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1 CYP8B1 expression could contribute to the decreased toxi
3 inding to the native promoters of CYP7A1 and CYP8B1 but resulted in dissociation of PGC-1 and concomi
5 to derepression of rate-limiting CYP7A1 and CYP8B1 hydroxylase enzymes in the biosynthetic pathway.
6 of CYP7B1 and down-regulated the CYP7A1 and CYP8B1, shifting bile acid synthesis toward the acidic p
9 sociated protein 4 (MRP4) overexpression and CYP8B1 inhibition that are involved in BA uptake, basola
10 me P450 (CYP) isoform 7A1 (CYP7A1), CYP27A1, CYP8B1, uridine 5'-diphospho-glucuronosyltransferase 1A1
11 4alpha (HNF4alpha) strongly activated human CYP8B1 promoter activities, whereas cholesterol 7alpha-h
17 is, notably cholesterol 12alpha-hydroxylase (CYP8B1), which was strongly reexpressed in the SHP null
21 these enzymes is sterol 12alpha-hydroxylase/CYP8B1 (12alpha-hydroxylase), the specific enzyme requir
23 duction of RORalpha to mice strongly induced CYP8B1 expression, and increased liver cholesterol and 1
26 r of diurnal rhythm and fasting induction of CYP8B1, which regulates bile acid composition and serum
28 This contrasts with the strong repression of CYP8B1 observed with short term bile acid feeding, as we
29 of fasting induction and circadian rhythm of CYP8B1 by a cholesterol-activated nuclear receptor and c
32 evealed the critical roles HNF4alpha play on CYP8B1 transcription and its repression by bile acids.
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