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)

A pronounced effect of concanavalin A (Con A) upon activity of ecto-5'-nucleotidase of intact C6 glioma cells in culture has been demonstrated. A near linear rate of decrease in 5'-nucleotidase activity was observed upon treatment with concentrations of Con A up to 0.25 muM. Nonspecific phosphatase activity and Ca2+-dependent ATPase activity were not inhibited by Con A treatment of the cells. Of the total 5'-nucleotidase activity of C6 cells (Vmax = 5.0 mumol of Pi liberated/mg of cell protein/hour), approximately 20% still remained after treatment with high concentrations of Con A. The inhibitory effect of Con A operated to reduce substantially Vmax for ecto-5'-nucleotidase. Inhibition was reversed by briefly incubating the Con A-treated cells with alpha-methyl-D-glucoside, or alpha-methyl-D-mannoside, the later being more effective. These findings suggest that a relatively specific, reversible, inhibition of ecto-5'-nucleotidase results from Con A binding to the surface of the intact cultured mammalian cells.
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PMID:Concanavalin A inhibition of ecto-5'-nucleotidase of intact cultured C6 glioma cells. 12 59

Myosin has been isolated from the clonal lines of murine neuroblastoma and rat glioma cells. Partial characterization of the two cellular myosins indicates that both possess the following properties: (1) the same elution position as rabbit skeletal muscle myosin by Sepharose 4B chromatography; (2) the presence of heavy (molecular weight about 200,000) and light subunit polypeptides by sodium dodecyl sulfate polyacrylamide gel electrophoresis; (3) EDTA and Ca2+ activated but Mg2+-inhibited ATPase activity in 0.6 M KCl; and (4) binding to rabbit skeletal muscle F-actin which is inhibited by Mg2+-ATP. For both mouse neuroblastoma and rat glioma cells, approximately 0.5-1.5% of the total cell protein is present as myosin. Cellular myosin appears to be indistinguishable in quantity and biochemical properties regardless of whether it is isolated from monolayer or suspension neuroblastoma cells.
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PMID:Isolation and characterization of myosin from cloned rat glioma and mouse neuroblastoma cells. 13 25

Catecholamines cause an elevation of both cyclic GMP and cyclic AMP levels in the rat C-6 glioma cell line. The response is mediated by a beta-receptor, with a Ka for stimulation of cyclic GMP of 2.6 X 10(-7)M. Maximum levels of cyclic GMP are reached by 5 min. whereas cyclic AMP levels are maximal by 10 min. Removal of calcium decreases the cyclic GMP elevation by 60%. Refractoriness to a second treatment with catecholamine develops for both responses. Catecholamine sensitivity of the cyclic GMP-generating system appears in the cells only as they start to contact and enter the stationary growth phase. In contrast to the effects of catecholamines, cholinergic agonists have no effect on either cyclic GMP or cyclic AMP levels.
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PMID:Catecholamine-mediated elevation of cyclic GMP in the rat C-6 glioma cell line. 18 27

Synapses form between cells of a neuroblastoma X glioma hybrid clone and cultured mouse skeletal myotubes. The synapses are cholinergic, and the acetylcholine release mechanism is dependent on calcium ions. The transmitter output of the synapses is low, with considerable variability in the latency and amplitude of the postsynaptic responses to presynaptic action potentials. The fine structure of physiologically identified functional junctions was examined electron microscopically. Small (50 nm) clear vesicles were seen presynaptically and there were areas with a wide (approx. 50 nm) gap containing basement membrane-like material between the pre- and postsynaptic cells. In addition, in some regions there was a densely staining material lining the muscle membrane and some suggestion of infolding of the muscle membrane. In none of the cases, however, have areas been found where small, clear vesicles cluster around pre- and postsynaptic membrane densities. Thus, functional synapses can occur in the absence of the highly organized synaptic structure seen at mature synapses.
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PMID:Formation of synapses between cells of a neuroblastoma X glioma hybrid clone and mouse myotubes. 20 14

Electrical excitability is one of the various neuronal properties of neuroblastoma X glioma hybrid cells. At a Ca2+ concentration of 1.8 mM the action potential is inhibited by tetrodotoxin, suggesting that the inward current is carried by Na+ ions. In contrast, at a Ca2+ concentration of 20-36 mM and even in the absence of Na+, spikes (sometimes repetitive) with strong hyperpolarizing afterpotential occur, which are no longer affected by tetrodotoxin. They are, however, blocked by antagonists of Ca2+ like La3+, Co2+, Mn2+, and the synthetic compounds D-600 and BAY a-1040. This seems to indicate that at high concentrations of Ca2+, the inward current of the action potential is essentially carried by Ca2+. Sr2+, but not Mg2+ can effectively substitute for Ca2+. It slows down the time course of the action potential. Ba2+ depolarizes the membrane gradually. If Ca2+ is also present, Ba2+ causes a reduced depolarization and spontaneous action potentials with no hyperpolarizing after-potential are observed.
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PMID:Influence of cations on the electrical activity of neuroblastoma X glioma hybrid cells. 89 Apr 47

A biphasic response to changes in Ca2+ concentration was observed for basal and norepinephrine-stimulated adenylate cyclase activity in homogenates of C-6 glioma cells. The enzyme was stimulated approximately 40% by low concentrations of free Ca2+ (less than or equal to 1 muM) and inhibited to successively greater extents as free Ca2+ concentrations were increased to approximately 100 muM. Ca2+ did not alter the concentration of norepinephrine required for enzyme activation. Homogenates of C-6 cells were separated into particulate and supernatant fractions by centrifugation at 27,000 X g for 20 min. The particulate fraction contained nearly all of the adenylate cyclase activity. This activity was stimulated approximately 40% by the addition of untreated supernatant fraction, by boiled or dialyzed supernatant fraction, and by a homogenous Ca2+-binding protein (calcium-dependent regulator (CDR) prepared from brain. Addition of either the supernatant fraction or CDR lowered the Ca2+ concentration required for maximal stimulation of the adenylate cyclase. The factor in the supernatant fraction which activated the particulate enzyme was subsequently identified in acrylamide gel electrophoretic studies to be CDR. The amount of CDR required for maximal activation of the enzyme was found to be lowered as the Ca2+ concentration in the assay was increased. High amounts of added CDR (100 to 1000 ng) were inhibitory. Use of the monionic detergent, Lubrol PX, to prepare dispersed adenylate cyclase from the particulate fraction resulted in large losses of activity. The resultant preparation of enzyme contained some CDR which could not be removed by chromatography of the preparation on anion exchange columns. Addition of homogeneous CDR to the assay activated the enzyme several-fold at low Ca2+ concentrations. At higher Ca2+ concentrations the enzyme was activated fully by the CDR endogenous to the preparation and added Ca2+. CDR was inhibitory.
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PMID:Regulation of adenylate cyclase from glial tumor cells by calcium and a calcium-binding protein. 94 8

The mechanism and the clinical significance of calcium deposits in glioma have been still obscure. Excluding pinealomas, 221 histologically proven intracranial gliomas were studied. The presence of roentgenological calcification in 27 of the authers' series represented an incidence of 12 percent. The incidence of roentgenological calcification in various types of glioma were as follows: astrocytoma grades 1 & 2-15%, astrocytoma grades 3 & 4-7%, medulloblastoma-5%, ependymoma-17%, oligodendrogioma-60%, and choroid plexus papilloma-25%. There was no characteristic relationship between the incidence of calcification and the age distribution. One exception was noted that in astrocytoma grades 1 & 2 the incidence of roentgenological calcification tended to be higher in younger patients than in older patients. The percentage of calcified tumors in both sexes was the same. In astrocytoma and ependymoma the incidence of roentgenological calcification was far greater in the supratentorial tumor than in the infratentorial tumor. According to their roentgenological appearance, calcified tumors were separated into four groups, but any specific appearance could not be claimed for any particular type of glial tumors. Only in astrocytoma both the duration of symptoms and the postoperative survival time of the calcified cases were longer than those of the uncalcified. But in other types of glioma there were no significant differences in the postoperative survival time between the calcified cases and the uncalcified ones. In 5 cases of astrocytomas the calcium deposits did not exist on preoperative radiographs, which were found postoperatively after chemotherapy and/or radiotherapy. In conclusion, it is not the histological type but the duration of the clinical course that plays more important role in calcification of gliomas.
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PMID:[Calcification in gliomas: first report with special reference to roentgenological calcification (author's transl)]. 123 29

Single potassium channels in the membrane of human malignant glioma cells U-118MG were studied using the technique of patch clamp in cell-attached and inside-out configurations. Three types of potassium channels were found which differed from each other under conditions close to physiological in their conductance and gating characteristics. The lowest-conductance channel (20 pS near the reversal potential) showed a mild outward rectification up to 45 pS at positive voltages and spontaneous modes of high and low activity. At extreme values of potentials its activity was generally low. The intermediate conductance channel had an S-shaped I-V curve, giving a conductance of 63 pS at reversal, and a low and voltage independent opening probability. The high-conductance (215 pS) channel was found to be activated by both membrane potential and Ca2+ ions and blocked by internal sodium at high voltages. The current-voltage curves of all three channel types displayed saturation.
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PMID:Single potassium channels of human glioma cells. 128 97

Because increasing evidence indicates that glial cells are a target of endothelin, we have characterized endothelin-induced phosphoinositide (PI) turnover and Ca2+ homeostasis in C6 glioma cells. Endothelin-1 (ET) increased formation of 3H-inositol phosphate (IP) from PI and elicited an increase in cytosolic free Ca2+ ([Ca2+]i) in rat C6 glioma. In the presence of Li+, the increase in 3H-inositol trisphosphate formation was rapid, reaching its peak at 5 min after stimulation. ET also elicited a rapid and sustained increase in [Ca2+]i in a dose-dependent manner (1-100 nM). The rank orders of efficacy for ET-related peptides in increasing [Ca2+]i were ET = ET-2 greater than sarafotoxin greater than ET-3. Both ET-mediated stimulation of IP formation and [Ca2+]i increase were largely inhibited in the absence of external Ca2+ but unaffected by the depletion of external Na+ and the presence of dihydropyridine derivatives or verapamil. Inorganic Ca2+ channel blockers Cd2+, La3+, and Mn2+ at 1 mM inhibited both responses induced by ET. Cross-desensitization and nonadditivity were observed for both events among ET-related peptides tested, but not between ET and ATP. Pretreatment of cells with pertussis toxin (PTX) attenuated the PI response to ET, but had no effect on ET-elicited [Ca2+]i increase. ET-induced Ca2+ mobilization (measured in Ca(2+)-free medium) was only transient and was inhibited by 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate. Moreover, the intracellular Ca2+ pools mobilized by ET and ATP appeared to overlap, as indicated by their partial heterologous desensitization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacological characterization of endothelin-stimulated phosphoinositide breakdown and cytosolic free Ca2+ rise in rat C6 glioma cells. 131 33

The dinoflagellate toxin maitotoxin (MTX) elicited a sustained increase of [Ca2+]i in C6 glioma cells. This response was inhibited by SK&F 96365, a blocker of receptor-mediated calcium entry. In C6 cells, endothelin-1 elicited a rapid but transient increase in [Ca2+]i, followed by a smaller sustained increase. SK&F 96365 inhibited the sustained increase in [Ca2+]i. In both C6 glioma cells and RIN insulinoma cells, MTX elicited a marked influx of 45Ca2+. SK&F 96365 inhibited MTX-induced 45Ca2+ influx by 95% at 30 microM. The L-type calcium channel blocker nifedipine, even at 10 microM, inhibited MTX-induced calcium uptake by only 20% in RIN cells and by only 10% in C6 cells. MTX elicited calcium-dependent phosphoinositide breakdown in both C6 and RIN cells. In both cell lines, the MTX-induced phosphoinositide breakdown was inhibited by 90% by SK&F 96365 at 30 microM. Endothelin-1 and carbamylcholine elicited phosphoinositide breakdown in C6 cells and RIN cells, respectively. The stimulations were unaffected by the presence of SK&F 96365 up to 100 microM. In RIN insulinoma cells, MTX elicited calcium-dependent release of insulin. SK&F 96365 at 30 microM inhibited MTX-induced insulin release by 75%, whereas nifedipine, even at 30 microM, inhibited release by only 10%. The blockade of MTX-induced responses by SK&F 96365 indicates that MTX increases intracellular calcium by interacting directly with a calcium-entry system that is similar, in its sensitivity to SK&F 96365, to the calcium-entry system activated by receptors that elicit phosphoinositide breakdown. Activation of phospholipase C and hormone release by MTX also are blocked by SK&F 96365 and, thus, may be secondary to the activation of such a calcium-entry system.
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PMID:Maitotoxin effects are blocked by SK&F 96365, an inhibitor of receptor-mediated calcium entry. 131 15


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