ライフサイエンスコーパス: lithocholic acid

1 oxycholic, deoxycholic, ursodeoxycholic, and lithocholic acid.

2 were synthesized from either deoxycholic or lithocholic acid.

3 cholic acid, 43%; deoxycholic acid, 11%, and lithocholic acid, 1%.

4 odeoxycholic acid (3alpha-OH, 7beta-OH), and lithocholic acid (3alpha-OH).

5 We show that vitamin K2 and lithocholic acid, a by-product of intestinal flora, acti

6 GR5 agonists, taurochenodeoxycholic acid and lithocholic acid, activated AKT and inhibited GSK3beta,

7 N-Lithocholic acid acylated insulin [Lys(B29)-lithocholyl

8 Furthermore, two of these ligands, lithocholic acid and estradiol disulfate, unexpectedly e

9 analysis revealed a significant decrease in lithocholic acid and its derivatives after UDCA withdraw

10 f free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the far

11 c P450 that catalyzes 6beta-hydroxylation of lithocholic acid, and the pattern of GH secretion is dir

12 thinyl estradiol, chenodeoxycholic acid, and lithocholic acid by either PCN or TCDD in small intestin

13 Lithocholic acid causes colon cancer; thus, decreasing l

14 However, the bile acid lithocholic acid competed efficiently with 9-cis-RA for

15 gate the ability of synthetic enantiomers of lithocholic acid (ent-LCA), chenodeoxycholic acid (ent-C

16 e report the first synthesis of enantiomeric lithocholic acid (ent-LCA, ent-1) and chenodeoxycholic a

17 When 0.4% UDCA was added to the diet, lithocholic acid increased in the insoluble fraction (40

18 rations of secondary BA deoxycholic acid and lithocholic acid, indicating reduced activity of the nuc

19 o being a ligand for the vitamin D receptor, lithocholic acid is also a substrate for CYP3A enzymes.

20 se A (SrtA 7M) was N-terminally labeled with lithocholic acid (LA)-an inexpensive bile acid that exhi

21 We studied lithocholic acid (LCA) (the natural 3alpha-OH isomer), g

22 that PXR is activated by the toxic bile acid lithocholic acid (LCA) and its 3-keto metabolite.

23 We recently identified lithocholic acid (LCA) as a small molecule able to block

24 o screening and confirmed by experiment that lithocholic acid (LCA) binds to the p53 binding sites of

25 patotoxicity of secondary bile acids such as lithocholic acid (LCA) by inducing expression of the hyd

26 The endogenous steroid lithocholic acid (LCA) dilates cerebral arteries via BK

27 Huh7 cells treated with lithocholic acid (LCA) exhibited a similar pattern of ch

28 ue uptake, distribution, and cytotoxicity of lithocholic acid (LCA) in relation to various experiment

29 Lithocholic acid (LCA) is an endogenous compound associa

30 rticular, the secondary bile acid derivative lithocholic acid (LCA) is highly hepatotoxic and, as we

31 Lithocholic acid (LCA) treatment of primary human hepato

32 Lithocholic acid (LCA), a bile acid implicated in the pr

33 We investigated the effects of lithocholic acid (LCA), an inhibitor of the key BER enzy

34 roduction of hepatotoxic bile acids, such as lithocholic acid (LCA), because of limited small bowel a

35 ns as a receptor for the secondary bile acid lithocholic acid (LCA), which is hepatotoxic and a poten

36 mice confers a female-specific resistance to lithocholic acid (LCA)-induced hepatotoxicity and bile d

37 o confer resistance to the hepatotoxicity of lithocholic acid (LCA).

38 ective response to the hydrophobic bile acid lithocholic acid (LCA).

39 , acts also as a bile acid sensor by binding lithocholic acid (LCA).

40 The GPBAR1 agonist, tauro-lithocholic acid (LCA, 10 microm) mimicked the effect of

41 c acid causes colon cancer; thus, decreasing lithocholic acid levels in the intestine by up-regulatin

42 Application of deoxycholic acid, lithocholic acid, or oleanolic acid (a selective agonist

43 sion was increased synergistically by RA and lithocholic acid (P<0.05).

44 s that an increased level of glyco and tauro lithocholic acid, perhaps because of a decreased capacit

45 lenic acid, cholenic acid 3beta-acetate, and lithocholic acid, respectively.

46 ary bile acids, such as deoxycholic acid and lithocholic acid, than those fed the LFCO or HFFO diets.

47 ng of the mitochondrial lipid composition by lithocholic acid treatment or by ablation of the lipid t

48 A regimen of lithocholic acid treatment, which was tolerated by wild-

49 ic acid (EC50=5.7 muM; its endogenous analog lithocholic acid was virtually equipotent), and the most

50 levels, with or without induction by RA and lithocholic acid, were determined by quantitative revers

51 n calcium homeostasis, or it is activated by lithocholic acid when its levels are elevated after a me