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PubMed1985

Purification and properties of gamma-oxalomesaconate hydratase from Pseudomonas ochraceae grown with phthalate.

Pseudomonas ochraceae produced inducibly a hydro-lyase which catalyzes the reversible conversion of gamma-oxalomesaconate into (-)-gamma-oxalocitramalate. The enzyme has been purified to homogeneity from the bacteria grown with phthalate. The enzyme was a dimeric protein (pI=4.9) with a Mr of 68,000 and showed a high specificity for gamma-oxalomesaconate (Km=14 microM) and (-)-gamma-oxalocitramalate (Km=6.4 microM). Equilibrium constant for the hydration of gamma-oxalomesaconate at pH 8.0 and 24 degrees C was 2.5. Various thiols activated the enzyme.

Bacterial Proteins↗
PubMed1988

Characterization of the inhibition of U46619-mediated human platelet activation by the trimetoquinol isomers. Evidence for endoperoxide/thromboxane A2 receptor blockade.

Sites of inhibition for the trimetoquinol (TMQ) isomers on 15S-hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5Z,13E-dienoic acid (U46619)-, 12-O-tetradecanoylphorbol 13-acetate (TPA)- and A23187-induced human platelet activation were investigated. Experiments using washed human platelets were designed to characterize relationships among functional (aggregation, secretion) and biochemical (protein phosphorylation, metabolism of inositol phospholipids and radioligand displacement analysis) processes of platelet activation by U46619 and the specificity of inhibition by the TMQ isomers. Thromboxane A2 receptor stimulation by U46619 in human platelets resulted in a time- and concentration-dependent breakdown of inositol phospholipids [phosphatidylinositol 4,5-bisphosphate (PIP2), phosphatidylinositol 4-monophosphate (PIP), and phosphatidylinositol (PI)], phosphatidic acid (PA) accumulation, phosphorylation of 20 and 45 kD proteins, aggregation and serotonin secretion. The TMQ isomers stereoselectively inhibited all U46619-mediated platelet activation processes. R(+)-TMQ was 40- and 22-fold more potent than S(-)-TMQ as an inhibitor of U46619-induced platelet aggregation and serotonin secretion respectively. In addition, R(+)-TMQ blocked U46619-induced 20 kD protein phosphorylation, 45 kD protein phosphorylation, PIP2, PIP and PI breakdown, and PA accumulation with a potency which was 8-, 13-, 45-, 37-, 33- and 33-fold greater than the S(-)-isomer respectively. In contrast to S(-)-TMQ, R(+)-TMQ produced a concentration-dependent inhibition of specific [3H]U46619 binding to endoperoxide/thromboxane A2 receptor sites in washed platelets. In other experiments, S(-)-TMQ was more potent than R(+)-TMQ as an inhibitor of TPA- and A23187-induced platelet aggregation and serotonin secretion, and of TPA-induced phosphorylation of 45 and 20 kD proteins. The inhibitory potencies of S(-)-TMQ against TPA- or A23187-induced responses were similar to those needed for antagonism of U46619-mediated platelet activation. In contrast, much higher concentrations of R(+)-TMQ were required for blockade of TPA or A23187 versus U46619-mediated responses in human platelets. Taken collectively, the data show that the TMQ isomers interfered with the endoperoxide/thromboxane A2 receptor-mediated phospholipase C-signal cascade of inositol phospholipid hydrolysis, calcium mobilization, and protein phosphorylation leading to platelet aggregation and secretion. R(+)-TMQ acted as a pharmacologically selective and highly stereospecific [R(+)-TMQ much greater than S(-)-TMQ] antagonist of endoperoxide/thromboxane A2 receptor sites in platelets.(ABSTRACT TRUNCATED AT 400 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1983

Synthesis of a nona- and an undeca-saccharide that form part of the complex type of carbohydrate moiety of glycoproteins.

Silver trifluoromethanesulfonate-promoted condensation of 3,6-di-O-acetyl-2-deoxy-2-phthalimido-4-O-(2,3,4,6-tetra-O-acetyl-beta-D- galactopyranosyl)-beta-D-glucopyranosyl bromide with benzyl 2,4,-di-O-benzyl-6-O-(3,4-di-O-benzyl-alpha-D-mannopyranosyl)-3-O-(3,6-di-O- benzyl-alpha-D-mannopyranosyl)-alpha-D-mannopyranoside gave nonasaccharide and undecasaccharide derivatives. The nonasaccharide 2 and the undecasaccharide 3 were obtained by removal of the protecting groups followed by N-acetylation. (formula; see text).

Carbohydrate Conformation↗
PubMed1983

[Synthesis of beta-L-rhamnoside linked oligosaccharides of lipopolysaccharides from Shigella flexneri serotype 6].

The synthesis of the trisaccharide O-beta-L-rhamnopyranosyl-(1 leads to 4)-O-beta-L-rhamnopyranosyl-(1 leads to 2)-L-rhamnopyranose (14) and the tetrasaccharide O-2-acetamido-2-deoxy-beta-D-galactopyranosyl)-(1 leads to 2)-O-[beta-L-rhamnopyranosyl-(1 leads to 4)]-O-beta-L-rhamnopyranosyl-(1 leads to 2)-L-rhamnopyranose (21) is described. The latter structure has been proposed as the repeating unit of the O-specific side-chain of the lipopolysaccharide obtained from Shigella flexneri Serotype 6. The key-intermediate was 4-O-acetyl-2-O-allyl-3-O-benzyl-alpha-D-rhamnopyranosyl bromide, which was first linked to benzyl 3,4-di-O-benzyl-alpha-L-rhamnopyranoside, to give a blocked beta-linked disaccharide. This was O-deacetylated and coupled with 2,3,4-tri-O-benzyl-alpha-L-rhamnopyranosyl bromide at O-4' to afford benzyl O-(2,3,4-tri-O-benzyl-beta-L-rhamnopyranosyl)-(1 leads to 4)-O-(2-O-allyl-3-O-benzyl-beta-L-rhamnopyranosyl)-(1 leads to 2)-3,4-di-O-benzyl-alpha-L-rhamnopyranoside (11), which was deprotected to give 14. Deallylation of 11 and coupling with 6-O-acetyl-2-azido-3,4-di-O-benzyl-2-deoxy-alpha-D-galactopyranosyl bromide led to a protected tetrasaccharide from which 21 was obtained. The method of catalysis by silver silicate was employed to obtain the beta-glycosidic linkage of all monosaccharide units.

Carbohydrate Conformation↗
PubMed1983

Synthesis and conformational properties of methyl 6,6-di-C-methyl-beta-D-galactopyranoside. Probes for the combining sites of D-galactosyl-binding proteins.

The binding of D-galactopyranosyl groups by lectins and antibodies can involve the 5-hydroxymethyl group. In order to examine the nature of these binding reactions, it was of interest to synthesize 6,6-di-C-methyl-D-galactose which was found to exist, like D-galactose, extensively in the pyranose forms. 2,3,4,6-Tetra-O-acetyl-7-deoxy-6-C-methyl-alpha-D-galacto-heptopyranosyl bromide was prepared under standard conditions and converted into methyl 6,6-di-C methyl-beta-D-galactopyranoside (6). Evidence based on 13C-n.m.r. studies indicates that the favored conformer of 6 has O-4 and O-6 in syn-axial-like relationship. General comments are presented on the nature of the binding of oligosaccharides by proteins.

Binding Sites↗
PubMed1983

Structure of the 3-deoxy-D-manno-octulosonic acid-(KDO)-containing capsular polysaccharide (K14 antigen) from Escherichia coli 06:K14:H31.

The chemical structure of the K14-antigenic polysaccharide (K14 antigen) of Escherichia coli 06:K14:H31 was elucidated by determination of the composition, 1H- and 13C-n.m.r. spectroscopy, periodate oxidation, and study of the oligosaccharides obtained by partial hydrolysis. The polysaccharide consists of [O-(2-acetamido-2-deoxy-beta-D-galactopyranosyl)-(1 leads to 5)-O-(3-deoxy-beta-D-manno-octulopyranosylonic acid)-(2 leads to 6)] repeating units, approximately 60% of the octonic acid units being O-acetylated and approximately 10% O-propionylated at O-8. The sequence of acetylated and propionylated residues is not known. The serologically-specific part of the K14 antigen residues in the polysaccharide part.

Bacterial Capsules↗
PubMed1983

Oligosaccharides from "standardized intermediates". Synthesis of a branched tetrasaccharide glycoside isomeric with the blood-group B, type 2 determinant.

Building block derivatives of the component monosaccharides were used to construct the tetrasaccharide glycoside 15, in which an alpha-D-Galp-(1 leads to 4)-D-Gal linkage replaces the alpha-(1 leads to 3) linkage of the human blood-group B, type 2, determinant structure. The initial coupling of 2-O-benzoyl-3,6-di-O-benzyl-4-O-(tetrahydropyran-2-yl)-alpha-D-galactopyranosyl chloride to allyl 2-acetamido-3,6-di-O-benzyl-2-deoxy-beta-D-glucopyranoside was followed by selective deprotection of the disaccharide product, either at O-4' (to give 8) or O-2' (to give 3). The conversion of 8 into 15 involved successive coupling with tetra-O-benzyl-alpha-D-galactopyranosyl bromide (8 leads to 11), O-debenzoylation at O-2' (11 leads to 12), coupling with tri-O-benzyl-alpha-L-fucopyranosyl bromide (12 leads to 14), and O-debenzylation by hydrogenolysis (14 leads to 15). Alternatively, 3 was alpha-L-fucosylated to give 6, and 6 was selectively deprotected at O-4' to give 7. However, attempts to alpha-D-galactosylate 7 were unsuccessful. The unsubstituted forms of the intermediate disaccharide (8) and trisaccharide (12) glycosides were obtained by appropriate deblocking procedures.

ABO Blood-Group System↗
PubMed1983

Oligosaccharides from "standardized intermediates". The 2-amino-2-deoxy-D-galactose analog of the blood-group O(H) determinant, type 2, and its precursors.

The selectively benzylated glycoside allyl 2-acetamido-4,6-di-O-benzyl-2-deoxy-beta-D-galactopranoside (4) was prepared from the corresponding derivative of 2-acetamido-2-deoxy-D-glucose via the p-bromobenzenesulfonate and the benzoate. 2-O-Benzoyl-3,4,6-tri-O-benzyl-alpha-D-galactopyranosyl (10) was obtained from allyl 6-O-benzyl-2-O-(2-butenyl)-alpha-D-galactopyranoside via known intermediates. To complete the sequence, the 1-propenyl 3,4,6-tri-O-benzyl galactoside was successively converted into the 2-benzoate, the free sugar, and the chloride 10. A fully protected form (11) of the trisaccharide alpha-L-Fucp-(1 leads to 2)-beta-D-Galp-(1 leads to 4)-D-GalNAc was then synthesized by coupling 10 to 4, partially deblocking the disaccharide product, and L-fucosylating the resulting intermediate. Cleavage of the O-benzyl groups from 11, with concomitant saturation of the allyl group, gave the propyl beta-glycoside of the unsubstituted trisaccharide.

ABO Blood-Group System↗