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1 oxycholic, deoxycholic, ursodeoxycholic, and lithocholic acid.
2  were synthesized from either deoxycholic or lithocholic acid.
3 xylated bile acids, ursodeoxycholic acid and lithocholic acid.
4  (DTX-PC) and poly(ethylene glycol)-tethered lithocholic acid.
5 cholic acid, 43%; deoxycholic acid, 11%, and lithocholic acid, 1%.
6                           Among these, 3-oxo-lithocholic acid (3-oxo-LCA) and isoallo-LCA have been r
7 odeoxycholic acid (3alpha-OH, 7beta-OH), and lithocholic acid (3alpha-OH).
8  P. goldsteinii or its BA metabolite, 7-keto-lithocholic acid (7-keto-LCA), showed reduced aspirin-me
9                  We show that vitamin K2 and lithocholic acid, a by-product of intestinal flora, acti
10 GR5 agonists, taurochenodeoxycholic acid and lithocholic acid, activated AKT and inhibited GSK3beta,
11 evation of unconjugated deoxycholic acid and lithocholic acid activates the G-protein-coupled bile ac
12                                            N-Lithocholic acid acylated insulin [Lys(B29)-lithocholyl
13 ve to FAP, UC pouches have reduced levels of lithocholic acid and deoxycholic acid (normally the most
14                                              Lithocholic acid and deoxycholic acid, the principal lig
15           Furthermore, two of these ligands, lithocholic acid and estradiol disulfate, unexpectedly e
16 xycholic acid, higher conjugated fraction of lithocholic acid and hyodeoxycholic acid, and higher rat
17  analysis revealed a significant decrease in lithocholic acid and its derivatives after UDCA withdraw
18                                              Lithocholic acid and the synthetic GPBAR1 agonist, L3740
19 f free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the far
20                                   Total SBA, lithocholic acid, and deoxycholic acid concentrations we
21 c P450 that catalyzes 6beta-hydroxylation of lithocholic acid, and the pattern of GH secretion is dir
22 tor design entailed the functionalization of lithocholic acid at C(3) and at the cyclopentane ring si
23 d herein report the identification of 12-oxo-lithocholic acid (BAA485), a potential microbiome-derive
24 thinyl estradiol, chenodeoxycholic acid, and lithocholic acid by either PCN or TCDD in small intestin
25                                              Lithocholic acid causes colon cancer; thus, decreasing l
26                       However, the bile acid lithocholic acid competed efficiently with 9-cis-RA for
27                                              Lithocholic acid concentrations were positively correlat
28         Here, we develop a polyethyleneimine-lithocholic acid conjugate (2E'), which forms a hydropho
29 ine derivative of docetaxel (DTX)-conjugated lithocholic acid (DTX-PC) and poly(ethylene glycol)-teth
30 gate the ability of synthetic enantiomers of lithocholic acid (ent-LCA), chenodeoxycholic acid (ent-C
31 e report the first synthesis of enantiomeric lithocholic acid (ent-LCA, ent-1) and chenodeoxycholic a
32     Consistently, serum deoxycholic acid and lithocholic acid (FXR antagonists) were increased, and t
33        When 0.4% UDCA was added to the diet, lithocholic acid increased in the insoluble fraction (40
34 rations of secondary BA deoxycholic acid and lithocholic acid, indicating reduced activity of the nuc
35 n and ceramide(d18:1/18:1) treatment prevent lithocholic-acid-induced cell death in human-liver-deriv
36 d oxidative stress, whereas the secondary BA lithocholic acid inhibited T cell function through endop
37 enzymes that convert the secondary bile acid lithocholic acid into 3-oxoLCA as well as the abundant g
38 o being a ligand for the vitamin D receptor, lithocholic acid is also a substrate for CYP3A enzymes.
39 se A (SrtA 7M) was N-terminally labeled with lithocholic acid (LA)-an inexpensive bile acid that exhi
40                                   We studied lithocholic acid (LCA) (the natural 3alpha-OH isomer), g
41 that PXR is activated by the toxic bile acid lithocholic acid (LCA) and its 3-keto metabolite.
42 ntestinal levels of the bacterial metabolite lithocholic acid (LCA) are decreased after SG in mice an
43                       We recently identified lithocholic acid (LCA) as a small molecule able to block
44 o screening and confirmed by experiment that lithocholic acid (LCA) binds to the p53 binding sites of
45 patotoxicity of secondary bile acids such as lithocholic acid (LCA) by inducing expression of the hyd
46                       The endogenous steroid lithocholic acid (LCA) dilates cerebral arteries via BK
47                      Huh7 cells treated with lithocholic acid (LCA) exhibited a similar pattern of ch
48 rmin in interleukin 8 (IL-8) upregulation by lithocholic acid (LCA) in HCT116 colorectal cancer (CRC)
49 ue uptake, distribution, and cytotoxicity of lithocholic acid (LCA) in relation to various experiment
50                     The endogenous bile acid lithocholic acid (LCA) inhibits NAPE-PLD activity (with
51                                              Lithocholic acid (LCA) is accumulated in mammals during
52                                              Lithocholic acid (LCA) is an endogenous compound associa
53 rticular, the secondary bile acid derivative lithocholic acid (LCA) is highly hepatotoxic and, as we
54 E undergo a morphotype switch in response to lithocholic acid (LCA) to facilitate gastrointestinal (G
55                                              Lithocholic acid (LCA) treatment of primary human hepato
56 tes and identify two distinct derivatives of lithocholic acid (LCA), 3-oxoLCA and isoalloLCA, as T ce
57                                              Lithocholic acid (LCA), a bile acid implicated in the pr
58 in hospitalized patients. We discovered that lithocholic acid (LCA), a secondary bile acid prevalent
59               We investigated the effects of lithocholic acid (LCA), an inhibitor of the key BER enzy
60  metabolites such as deoxycholic acid (DCA), lithocholic acid (LCA), and ursodeoxycholic acid (UDCA)
61 roduction of hepatotoxic bile acids, such as lithocholic acid (LCA), because of limited small bowel a
62 l administration of secondary BAs, including lithocholic acid (LCA), deoxycholic acid, and 3-oxoLCA,
63         We show that a microbial metabolite, lithocholic acid (LCA), is increased in murine portal ve
64 ondary bile acids deoxycholic acid (DCA) and lithocholic acid (LCA), which accumulate at concentratio
65 ns as a receptor for the secondary bile acid lithocholic acid (LCA), which is hepatotoxic and a poten
66 mice confers a female-specific resistance to lithocholic acid (LCA)-induced hepatotoxicity and bile d
67 , acts also as a bile acid sensor by binding lithocholic acid (LCA).
68 o confer resistance to the hepatotoxicity of lithocholic acid (LCA).
69 ective response to the hydrophobic bile acid lithocholic acid (LCA).
70 ry bile acids, including various isoforms of lithocholic acid (LCA): iso-, 3-oxo-, allo-, 3-oxoallo-
71                    The GPBAR1 agonist, tauro-lithocholic acid (LCA, 10 microm) mimicked the effect of
72 c acid causes colon cancer; thus, decreasing lithocholic acid levels in the intestine by up-regulatin
73                            Administration of lithocholic acid or a vitamin D receptor agonist resulte
74             Application of deoxycholic acid, lithocholic acid, or oleanolic acid (a selective agonist
75          Women taking UDCA had higher faecal lithocholic acid (p < 0.0001), with more unconjugated bi
76      The stearic acid diet resulted in lower lithocholic acid (P = 0.01) and total secondary bile aci
77 sion was increased synergistically by RA and lithocholic acid (P<0.05).
78 s that an increased level of glyco and tauro lithocholic acid, perhaps because of a decreased capacit
79 lenic acid, cholenic acid 3beta-acetate, and lithocholic acid, respectively.
80 induction by BA pools is driven primarily by lithocholic acid signaling via the vitamin D receptor.
81 ary bile acids, such as deoxycholic acid and lithocholic acid, than those fed the LFCO or HFFO diets.
82 ng of the mitochondrial lipid composition by lithocholic acid treatment or by ablation of the lipid t
83                                 A regimen of lithocholic acid treatment, which was tolerated by wild-
84 ic acid (EC50=5.7 muM; its endogenous analog lithocholic acid was virtually equipotent), and the most
85  levels, with or without induction by RA and lithocholic acid, were determined by quantitative revers
86 n calcium homeostasis, or it is activated by lithocholic acid when its levels are elevated after a me