Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.4.99.6 (sialyltransferase)
 1,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The morphological changes induced by butyrate in HeLa cells and by monobutyryl or dibutyryl cAMP in CHO cells are prevented by micromolar concentrations of the divalent cation ionophore A23187. The ionophore is unable to prevent such changes in medium from which calcium is omitted. At slightly higher (but nontoxic) concentrations, the ionophore inhibits the butyrate-mediated induction of the ganglioside biosynthetic enzyme, sialyltransferase, in HeLa. In CHO, sialyltransferase activity is normally high and not altered by any of the compounds tested.
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PMID:Morphological changes in cultured mammalian cells: prevention by the calcium ionophore A23187. 16 98

The mononuclear cells separated from human blood by Ficoll-Hypaque centrifugation contained and released sialyltransferase, galactosyltransferase, and fucosyltransferase. Granulocytes contained and released lesser amounts of glycosyltransferases, whereas platelets released more fucosyltransferase than sialyltransferase or galactosyltransferase. When mononuclear cells were incubated with 12-O-tetradecanoyl-phorbol-13-acetate (TPA), the release of these three glycosyltransferases increased two- to six-fold, and cell suspension glycosyltransferase activities decreased 10-50%. Mononuclear cells were fractionated into lymphocytes and monocytes using baby hamster kidney cells microexudate-coated flasks. TPA stimulated the release of glycosyltransferases from lymphocytes but not from monocytes. The release of glycosyltransferases by TPA-treated mononuclear cells was not further stimulated by reincubation with TPA and was not affected by puromycin, cAMP, or cGMP. Concanavalin A, a mitogenic stimulator of lymphocytes, also stimulated the release of glycosyltransferases from mononuclear cells, but to a lesser extent. TPA did not stimulate the release of 5'-nucleotidase or decrease its activity on the cell pellet. Triton X-100 (0.2%) stimulated the release of glycosyltransferases to the same extent as TPA, but also caused the release of 5'-nucleotidase. [(3)H]TPA bound specifically and reversibly to mononuclear cells. The possible relationship between glycosyltransferase release and TPA effect on the plasma membrane is discussed.
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PMID:12-O-tetradecanoyl-phorbol-13-acetate release of glycosyltransferases from human blood cells. 644 9

The up- and downregulation of polysialic acid-neural cell adhesion molecule (PSA-NCAM) expression on motorneurons during development is associated respectively with target innervation and synaptogenesis, and is regulated at the level of PSA enzymatic biosynthesis involving specific polysialyltransferase activity. The purpose of this study has been to describe the cellular mechanisms by which that regulation might occur. It has been found that developmental regulation of PSA synthesis by ciliary ganglion motorneurons is not reflected in the levels of polysialyltransferase-1 (PST) or sialyltransferase-X (STX) mRNA. On the other hand, PSA synthesis in both the ciliary ganglion and the developing tectum appears to be coupled to the concentration of calcium in intracellular compartments. This study documents a calcium dependence of polysialyltransferase activity in a cell-free assay over the range of 0.1-1 mM, and a rapid sensitivity of new PSA synthesis, as measured in a pulse-chase analysis of tissue explants, to calcium ionophore perturbation of intracellular calcium levels. Moreover, the relevant calcium pool appears to be within a specific intracellular compartment that is sensitive to thapsigargin and does not directly reflect the level of cytosolic calcium. Perturbation of other major second messenger systems, such as cAMP and protein kinase-dependent pathways, did not affect polysialylation in the pulse chase analysis. These results suggest that the shuttling of calcium to different pools within the cell can result in the rapid regulation of PSA synthesis in developing tissues.
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PMID:Regulation of neural cell adhesion molecule polysialylation: evidence for nontranscriptional control and sensitivity to an intracellular pool of calcium. 949 Jul 30

This paper reviews experiments from this lab that have tested the hypothesis that pH of the Golgi (pH(G)) of cystic fibrosis (CF) airway epithelial cells is alkaline compared to normal, that this altered pH affects sialyltransferase and other Golgi enzymes controlling biochemical composition of the plasma membrane and that altered surface biochemistry increases bacterial binding. We generated a plasmid encoding a modified green fluorescence protein-sialyltransferase (GFP-ST) chimera protein that was pH-sensitive and localized to the Golgi when transfected into HeLa cells and also CF and normal or cystic fibrosis transmembrane conductance regulator- (CFTR)-corrected airway epithelial cells. Digital imaging microscopy of these Golgi-localized probes showed that there was no correlation between pH(G) (6.4-7.0) and the presence of CFTR, whether cells were in HCO(3)(-)/CO(2)-containing or in HCO(3)(-)/CO(2)-free solutions. Activation of CFTR by raising cell [cAMP] had no effect on pH(G). Thus, CFTR seemed not to be involved in controlling pH(G). Experiments on HeLa cells using an avidin-sialyltransferase chimera in combination with a pH-sensitive fluorescent biotin indicated that even in cells that do not express CFTR, Cl(-) and K(+) conductances of the Golgi and other organelle membranes were large and that pH(G) was controlled solely by the H(+) v-ATPase countered by a H(+) leak. A mathematical model was applied to these and other published data to calculate passive H(+) permeability (P(H+)) of the Golgi, endoplasmic reticulum, trans-Golgi network, recycling endosomes and secrety granules from a variety of cells. An organelle's acidity was inversely correlated to its calculated P(H+). We conclude that the CFTR plays a minor role in organelle pH regulation because other (Cl(-) and K(+)) channels are present in sufficient numbers to shunt voltages generated during H(+) pumping. Acidity of the Golgi (and perhaps other organelles) appears to be determined by the activity of H(+) pumps countered by H(+) leaks.
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PMID:Cystic fibrosis transmembrane conductance regulator and H+ permeability in regulation of Golgi pH. 1187 64