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1 sm, lysine biosynthesis and degradation, and bile acid biosynthesis.
2 ceptor LRH-1 (also known as NR5A2) regulates bile acid biosynthesis.
3 the classical homeostatic control of hepatic bile acid biosynthesis.
4 id clearance and represses genes involved in bile acid biosynthesis.
5 e by which high levels of bile acids repress bile acid biosynthesis.
6 te-limiting enzyme in the neutral pathway of bile acid biosynthesis.
7 effect of the C-36 serpin peptide on hepatic bile acid biosynthesis.
8 lation of genes encoding critical enzymes of bile acid biosynthesis.
9 ), which catalyzes the rate-limiting step in bile acid biosynthesis.
10 eroxisome and that this is a crucial step in bile acid biosynthesis.
11 ession of CYP7A1 and other genes involved in bile acid biosynthesis.
12 es the reduction of key intermediates during bile acid biosynthesis.
13 abolism, vitamin A (retinol) metabolism, and bile acid biosynthesis.
14  sparing the expression of genes involved in bile acids biosynthesis.
15 getic effects that contribute to its role in bile acid biosynthesis: 1) it has the ability to activat
16 r basal levels in PRH dramatically increased bile acid biosynthesis (586% +/- 82%, P < 0.001) but did
17 A1) plays an important role in regulation of bile acid biosynthesis and cholesterol homeostasis.
18  PGC-1alpha is a key activator of CYP7A1 and bile acid biosynthesis and is likely responsible for the
19 (AKR1D1) and AKR1C enzymes are essential for bile acid biosynthesis and steroid hormone metabolism.
20                    Consequences of defective bile acid biosynthesis and transport have been clarified
21           Pathway analysis (p < 0.05) showed bile acid biosynthesis and tryptophan metabolism as the
22 a novel mechanism for feedback repression of bile acid biosynthesis and underscores the vital role of
23  involvement of arachidonic acid metabolism, bile acid biosynthesis, and the pentose phosphate pathwa
24 tivates CYP7A1 gene expression and increases bile acid biosynthesis as well.
25 e small heterodimer partner (SHP) suppresses bile acid biosynthesis by heterodimerizing with FTF.
26 hysiological pathway, feedback inhibition of bile acid biosynthesis, by differentially targeting SHP
27 ibits transcription of CYP7A1, a key gene in bile acid biosynthesis, by recruiting histone deacetylas
28 fine a potentially treatable inborn error of bile acid biosynthesis caused by ACOX2 deficiency.
29 To determine whether the primary products of bile acid biosynthesis, cholic acid and chenodeoxycholic
30 erconversion, amino acid metabolism, primary bile acid biosynthesis, citric acid cycle, and lipid met
31 nd in Abcd3-/- mice, there was evidence of a bile acid biosynthesis defect.
32 ed increased expression of genes involved in bile acid biosynthesis, efflux transport, and reduced ex
33 tion scores of 3 metabolic pathways, primary bile acid biosynthesis, fatty acid biosynthesis, and bio
34 iting step in the classic pathway of hepatic bile acid biosynthesis from cholesterol.
35 ediated suppression of the expression of two bile acid biosynthesis genes resulted in a 3-fold lower
36                  However, the role of FTF in bile acid biosynthesis has been studied only in tissue c
37 on of propanoate, amino acid metabolism, and bile acid biosynthesis in the subspecies and sex compari
38 teroid hydroxylases and modulates sterol and bile acid biosynthesis in vivo.
39 of genes involved in cholesterol and primary bile acid biosynthesis including Cyp7a1.
40 a key hepatic activator of genes involved in bile acid biosynthesis including the cholesterol 7-alpha
41 le products, a dramatic increase was seen in bile acid biosynthesis intermediates (27- and 7,27-hydro
42                       The classic pathway of bile acid biosynthesis is downregulated in PEX2(-/-) mic
43 rd regulation of the rate limiting enzyme in bile acid biosynthesis is provided by oxysterols through
44                                              Bile acid biosynthesis is regulated by both feed-forward
45 dy, the induction of an alternate pathway of bile acid biosynthesis is shown to underlie this unusual
46                                              Bile acid biosynthesis is subjected to feedback regulati
47 te-limiting enzyme in the neutral pathway of bile acid biosynthesis, is feedback-inhibited at the tra
48 1, which catalyzes the rate-limiting step in bile acid biosynthesis, is strongly suppressed.
49 n of hepatic transporters and alterations of bile acid biosynthesis may contribute to development of
50 ial cholesterol transport protein, increases bile acid biosynthesis more than 5-fold via the acidic p
51 els, and CYP7A1, the rate-limiting enzyme in bile acid biosynthesis (p<0.05).
52 zyme that commits cholesterol to the neutral bile acid biosynthesis pathway and is highly regulated.
53            Two key regulatory enzymes in the bile acid biosynthesis pathway are cholesterol 7alpha-hy
54 lesterol 7 alpha-hydroxylase (CYP7A1) of the bile acid biosynthesis pathway is suppressed by bile aci
55 he side chain of C27 steroids in the hepatic bile acid biosynthesis pathway, which begins with 7alpha
56 7a1, the rate-limiting enzyme in the classic bile acid biosynthesis pathway.
57 sic" (neutral) or the "alternative" (acidic) bile acid biosynthesis pathways.
58 specific deletion of SIRT1 increased hepatic bile acid biosynthesis, reduced hepatic accumulation of
59 ogenase (AKR1C4) plays a significant role in bile acid biosynthesis, steroid hormone metabolism, and
60  and eicosanoids; cholesterol metabolism and bile-acid biosynthesis; steroid synthesis and metabolism
61 nisms underlying PXR-mediated suppression of bile acid biosynthesis, we examined the functional cross
62 pha-hydroxylase, the rate-limiting enzyme of bile acid biosynthesis, were constructed by targeted dis