ライフサイエンスコーパス: deoxycholic acid

1 s as well as by efficient rehydroxylation of deoxycholic acid.

2 en the two porins, namely the sensitivity to deoxycholic acid.

3 hypersensitive to the anionic bile detergent deoxycholic acid.

4 ed with cholylglycine, 7-oxocholic acid, and deoxycholic acid.

5 holic acid, 45%; chenodeoxycholic acid, 43%; deoxycholic acid, 11%, and lithocholic acid, 1%.

6 cholic acid, 85%; chenodeoxycholic acid, 7%; deoxycholic acid, 3%; allocholic acid, 3%; and unidentif

7 Instead of deoxycholic acid, 3alpha,6beta,12alpha-trihydroxycholani

8 P < .05), cholic acid (-72%, P < .005), and deoxycholic acid (-62%, P < .05).

9 Deoxycholic acid, a strong detergent, greatly enhanced t

10 sed intratesticular BA levels in general and deoxycholic acid, a TGR5 agonist, in particular.

11 The results are interpreted as deoxycholic acid acting as an open-channel blocker, whic

12 chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR

13 he liver after mice were given injections of deoxycholic acid and an increase after they were fed fen

14 and decreased concentrations of secondary BA deoxycholic acid and lithocholic acid, indicating reduce

15 gher levels of secondary bile acids, such as deoxycholic acid and lithocholic acid, than those fed th

16 suggests that the active form is the neutral deoxycholic acid and not the negatively charged species.

17 Bile acids deoxycholic acid and ursodeoxycholic acid differentially

18 re properties, such as conductance, block by deoxycholic acid, and sensitivity to acidic pH.

19 brane sensitizes cells to the bile component deoxycholic acid, and the repression of OmpT in the inte

20 eased 12alpha-hydroxylated BAs (cholic acid, deoxycholic acid, and their conjugated forms).

21 The addition of an individual bile acid (deoxycholic acid, chenodeoxycholic acid, ursodeoxycholic

22 p-1/WAF1/mda6 (p21) enhanced the toxicity of deoxycholic acid (DCA) + MEK1/2 inhibitor.

23 In this study, the mechanism(s) by which deoxycholic acid (DCA) activates the JNK pathway were ex

24 We investigated the roles of hydrophobic deoxycholic acid (DCA) and hydrophilic ursocholic acid (

25 to test this by investigating the effects of deoxycholic acid (DCA) and ursodeoxycholic acid on the e

26 Secondary bile acids like deoxycholic acid (DCA) are well-established tumor promot

27 e identified ursodeoxycholic acid (UDCA) and deoxycholic acid (DCA) as the two most potent inhibitors

28 Deoxycholic acid (DCA) caused prolonged activation of th

29 Deoxycholic acid (DCA) is an endogenous secondary bile a

30 Secondary bile acids (BA) such as deoxycholic acid (DCA) promote the development of severa

31 tudies have demonstrated in hepatocytes that deoxycholic acid (DCA) promotes inactivation of protein

32 tio of dihomo-gamma-linolenic acid (DGLA) to deoxycholic acid (DCA) species (DCAS) was significantly

33 Deoxycholic acid (DCA) was instilled into the rat colon

34 Deoxycholic acid (DCA) was the best activator of ERK (3.

35 bile acids enhanced DR5/TRAIL-R2 expression, deoxycholic acid (DCA) was the most potent.

36 )/FXR, only chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) were able to stimulate a heterolo

37 Second, CDCA, deoxycholic acid (DCA), and other synthetic FXR agonists

38 Secondary bile acids, particularly deoxycholic acid (DCA), are implicated in promoting colo

39 a) determine if UDCA inhibits apoptosis from deoxycholic acid (DCA), as well as from ethanol, TGF-bet

40 Treatment of hepatocytes with deoxycholic acid (DCA), chenodeoxycholic acid (CDCA) or

41 Deoxycholic acid (DCA), chenodeoxycholic acid (CDCA), ta

42 CA, CDCA, and deoxycholic acid (DCA), fed as a supplement to the diet,

43 ransit, and an increase in the proportion of deoxycholic acid (DCA), have been implicated in the path

44 BAs (deoxycholic acid (DCA), taurolithocholic acid) and the s

45 ing with methyl-beta-cyclodextrin suppressed deoxycholic acid (DCA)-induced apoptosis, and staining f

46 Previously, we demonstrated that deoxycholic acid (DCA)-induced ERK1/2 and AKT signaling

47 Previously, we have demonstrated that deoxycholic acid (DCA)-induced signaling of extracellula

48 (AP-1) transcription factor was crucial for deoxycholic acid (DCA)-mediated GADD153 gene transcripti

49 use fecal secondary bile acids [particularly deoxycholic acid (DCA)] are considered to promote format

50 hepatocytes exposed to low concentrations of deoxycholic acid (DCA, 50 microM).

51 Bile acids (deoxycholic acid, DCA; taurocholic acid, TCA) activated

52 th the highly chaotropic bile salt detergent deoxycholic acid demonstrated that some Bdr paralogs may

53 id, 1-hydroxy-2-naphthoic acid, cholic acid, deoxycholic acid, dioctylsulfosuccinic acid, and pamoic

54 completed a total synthesis of enantiomeric deoxycholic acid (ent-DCA) from achiral 2-methyl-1,3-cyc

55 -LCA), chenodeoxycholic acid (ent-CDCA), and deoxycholic acid (ent-DCA) to induce toxicity and apopto

56 neurological decline, whereas cholic acid or deoxycholic acid feeding worsened AOM-induced neurologic

57 on in vitro assays with substrate preference deoxycholic acid > chenodeoxycholic acid > cholic acid >

58 Treatment of serum with 0.5% deoxycholic acid in the absence of salt produced HCV wit

59 s of cholic acid, chenodeoxycholic acid, and deoxycholic acid in their conjugated (glycine and taurin

60 the effects of chenodeoxycholic, cholic, and deoxycholic acid in unconjugated (CDCA, CA, and DCA) and

61 In wild-type hepatic macrophages, deoxycholic acid induced the association of Gal3 and NLR

62 Deoxycholic acid inhibited contractility of colonic long

63 Application of deoxycholic acid, lithocholic acid, or oleanolic acid (a

64 siRAGE) was delivered to myocardium by using deoxycholic acid-modified polyethylenimine (PEI-DA) as a

65 iated with HCV after treatment of serum with deoxycholic acid or NP-40, whereas ApoE was removed from

66 icant changes were detected for cholic acid, deoxycholic acid, or chenodeoxycholic acid.

67 sed with increasing temperature, addition of deoxycholic acid, or treatment with heparinase I.

68 an open-channel blocker, which may relate to deoxycholic acid permeation.

69 The ratio of dihomo-gamma-linolenic acid to deoxycholic acid species is a potential biomarker for th

70 brella conjugates, derived from cholic acid, deoxycholic acid, spermidine, lysine, and 5-mercapto-2-n

71 d with cholesterol, sitosterol, cholic acid, deoxycholic acid, ursodeoxycholic acid, cholestyramine,

72 etergents such as sodium dodecyl sulfate and deoxycholic acid were inhibitory.

73 ts low affinity for common bile acids except deoxycholic acid, which uniquely lacks a 7alpha-hydroxyl