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2 d that "high-risk" patients are treated with hydroxymethylglutaryl CoA reductase inhibitors to reduce
3 nhibited by both lovastatin, an inhibitor of hydroxymethylglutaryl CoA reductase, and alendronate.
4 e, we evaluated mice lacking mitochondrial 3-hydroxymethylglutaryl CoA synthase (HMGCS2) to determine
5 his enzyme is unique in that it is the first hydroxymethylglutaryl CoA synthase that is insensitive t
7 In this study, the comparative effects of hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors
10 acetoacetyl-CoA, succinyl-CoA, malonyl-CoA, hydroxymethylglutaryl-CoA (HMG-CoA), and acetyl-CoA in I
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 cutely injured lungs from sepsis (SAILS) and hydroxymethylglutaryl-CoA reductase inhibition with simv
18 or the hepatic uptake of this liver-specific hydroxymethylglutaryl-CoA reductase inhibitor in rat and
19 hamster ovary cell lines with lovastatin (a hydroxymethylglutaryl-CoA reductase inhibitor) and meval
20 sulfate, and thyroid hormone, as well as the hydroxymethylglutaryl-CoA reductase inhibitor, pravastat
21 dence suggests that long term treatment with hydroxymethylglutaryl-CoA reductase inhibitors, or stati
22 ord "surgery" and the MeSH term for statins "hydroxymethylglutaryl-CoA reductase inhibitors." Studies
25 carboxykinase, and type I deiodinase but not hydroxymethylglutaryl-CoA reductase, cytochrome c, and a
26 e stimulated the rapid inactivation of their hydroxymethylglutaryl-CoA reductase, presumably through
31 n regulatory factor 1 (IRF-1), mitochondrial hydroxymethylglutaryl-CoA synthase (HMG-CoA synthase), a
35 nd catalase, and show that these, as well as hydroxymethylglutaryl-CoA synthase and sarcosine dehydro
36 nding cassette transporters ABCA1 and ABCG5, hydroxymethylglutaryl-CoA synthase and the LDL receptor)
37 odular polyketide synthase (PKS) proteins, a hydroxymethylglutaryl-CoA synthase cassette and three fl
38 -methyl and beta-ethyl branches catalyzed by hydroxymethylglutaryl-CoA synthase homologues that utili
39 ency resulted in up-regulation of intestinal hydroxymethylglutaryl-CoA synthase mRNA and an increase
42 f acetyl-CoA, acetoacetyl-CoA, succinyl-CoA, hydroxymethylglutaryl-CoA, and malonyl-CoA confirmed tha
43 iNOS expression, and NF-kappaB activation by hydroxymethylglutaryl-CoA, mevalonate, and farnesyl pyro
46 domized trials, calcium channel blockers and hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inh
49 his study aimed to investigate the impact of hydroxymethylglutaryl coenzyme A reductase inhibitor (st
50 nse of C-reactive protein to initiation of a hydroxymethylglutaryl coenzyme A reductase inhibitor (st
53 We sought to determine whether therapy with hydroxymethylglutaryl coenzyme A reductase inhibitors (s
54 f the most recent clinical trials with the 3-hydroxymethylglutaryl coenzyme A reductase inhibitors (s
57 , including cholesterol metabolic processes, hydroxymethylglutaryl-coenzyme A (CoA) reductase activit
58 sterol pathways, I found that mRNA levels of hydroxymethylglutaryl-coenzyme A (HMG-CoA) synthase, squ
59 (FPP), which are lipids downstream from the hydroxymethylglutaryl-coenzyme A block, were also examin
60 ylase [At1g03090 and At4g34030] and putative hydroxymethylglutaryl-coenzyme A lyase [At2g26800]) base
62 of previously reported methods for screening hydroxymethylglutaryl-coenzyme A reductase (HMGR) inhibi
65 nate, indicating a direct effect of vascular hydroxymethylglutaryl-coenzyme A reductase inhibition.
66 Pretreatment of Jurkat T-cells with the 3-hydroxymethylglutaryl-coenzyme A reductase inhibitor, lo
68 sterol regulatory element-binding protein 1, hydroxymethylglutaryl-coenzyme A reductase, and apolipop
71 ame deletion mutants confirmed the role of a hydroxymethylglutaryl-coenzyme A synthase cassette, thre
74 l1L) is an adaptor protein for the E3 ligase hydroxymethylglutaryl reductase degradation protein 1 (H
75 e stability of the E3 ubiquitin ligase Hrd1 (hydroxymethylglutaryl reductase degradation protein 1),
76 lean proof for the reversible dehydration of hydroxymethylglutaryl-S-PksL via incorporation of 2H or