ライフサイエンスコーパス: cholate

1 an unconjugated bile salts (deoxycholate and cholate).

2 hain acyl-CoA synthetase (VLCS) can activate cholate.

3 uires an equal molar concentration of sodium cholate.

4 not reassociate upon the addition of sodium cholate.

5 old), but did not enhance absorption of (3)H-cholate.

6 olesterol, but repressed normally by dietary cholate.

7 alpha-hydroxylase transcription by FGFR4 and cholate.

8 CoA synthetases were incapable of activating cholate.

9 F subunit in all concentrations of Chaps and cholate.

10 ole for MrpF as an efflux system for Na+ and cholate.

11 onic acid, and a low concentration of sodium cholate.

12 rophilic or hydrophobic BS; and 4) 10 mmol/L cholate.

13 of both dimyristoylglycerophosphocholine and cholate.

14 icities, where mEH preferentially transports cholate.

15 lized equally from E2M11 membranes by sodium cholate.

16 ids, with CE and TG hydrolysis stimulated by cholate.

17 dium-dependent transport of taurocholate and cholate.

18 that for HDL3-CE at either 10 or 100 microM cholate.

19 to the unconventional aggregation of sodium cholate.

20 n the presence of solubilizing factor sodium cholate.

21 ith Bio-Beads SM-2 in the presence of sodium cholate.

22 le HDL and LDL to mixed micelles with sodium cholate.

23 titive solvents with as few as three or four cholates.

24 a monomer to prepare amide-linked oligomeric cholates.

25 h EYPC/taurochenodeoxycholate = 0.6 and EYPC/cholate = 1.0 in 0.15 M NaCl, independent micelles grow

26 The systems EYPC/cholate = 1.0 in 0.4 M NaCl, EYPC/cholate = 1.2 in 0.15

27 stems EYPC/cholate = 1.0 in 0.4 M NaCl, EYPC/cholate = 1.2 in 0.15 M NaCl, and EYPC/octyl glucoside =

28 ed with purified porcine CEL without or with cholate (10 or 100 microM, concentrations achievable in

29 e (Cyp8b1) in mice prevents the synthesis of cholate, a primary bile acid, and its metabolites.

30 very of (3)H-taurocholate ((3)H-TC) and (3)H-cholate administered into proximal and distal intestines

31 ide, dodecyl maltoside, Tween 20, and sodium cholate allow varying degrees of Bax hetero- and homodim

32 Solubilization of rhodopsin in cholate allowed binding of the antibody, but the binding

33 rast, beta gamma in ionic detergents such as cholate and 3-[(cholamidopropyl)diethylammonio]-1-propan

34 ains underneath the concave steroid rings of cholate and capping with another rigid, symmetrically tr

35 ma2 subunit was disrupted in two detergents, cholate and Chaps (3-[(3-cholamidopropyl) dimethylammoni

36 MR and DSF, it was shown that the bile salts cholate and chenodeoxycholate interact with purified Tox

37 M demonstrated that the transporter binds to cholate and deoxycholate with micromolar affinity, and t

38 Surprisingly, cholate and deoxycholate, two of the most abundant and v

39 In wild-type mice, cholate and diosgenin both increased biliary cholesterol

40 biliary cholesterol secretion in response to cholate and diosgenin, but the choleretic effects of the

41 lesterol and by the non-cholesterol steroids cholate and diosgenin.

42 human plasma lipoproteins (TLP) with sodium cholate and its subsequent removal, has been used to stu

43 Among several determinants of cholate and lysozyme resistance in E. faecalis, IreK was

44 h concentrations of GIT antimicrobials, like cholate and lysozyme, leading us to hypothesize that res

45 Second, reutilization of cholate and other C24 bile acids requires reactivation p

46 wo 15-hLO isozymes and demonstrate that both cholate and specific LO products affect substrate specif

47 ining mixed micelles composed of bile salts (cholate and taurochenodeoxycholate, both cholanoyl deriv

48 Conjugated cholate and taurocholate directly and secondary to prima

49 Here we show that cholate and taurocholate elicit more dramatic Ca(2+) sig

50 Sodium cholate and taurocholate induced cytosolic Ca(2+) elevat

51 nation of C. difficile spores in response to cholate and taurocholate.

52 the fatty acid palmitate, and the bile acids cholate and taurocholate.

53 amples were solubilized with octyl glucoside/cholate and the subunit a was purified via the oligohist

54 l centrifugation and solubilized with sodium cholate and urea.

55 was strongly influenced by the number of the cholates and the topology of the scaffold.

56 uding the use of amides, mixed amide esters, cholate, and alkyl bridges, was explored.

57 n of GAPDH prevented repression of CYP7A1 by cholate, and blocking nuclear transport of nitrosylated

58 s, mixed micelles of phosphatidylcholine and cholate, and in vivo with native spherical lipoprotein p

59 , polydocanol, dodecyl maltoside, and sodium cholate, and no exposure of this epitope was observed in

60 different detergents, RapiGest SP and sodium cholate, and two different trypsins, sequencing grade mo

61 The results implicate cholate as an important negative regulator of bile acid

62 also exhibited sodium-dependent transport of cholate at levels 150% of taurocholate in contrast to he

63 We describe cholate-based cage amphiphiles with a unique architectur

64 Dye- and cholate-binding functions can be separated on sequences

65 Alkyl and cholate bridges were significantly less potent against H

66 than larger, more flexible ones because the cholate building blocks in the latter could rotate outwa

67 phosphatidylcholine followed by removing the cholate by dialysis.

68 6% kcal from fat and 2% cholesterol and 0.7% cholate by weight) (atherogenic diet group, n = 13), and

69 gh-fat/high-cholesterol (HF), control and 1% cholate (CA) and HF + CA.

70 , galactose elimination capacity (GEC), dual cholate (CA) clearances and shunt, perfused hepatic mass

71 henodeoxycholate (CDCA), deoxycholate (DCA), cholate (CA), and ursodeoxycholate (UDCA), act as select

72 hosphatidylcholine with the bile salts (BSs) cholate (Ch), glycocholate (GC), chenodeoxycholate (CDC)

73 O mice on the C57BL/6J background when fed a cholate-cholesterol diet.

74 expressed in COS-1 cells, hVLCS-H2 exhibited cholate:CoA ligase (choloyl-CoA synthetase) activity wit

75 the full-length A22 will bind either dye or cholate columns and elute with the other ligand, as if b

76 g an amino group at the C(3) position of the cholate component markedly increased potency (IC50 value

77 These results establish that cholesterol and cholate components of the Ath diet have distinct proathe

78 in-associated CE (4 microM), with increasing cholate concentration there was an increase in the hydro

79 in 20 mM phospholipid requires 50 mM sodium cholate, concentrations that are commonly used to recons

80 se plasma lipoprotein levels and, when fed a cholate-containing diet, decrease foam-cell lesion size.

81 tar-like copolymer emanating from the methyl cholate core provided the requisite modification in the

82 is induced in the presence of the bile salts cholate, deoxycholate, and chenodeoxycholate, and EMSA s

83 Expression pattern and cholate-dependent, cholesterol-induced hepatomegaly in t

84 We found that cholate derivatives and the amino acid glycine act as co

85 Some cholate derivatives that are normal components of bile c

86 eroidal)-4,7-ACQ derivatives and bis(4,7-ACQ)cholate derivatives; both classes provided inhibitors wi

87 fts in both of these cell lines and that the cholate detergent removed cholesterol from these microdo

88 d through partial solubilization with sodium cholate detergent, and the partially purified receptor c

89 tituted HDL particles prepared by the sodium cholate dialysis method, has shown that mutants (Pro165-

90 1ra knockout C57BL/6J mice fed a cholesterol/cholate diet for 3 mo had a 3-fold decrease in non-high-

91 In contrast to cholate, diosgenin treatment did not affect G5G8 express

92 treated with the above antibody in DM and in cholate, enhanced destabilization (5-fold) was observed

93 Cholate esters with phenylurea groups at the 7alpha- and

94 Cholesterol/cholate feeding resulted in down-regulation of intestina

95 Cholate feeding to rats with intact enterohepatic circul

96 The conformations of three cholate foldamers and one molecular basket were studied

97 constituted into lipid bilayers by mixing in cholate followed by dilution to re-form membranes.

98 g single-walled carbon nanotubes with sodium cholate, followed by surfactant exchange to form phospho

99 15% fat, 1.25% cholesterol, and 0.5% sodium cholate for 12 weeks, and atherosclerotic lesions at the

100 -48-deficient mice fed Paigen's diet without cholate for 20 weeks received rPAI-1(23) treatment (n=21

101 LA2 with the naturally occurring bile salts: cholate, glycocholate, taurocholate, glycochenodeoxychol

102 rom the immobilized gamma2HF subunit using a cholate gradient from 0.05 to 1.0% and greater than 40%

103 e obtained by attaching facially amphiphilic cholate groups to a covalent scaffold (calix[4]arene or

104 ained by attaching four facially amphiphilic cholate groups to a tetraaminocalixarene scaffold.

105 between the cholates) require at least five cholate groups to fold cooperatively, the 4-aminobutyroy

106 energy transfer (FRET) occurred readily in a cholate hexamer labeled with a naphthyl donor and a dans

107 In contrast to the parent cholate hexamer that folded in all micelles investigated

108 The conformation of a cholate hexamer with a clicked tether in between two tri

109 Mice fed high fat, high cholesterol, cholate (HFHCC) diet for three weeks consistently develo

110 a high-cholesterol/high-fat diet containing cholate, however, a statistically significant 40% decrea

111 GF19 each increased the ratio of muricholate:cholate in bile, inducing a more hydrophilic bile salt p

112 ms induced by an atherogenic diet containing cholate in mice deficient in apolipoprotein E.

113 nylpropionic acid, N-acetylglycoprotein, and cholate in samples from female animals.

114 atio, 0.57; P = 0.004) and higher conjugated cholate increased the likelihood of significant fibrosis

115 Cholate induced binding of SHP to HDAC2 and its recruitm

116 In contrast, cholate induced expression of genes involved in extracel

117 epatocytes, L-NAME or dithiothreitol blocked cholate-induced down-regulation of CYP7A1 without impair

118 lear transport of nitrosylated GAPDH reduced cholate-induced nitrosylation of HDAC2 and SIRT1; this e

119 Since cholate is a known potent inhibitor of bovine oxidase an

120 Sodium cholate is critical because it does not interfere with t

121 Elution with 10 mmol/L cholate may introduce artifactual gel-filtration peaks a

122 tenuating amphiphile charge density within a cholate micelle environment.

123 he anionic sodium dodecyl sulfate and sodium cholate micelle systems.

124 r-HDL were made from cholate mixed micelles that contained PC, apo AI, and, i

125 In the presence of cholate, multiple equivalents of cationic charge were re

126 In the absence of surfactant (sodium cholate, NaC), multilayer graphene had higher adsorption

127 a polar solvent (e.g., alcohol or DMSO), the cholate oligomer folded into a helix with the hydrophili

128 These cholate oligomers fold into helical structures with nano

129 n found previously to enhance the folding of cholate oligomers in homogeneous solution.

130 F nor mrpFG expression in trans enhanced the cholate or Na+ resistance of the null mutant.

131 5% cholesterol supplemented with 0.5% sodium cholate) or given methotrexate intraperitoneally.

132 of the Ath diet in which either cholesterol, cholate, or fat were omitted.

133 An eluant of 10 mmol/L cholate overestimated vesicular cholesterol and in conce

134 o unconjugated chenodeoxycholate (P = 0.04), cholate (P = 0.0004), and total primary BAs (P < 0.0001)

135 Membrane additives such as cholate produced a 2-fold increase in protein-vesicle yi

136 Deoxycholate, a metabolite of cholate produced by the normal intestinal flora, also in

137 Dietary cholesterol and cholate produced discrete gene expression patterns.

138 In hepatocytes, cholate promoted S-nitrosylation of GAPDH and its transl

139 These studies suggest that dietary cholate regulates plasma levels of apoA-I primarily by a

140 ible, 4-aminobutyroyl spacers in between the cholate repeat units had been found previously to enhanc

141 lates (with no spacing groups in between the cholates) require at least five cholate groups to fold c

142 uggest that functions in addition to Na+ and cholate resistance and pH homeostasis will be found amon

143 Cholate restores CYP7A1 regulation in vivo and in vitro.

144 homeostasis in male Wistar rats placed on a cholate-rich diet for 5 days and in cultured primary hep

145 Rats placed on cholate-rich diets and given L-NAME had increased intrah

146 line, which required no additions to the 2% cholate s/i buffer.

147 e of sodium dodecyl sulfate (SDS) and sodium cholate (SC) in aqueous solutions with and without semic

148 rsely, dimerization of CcO induced by sodium cholate significantly increases its kinetic stability of

149 Other detergents, e.g., Tween 20, sodium cholate, sodium deoxycholate, CHAPS, or CHAPSO, are comp

150 pon the addition of bile salts, e.g., sodium cholate, sodium deoxycholate, or CHAPS.

151 CNTs coated with various surfactants (sodium cholate, sodium dodecyl sulfate, and cetyl trimethylammo

152 quired the addition of cholesterol to the 2% cholate solubilization/immobilization (s/i) buffer and t

153 In Triton X-100 and sodium cholate solutions, the aggregated, unfolded, and folded

154 Cholate-stimulated ATP hydrolysis was maximal at concent

155 y demonstrating in human aortic homogenate a cholate-stimulated cholesteryl ester hydrolytic activity

156 Feeding a cholate-supplemented diet (0.1%) resulted in a completel

157 Nonconjugated cholate supported the highest ATPase activity in ABCG5/G

158 this study, we describe the use of a sodium cholate suspension-dialysis method to adsorb the redox e

159 ell as those determined for benchmark sodium cholate suspensions of (6,5) SWNTs, are similar; likewis

160 The cyclic cholate tetramer, however, was more effective at permeat

161 A traW mutant was 100-fold more sensitive to cholate than the tra(+) strain but only marginally more

162 ydrolysis of LDL- and HDL3-CE; at 100 microM cholate, the present hydrolysis per hour was 32+/-2 and

163 herogenic diet rich in fat, cholesterol, and cholate, they rapidly developed hypercholesterolemia, at

164 of trimethylene carbonate (TMC) from methyl cholate through a combination of metal-free organo-catal

165 The total cholate to chenodeoxycholate ratio was significantly hig

166 After intravenous administration of cholate to Oatp1b2-null mice, its clearance was 50% lowe

167 den mice and did not require the addition of cholate to the diet.

168 lecules utilize the hydrophilic faces of the cholates to bind hydrophilic molecules such as glucose d

169 olecules employ the hydrophobic faces of the cholates to bind hydrophobic guests.

170 t stable in structures that allowed multiple cholates to form a microenvironment that could efficient

171 aurocholate in contrast to hepatocytes where cholate transport is only 30% of taurocholate levels, su

172 ion (88%) from DIDS inhibition of hepatocyte cholate transport, suggesting that taurocholate is also

173 In the cholate-treated NDH-1-enriched P. denitrificans membrane

174 Cholate treatment was associated with a farnesoid X rece

175 lvent (i.e., DMSO), the hydrophilic faces of cholates turned inward to form a reversed-micelle-like c

176 to a helix with the hydrophilic faces of the cholates turned inward.

177 olecular basket was obtained by linking four cholate units to a cone-shaped calix[4]arene scaffold th

178 s with 4-aminobutyroyl groups in between the cholate units were labeled with a naphthyl and a dansyl

179 levation of circulating serum amyloid A, and cholate was required for accumulation of collagen in the

180 l)dimethylammonio]-1-propanesulfonic acid or cholate), was purified to near-homogeneity by a single n

181 ium thermoautotrophicum was solubilized from cholate-washed membranes with Zwittergent 3-14 at 58 deg

182 ential solvation of the hydrophilic faces of cholates within the molecule by the polar solvent was co