Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of several inhibitors of oligosaccharide-processing on the high-affinity transport of D-aspartate was investigated in C6 glioma cells. Swainsonine, an inhibitor of mannosidase II, had no effect on the uptake of the amino acid. Castanospermine (100 micrograms/ml) and 1-deoxynojirimycin (1 mM), inhibitors of glucosidases, and 1-deoxymannojirimycin (1 mM), an inhibitor of mannosidase I, reduced the rate of transport by 35-45%. All inhibitory compounds decreased the Vmax for transport without affecting the Km which suggests that inhibition of oligosaccharide trimming reduces the number of competent transporters on the surface of the plasma membrane. Returning the cells to a drug-free medium for 24 h, following a 24 h exposure, resulted in complete recovery of uptake. Treatment of cells with neuraminidase from V. cholerae also decreased the Vmax for transport by about 20%. The results suggest that: (i) a partial complex carbohydrate chain on the high-affinity transporter for acidic amino acid transmitters is sufficient for activity and (ii) sialic acid residues may be necessary for normal operation of the transporter.
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PMID:Effect of inhibitors of N-linked oligosaccharide processing on the high-affinity transport of D-aspartate by C6 glioma cells. 153 37

In previous studies it was shown that cell surface oligosaccharide affinity class distributions and binding capacities were down-regulated as normal cells approach senescence. Using a sensitive, amplified, lectin/specific-ligand competition analysis three other growth regulation states were compared to that of cellular senescence. Non-senescent and senescent low-density and contact-induced growth inhibition was compared with neoplastic cell growth control. Non-senescent human fetal lung fibroblasts (IMR-90) down-regulated their mannosyl and galactosyl specificities in response to both low-density and contact-induced growth inhibition. Senescent IMR-90 down-regulate their mannosyl residues in response to contact conditions while they up-regulate their galactosyl residues under the same conditions. Growth-transformed transplantable canine glioma cells did not show density-dependent regulation of their cell surface oligosaccharide structures. Modulation of the CG cells with a specific alpha-mannosidase II inhibitor, Ricinus communis a galactosyl specific lectin, and pokeweed mitogen a cellular differentiating agent resulted in an altered growth phenotype and up-regulation of the mannosyl and galactosyl surface oligosaccharides. These data indicate a controller function for the cell surface oligosaccharides and a general influence on growth control.
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PMID:Cell surface oligosaccharide modulation during differentiation: IV. Normal and transformed cell growth control. 314 38