroxymethylglutaryl-CoA reductase inhibitors, or stati
21 ord "surgery" and the MeSH term for statins "hydroxymethylglutaryl-CoA reductase inhibitors." Studies
24 carboxykinase, and type I deiodinase but not hydroxymethylglutaryl-CoA reductase, cytochrome c, and a
25 e stimulated the rapid inactivation of their hydroxymethylglutaryl-CoA reductase, presumably through
30 e, we evaluated mice lacking mitochondrial 3-hydroxymethylglutaryl CoA synthase (HMGCS2) to determine
31 his enzyme is unique in that it is the first hydroxymethylglutaryl CoA synthase that is insensitive t
33 n regulatory factor 1 (IRF-1), mitochondrial hydroxymethylglutaryl-CoA synthase (HMG-CoA synthase), a
36 nd catalase, and show that these, as well as hydroxymethylglutaryl-CoA synthase and sarcosine dehydro
37 nding cassette transporters ABCA1 and ABCG5, hydroxymethylglutaryl-CoA synthase and the LDL receptor)
38 odular polyketide synthase (PKS) proteins, a hydroxymethylglutaryl-CoA synthase cassette and three fl
39 -methyl and beta-ethyl branches catalyzed by hydroxymethylglutaryl-CoA synthase homologues that utili
40 ency resulted in up-regulation of intestinal hydroxymethylglutaryl-CoA synthase mRNA and an increase
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