Disease relevance of cholate

• Sterilisation of hepatitis and HTLV-III viruses by exposure to tri(n-butyl)phosphate and sodium cholate [1].
• Blood product sterilisation with 0.3% tri(n-butyl)phosphate (TNBP)/0.2% sodium cholate (CA), a combination known to permit high recovery of factor VIII and factor IX, was evaluated for its effect on hepatitis B (HBV), non-A, non-B (NANB), and human T-lymphotropic type III (HTLV-III) viruses [1].
• Proteoliposomes were reconstituted by detergent dialysis of a sodium cholate extract of inverted vesicles derived from Escherichia coli plasma membrane [2].
• Membrane protein(s) responsible for the active transport of calcium in membrane vesicles from Mycobacterium phlei have been solubilized from membranes by sodium cholate treatment and partially purified using a hydrophobic resin [3].
• Crude membrane preparations from spleens of controls and patients representing the three clinical categories of Gaucher's disease were delipidated by extraction with sodium cholate and n-butanol [4].

High impact information on cholate

• Canine pancreas rough microsomes were solubilized in a high salt buffer containing sodium cholate, a detergent extract prepared by high speed centrifugation, and vesicles were reconstituted from the extract by a detergent dialysis procedure [5].
• In the presence of 10 mM sodium cholate, the CEH activity was maximal near pH 7 but was significant between pH 6 and 8 [6].
• Sepharose Cl-6B gel chromatography of photolabeled brain membranes solubilized with the nondenaturing detergent sodium cholate showed a radioactive complex with a Stoke's radius of 4.6 nm (Mr, 150,000) that may represent the intact sigma receptor complex [7].
• Göttingen miniature pigs were fed a semisynthetic diet containing 2% cholesterol and 1.1% sodium cholate [8].
• Analysis of the covalently labeled apamin binding protein/sodium cholate complex by density gradient centrifugation indicated a high molecular weight with S20,w = 20 S [9].

Chemical compound and disease context of cholate

• Exposure of Salmonella enterica to sodium cholate, sodium deoxycholate, sodium chenodeoxycholate, sodium glychocholate, sodium taurocholate, or sodium glycochenodeoxycholate induces the SOS response, indicating that the DNA-damaging activity of bile resides in bile salts [10].
• A multiple step procedure including treatment with 0.2% BPL, 0.05% sodium cholate, 10 mM BEI and 0.02% formaldehyde was designed to inactivate HIV-1 for use as an experimental vaccine [11].
• The effect of human bile juice and bile salts (sodium cholate, sodium taurocholate, sodium glycochenodeoxycholate and sodium chenodeoxycholate) on growth, sporulation and enterotoxin production by enterotoxin-positive and enterotoxin-negative strains of Clostridium perfringens was determined [12].
• Results showed that insignificant hemolysis from normal saline (P<0.05) occurred with the enhancer protamine sulphate while poly-l-arginine and sodium cholate demonstrated very low (<15%) hemolysis and caused insignificant protein and LDH release from the rat nasal mucosa [13].
• Mild hepatic fibrosis in cholesterol and sodium cholate diet-fed rats [14].

Biological context of cholate

• The saxitoxin (STX) binding protein has been solubilized by sodium cholate, both from axolemma and from synaptosomal membranes of mammalian brain [15].
• Among various bile salts tested, sodium cholate at a concentration of 1 microgram/microliter was found to be most effective in stimulating the hydrolysis of various glycosphingolipids with the exception of LacCer [16].
• The conformation of the binding site for PK11195 can be stabilized during solubilization in sodium cholate by relatively low concentrations of supplementary soybean lipid [17].
• The kinetics of recombination of sodium cholate solubilized opsin were also analyzed [18].
• Inhibitory activity was generally unaffected by anaerobiosis, light, changes in inoculum size or cation concentration, or addition of human serum or sodium cholate [19].

Anatomical context of cholate

• [3H]Perhydrohistrionicotoxin binding activity was largely reconstituted from 2% sodium cholate extracts of base-treated membranes [20].
• The apamin binding protein was solubilized from rat brain synaptic membranes using sodium cholate [9].
• The purification method involved solubilization of microsomes using sodium cholate, and recovery of cytochrome P-450 in the precipitate formed between 25 to 42% saturation of the digested microsomes with ammonium sulfate in the absence of glycerol [21].
• A 3beta-hydroxy-Delta5-C27-steroid dehydrogenase active in bile acid biosynthesis was purified from pig liver microsomes by solubilization with sodium cholate and by chromatography on DEAE-Sepharose, aminohexyl-Sepharose, and blue Sepharose [22].
• The turkey erythrocyte phospholipase C differed from the two mammalian phospholipases with respect to the effect of sodium cholate on the rate of polyphosphoinositide hydrolysis observed [23].

Associations of cholate with other chemical compounds

• The rate of dissolution of lecithin corresponding to formation of mixed micelles was studied in the presence of dihydroxy bile salts, sodium deoxycholate, sodium chenodeoxycholate, sodium ursodeoxycholate and one trihydroxy bile salt, sodium cholate [24].
• However, the slopes of these linear relationships for membranes treated with phospholipase A2 (m = 0.80), SDS (m = 0.94), and sodium cholate (m = 0.53) differed [25].
• The purification procedure included sodium cholate solubilization of total membranes followed by chromatography with DE53, Affi-Gel Blue, hydroxylapatite, Mono Q, and Superose 12 [26].
• In an incubation mixture of 50 microliters containing 30 nmol of GM1, 50 micrograms of sodium cholate, 20 microliters of 1-octanol, and 0.1 unit of CGase, the ratio between hydrolysis and transglycosylation was approximately 3:1 [27].
• Cytochrome P -450 was prepared either by sodium cholate treatment and ammonium sulfate fractionation or by subtilisin and sodium deoxycholate treatment followed by DEAE-cellulose chromatography [28].

Gene context of cholate

• Lecithin:cholesterol acyltransferase analysis, using reconstituted HDL particles prepared by the sodium cholate dialysis method, has shown that mutants (Pro165-->Ala,Gln172-->Glu) (Leu211-->Val,Leu214-->Val, Leu218-->Val,Leu219-->Val), Leu222-->Lys,Phe225-->Lys, Phe229-->Lys) and delta209-243 reduced LCAT activation (38-68%) [29].
• We further demonstrate that feeding mice with diets containing cholestyramine or sodium cholate increases mRNA-expression of ES-x in liver 2.5- to 3-fold [30].
• PLA2 activities in tissues and sera were quantitated by phosphatidyl-glycerol/sodium cholate mixed micelle assay [31].
• This study shows that sodium cholate is not necessary for the formation of atherosclerosis in LDLR(-/-) mice and that precisely defined semipurified diets are a valuable tool for the examination of diet-gene interactions [32].
• Artificial heterodimeric sigma 1, capable of NADPH oxidase activation, could be reconstituted in vitro by recombining purified monomeric rac1 p21 and rho GDI and removing the sodium cholate used to dissociate the native sigma 1 dimer [33].

Analytical, diagnostic and therapeutic context of cholate

• The purification method includes an aqueous two-phase separation technique, a treatment of the crude factor with sodium cholate and two successive column chromatographies on diethyl-aminoethyl-Sephadex A-50 [34].
• Activity of 7-alpha-Dehydroxylase was detected within a pH range of 5 to 9 and was 8-fold higher in specific activity in cell cultures in the presence of 0.1 mM sodium cholate than in its absence [35].
• Micellar electrokinetic chromatography (MEKC) with one kind of bile salt (sodium cholate) was used to separate three chiral polychlorinated biphenyls (PCBs; 84, 95, and 176), each one in its two enantiomers [36].
• The 400 MHz 1H-nuclear magnetic resonance spectrum of sodium cholate in dilute aqueous solution has been successfully resolved using a combination of decoupling, partial relaxation, and decoupled partial relaxation techniques [37].
• ApoE*3 Leiden mice developed marked hypercholesterolaemia, and early Type I 'fatty streak' lesions, following consumption of an atherogenic diet high in saturated fat and cholesterol, and containing sodium cholate, for up to 4 weeks [38].

References