Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.4.99.7 (sialyltransferase)
1,534 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Cytidine-5'-monophospho-N-acetylneuraminic acid: (galactosyl-N-acetyl-galactosaminyl-(N-acetylneuraminyl)-galactosyl-glucosylceramide sialyltransferase (CMP-NAcNeu: monosialoganglioside (GM1) sialyltransferase) activity was demonstrated in the neurohypophysis of the rabbit. 2. Optimum activity occurred at pH 6.5 and required the presence of exogenous galactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl)-galactosyl-glucosylceramide (GM1 ganglioside), detergent (Triton X-100), and divalent cation (Mn2+, Mg2+ or Ca2+). 3. The product of the reaction was characterized as N-acetylneuraminyl-galactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl)-galactosyl-glucosylceramide (GD1a) by ascending thin-layer chromatography. 4. Physiological stimulation of vasopressin secretion, by the substitution of 2.2% NaCl for drinking water for 14 days, had no effect on the enzyme activiity or the ganglioside content of the tissue.
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PMID:Cytidine-5'-monophospho-N-acetylneuraminic acid galactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl)-galactosyl-glucosylceramide sialyltransferase in the neurohypophysis of the rabbit. 0 25

Four different glycolipid:glycosyltransferase activities involved in the biosynthesis in vitro of gangliosides and blood group-related glycosphingolipids have been tested in a simian virus 40-transformed glial cell culture derived from the cerebrum of a fetus with Tay-Sachs disease (TSD). The TSD cultured brain cells contained little activity of either UDP-Gal:GM2(beta 1-3)galactosyltransferase (GalT-3; EC 2.4.1.62), which catalyzes the formation of GM1a from GM2 (tay-Sachs) ganglioside, or GDP-Fuc:nLcOse4Cer (alpha 1-2)fucosyltransferase (FucT-2; EC 2.4.1.89), which catalyzes the formation of H1 glycolipid from nLcOse4Cer. These cells contained a potent inhibitor of the second reaction (catalyzed by a Golgi-rich membrane fraction from bovine spleen), whereas no inhibition of the first reaction (catalyzed by a membrane fraction from 14-day-old embryonic chicken brain) was observed. The activity of UDP-Gal:LcOse3Cer(beta 1-4)galactosyltransferase (GalT-4; EC 2.4.1.86) was 30- to 80-fold higher than the activity of GalT-3. The presence of CMP-AcNeu:nLcOse4Cer sialyltransferase activity and the absence of either GalT-3 or FucT-2 suggested a probable pathway for the synthesis of sialylneolactotetraosylceramide [GM1b(GlcNAc)] in addition to a specific blockage of GM1a ganglioside synthesis from GM2 in these TSD transformed cells.
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PMID:Differential activities of glycolipid glycosyltransferases in Tay-Sachs disease: studies in cultured cells from cerebrum. 29 63

The developmental pattern of gangliosides in human fetal brain should reflect the activities of the respective glycosyltransferases. LA2-synthase activity, along with that of GM3-, GD3-, GM2-, and GM1-synthases, was determined in human fetal brain at 10-22 weeks of gestation. LA2-synthase is the pivotal enzyme in lacto series ganglioside formation. LA2-synthase activity decreased during the study period, mirroring a similar temporal decline in levels of the lacto series gangliosides, particularly 3'-isoLM1. The developmental profiles of the ganglio series glycosyltransferase activities demonstrate distinct changes that correspond to the ganglioside pattern between fetal weeks 10 and 22. In particular, the marked increase in GM2-synthase activity at 20 and 22 weeks of gestation and the decline in GD3-synthase activity after 15 weeks could explain the prominent expression of the a series gangliosides in this period of rapid neuronal outgrowth. However, a similar decline (two- to 2.5-fold) in GM3-synthase activity suggests a more likely conclusion, namely, that the two sialyltransferase activities are derived mainly from astroglial cells, which show a marked proliferation during the 10-15th fetal weeks. The data do not negate the hypothesis that GM3- and GD3-synthase are the critical enzymes in the regulation of ganglioside biosynthesis but do indicate a need to reevaluate the significance of GM2-synthase in expression of the a series gangliosides.
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PMID:Glycosphingolipid glycosyltransferases in human fetal brain. 190 91

The acceptor specificities of four sialytransferases (I, II, IV and V) involved in ganglioside biosynthesis were studied in Golgi vesicles derived from rat liver. The activities of these sialytransferases were strongly detergent-dependent. Competition experiments with different detergent concentrations using LacCer (Gal beta 1----4Glc beta 1----1Cer), GM1a [Gal beta 1----3GalNAc beta 1----4(NeuAc alpha 2----3)Gal beta 1----4Glc beta 1----1Cer] and GD1b [Gal beta 1----3GalNAc beta 1----4(NeuAc alpha 2----8NeuAc alpha 2----3)Gal beta 1----4Glc beta 1----1Cer] as substrates, and as mutual inhibitors for ganglioside sialyltransferase activity, suggested that sialyltransferase IV was able to catalyze the sialyltransfer in alpha 2----3 linkage to the galactose residues of LacCer as well as of GM1a and GD1b. The other three sialyltransferases (I, II and V) seemed to be quite specific for their respective glycolipid acceptors, LacCer, GM3 and GM1b, GD1a and GT1b. Furthermore the kinetic data showed that sialyltransferase I was inactive at higher detergent concentrations (greater than 75 micrograms Triton CF-54); under these conditions, formation of GM3 and GD1a was catalyzed only by sialyltransferase IV. These results have been integrated into a model for ganglioside biosynthesis and its regulation.
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PMID:Substrate specificity of alpha 2----3-sialyltransferases in ganglioside biosynthesis of rat liver golgi. 199 63

Partial or total loss of chromosome 22 is often associated with tumors of the central nervous system and in particular with meningiomas. As in the case of other tumors, the ganglioside pattern is modified in transformed tissues. Cytogenetic analysis of 30 human meningiomas has been performed and the results compared to biochemical analysis of ganglioside distribution on the membrane surface. The meningiomas were divided into 2 groups on the basis of the presence or absence of chromosome 22. Thirteen tumors exhibited partial or total monosomy of the chromosome, whereas 17 were normal or showed other chromosomal anomalies. The GM3 and GD3 content of the meningiomas belonging to the 2 groups revealed a significant correlation between amount and reciprocal ratio of these 2 gangliosides and cytogenetic data. Tumors with monosomy 22 had a higher content of ganglioside GD3 than samples without monosomy 22, where the main ganglioside was GM3. Other gangliosides such as GM1, GD1a, GD1b and GT were present in various amounts in the 2 groups. Considering the biosynthetic pathway of gangliosides, we hypothesize the involvement of a gene located on chromosome 22 in the regulation of the enzymes which catalyze either GD3 synthesis (sialyltransferase 2, SAT-2) or its degradation to GM3 (neuraminidase).
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PMID:Correlation between cytogenetic data and ganglioside pattern in human meningiomas. 199 40

The role of acidic glycosphingolipids in cell growth and differentiation was investigated using the multipotent leukemia cell line K562. When GM3 was added to cell culture media, the growth of K562 cells was remarkably inhibited and the cells were shown to have megakaryocytoid morphology. Ultrastructural study demonstrated that K562 cells treated with GM3 had platelet peroxidase-positive structures, which were considered to be the specific marker of megakaryocyte. Furthermore, AP-3 directed against an epitope present on membrane glycoprotein IIIa reacted with the GM3-treated cells. Free N-acetylneuraminic acid, GM1, GM2, GD1a, and a mixture of bovine brain gangliosides containing GD1a and GT1b did not affect growth of K562 cells or show morphological changes. According to chemical analyses, GM3 content increased in megakaryocytoid differentiation induced by tetradecanoylphorbol-13-acetate, whereas GM3 decreased in erythroid differentiation induced by hemin. Enzymatic analysis showed that the GM3 increase during megakaryocytoid differentiation was a result of the sialyltransferase activation. These results indicated that exogenous GM3 induced differentiation of K562 cells into a "GM3-rich" lineage, i.e., mainly megakaryocytoid lineage, and that GM3 accumulation in the GM3-rich lineage was the result of the activation of GM3 synthase. These findings strongly suggested that GM3 ganglioside, a minor membrane component, has a crucial role in not only the differentiation induction but also the determination of the differentiation direction in pluripotent K562 cells.
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PMID:Ganglioside GM3 can induce megakaryocytoid differentiation of human leukemia cell line K562 cells. 200 80

An alpha 2----3 glycolipid galactosyl sialyltransferase (SAT3/4) has been partially purified from embryonic chicken skeletal muscle. It is preserved in 50 mM Hepes buffer (pH 6.8) containing 1% Triton CF-54 and 20% glycerol at -70 degrees C for a period of 6 months without loss of activity. The SAT3+4 preparation transfers sialic acid to nLcOse4Cer, nLcOse6Cer and GgOse4Cer with respective Km values of 1.4, 0.83 and 0.45 mM. The activity is stimulated 2-3-fold at high substrate concentration and 6-8-fold at low substrate concentration; 0.01 and 0.005 mumol for asialo GM1 and 0.025 and 0.01 mumol for other glycolipids in the presence of phosphatidylcholine (PC) and sphingomyelin (SM) at an optimum concentration 0.75%. A higher concentration is inhibitory. SM from chicken muscle is more effective than that from bovine brain and the stimulation is qualitatively proportional to that of the saturated fatty acyl content of SM. Free fatty acids (palmitic and stearic), their sodium salts, other choline compounds including choline chloride, phosphorylcholine and acetylcholine either do not have any effect or are inhibitory. Acetylcholine, even in the presence of SM and PC, is strongly inhibitory (70%).
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PMID:Biosynthesis of GM1b and similar neolactoseries gangliosides by a partially purified chicken skeletal muscle sialyltransferase. Effect of sphingomyelin and acetylcholine. 222 21

A CMP-NeuAc:GM1 alpha 2-3 sialyltransferase (GD1a synthase, 2.4.99.2) has been purified from the Triton extract of rat brain. The enzyme was purified and resolved by affinity chromatography on CDP-Sepharose column by a linear NaCl gradient elution. Final purification was achieved by elution from a 'GM1-acid'-Sepharose column. SDS-PAGE of the enzyme revealed a single protein band with an apparent Mr 44 kDa. It catalyzed specifically the sialylation of GD1b, GM1 and asialo-GM1. Enzyme products were identified by TLC in three different solvent systems. The Km value for GM1 was 7.5 x 10(-2) M, and for CMP-NeuAc it was 6.5 x 10(-5) M.
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PMID:Purification and characterization of CMP-NeuAc:GM1 (Gal beta 1-4GalNAc) alpha 2-3 sialyltransferase from rat brain. 226 6

The patterns of acidic and neutral glycosphingolipids (GSLs) were examined in a syngeneic tumour system in Balb/c mice consisting of closely related cell lines with different colonisation potentials directed to the murine lungs (in vivo selected highly metastatic sublines of L1-fibrosarcoma cells and their WGA-resistant mutants with low metastatic potential). GSLs were analysed by high-performance thin-layer chromatography and structurally identified by fast atom bombardment mass spectrometry combined with compositional analyses and exo-glycosidase digestion. The results suggest that highly metastatic sublines L1-LM and L1-LM12 derived by in vivo selection from mouse fibrosarcoma cells (cell line L1) exhibit a drastic increase of polar ganglioside expression and a restriction to globo-series GSLs. Contrasting with this the low metastatic mutant cells (L1-LM13WGA) express a reduced portion of acidic GSLs and exhibit a shift to less polar ganglioside components. Total cellular and plasma membrane-integrated GSLs were demonstrated to exhibit largely identical patterns. Concomitant with a significant decrease in LacCer expression a substantial reduction of GM2 and a complete lack of GM3 expression can be assigned to the highly metastatic sublines of L1-cells. On the other hand, the more polar gangliosides GM1a and, to an even greater extent, GD1a (exceeding 70% of total gangliosides) accumulate on L1-LM and their clonal sublines. The shift to acidic GSLs of higher polarity is less pronounced on the low metastatic WGA-resistant mutant cells (L1-LM13WGA) showing a preponderance of GM1a. The portion of GD1a within the fractions of acidic GSLs does not correspond to the cellular activities of CMP-NeuAc/GM1 (alpha 2-3) sialyltransferase measured for high and low metastatic cell variants. Total sialic acid content of the various cell lines differs, but is not associated with the metastatic potential. Gangliosides on L1-cells exhibit a significant substitution of N-glycolyl for N-acetylneuraminic acid (13%) compared to their metastatic sublines and to mutant cells (less than 1%). A conversion of surface exposed GD1a to GM1a on membranes of metastatic cells by in situ treatment with Vibrio cholerae sialidase is associated with a significant reduction of tumour cell colonisation directed to the murine lungs.
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PMID:Glycosphingolipid expression on murine L1-fibrosarcoma cells: analysis of clonal in vivo and in vitro selected sublines with different lung colonisation potential. 237 82

The enrichment of gangliosides in neuronal membranes suggests that they play an important role in CNS development. We recently found a marked tetrasialoganglioside deficiency in twl/twl mutant mouse embryos at embryonic day (E)-11. The recessive twl/twl mutants die at embryonic ages E-9 to E-18 from failed neural differentiation in the ventral portion of the neural tube. In the present study, we examined the composition and distribution of gangliosides in twl/twl mutant mouse embryos at E-12. The total ganglioside sialic acid concentration was significantly lower in the mutants than in normal (+/-) embryos. The mutants also expressed significant deficiencies of gangliosides in the "b" metabolic pathway (GD3, GD1b, GT1b, and GQ1b) and elevations in levels of gangliosides in the "a" metabolic pathway (GM3, GM2, GM1, and GD1a). These findings suggest that the mutants have a partial deficiency in the activity of a specific sialyltransferase in the b pathway. Regional ganglioside distribution was also studied in E-12 normal mouse embryos. The ganglioside composition in heads and bodies was similar to each other and to whole embryos. Total ganglioside concentration and the distribution of b pathway gangliosides were significantly higher in neural tube regions than in nonneural tube regions. These findings suggest that b pathway gangliosides accumulate in differentiating neural cells and that the deficiency of these gangliosides in the twl/twl mutants is closely associated with failed neural differentiation.
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PMID:Ganglioside composition of normal and mutant mouse embryos. 291 Oct 26


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