Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Mg2+ATPase and (Na+ + K+)ATPase activities were measured in clonal line NN hamster astroblasts and in clonal lines M1 and N1E-115 mouse neuroblastoma cells after the cells had been subjected to the acute and chronic actions of 100 mM ethanol. Exposure of the astroblasts to ethanol for periods as long as 68 days produced an increase in total cellular Mg2+ ATPase activity, as measured in cell homogenates; however, activity reverted to control levels upon withdrawal of ethanol. Chronic exposure of clonal line N1E-115 neuroblastoma cells to ethanol produced an increase in Mg2+ATPase and (Na+ +K+)ATPase activities. In contrast, the activities of both ATPases of clonal line M1 neuroblasts were unaffected by chronic exposure to ethanol. Acute exposure of cell homogenates to 100 mM ethanol inhibited Mg2+ ATPase and (Na+ + K+)ATPase of astroblasts but not that of neublastoma cells. These findings suggest that neural cells in culture may serve as useful models for studying the effects of ethanol on specific cell types.
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PMID:The chronic and acute effects of ethanol on adenosine triphosphatase activity in cultured astroblast and neuroblastoma cells. 13 50

A biological system consisting of a cell membrane enzyme (Na+-K+)-ATPase responded to exposure to a weak A.C. magnetic field. Analysis of Na+ pump activity in normal mouse (A/J) tissue--(a) Kidney cortex and diaphragm after 11 days of exposure to a magnetic field of 55-60 gauss, 60Hz showed a significant reduction as did (b) liver tissue but at day 17 the levels had returned to the control values. Neuroblastoma cells (C1300) transplanted to A/J mice also showed a reduction in the (Na+-K+)-ATPase activity but this persisted at day 17.
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PMID:Weak A.C. magnetic field effects: changes in cell sodium pump activity following whole animal exposure. 15 71

The development of (Na+ + K+) ATPase, carbonic anhydrase and HCO3--stimulated ATPase activity was studied in developing rat brain in vivo, and in primary astrocyte cultures from 1--3-day-old rat brain as a function of increasing cell growth. The primary cultures showed an increase in all the above enzyme activities during cell growth, with time courses which were qualitatively similar to their development in vivo. Cell cultures grown separately from the cerebellum plus brain stem regions showed greater carbonic anhydrase activity than cerebral cultures over the entire 4-week growth period, corresponding to development of this activity in these same regions in vivo, HCO3-stimulated ATPase activity was slightly greater in cerebellar cultures and (Na+ + K+) ATPase activity was greater in cerebral cultures up to the second week of growth, resembling development of the same enzyme activities in vivo. C6 glioma and neuroblastoma cells showed no and 10-fold lower carbonic anhydrase activities respectively, compared to the primary astrocyte cultures. Addition of 1 mM N6-2'-O-dibutyryladenosine-3',5'-monophosphate (DBcAMP) in the presence of serum caused marked formation of cellular processes and increased carbonic anhydrase and (Na+ + K+) ATPase activity. Maximum effects were found 2 h after addition of 1 mM DBcAMP and thereafter declined. In the absence of serum such effects persisted for at least 24 h. Electron microscope studies showed large numbers of microtubule (approximately 20 nm diameter) and filamentous structures (less than or equal to 10 nm diameter) in the cytoplasm, which showed changes in distribution in cells treated with DBcAMP. This study suggests that the increase in ATPase and carbonic anhydrase activities in rat brain with increasing age may be in part a reflection of proliferation and development of astroglia cells. Together with the morphological data, it also provides additional evidence that primary cultures derived from neonatal rats may closely resemble developing astroglia in vivo.
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PMID:Enzymatic and morphological properties of primary rat brain astrocyte cultures, and enzyme development in vivo. 20 76

Neuroblastoma-glioma hybrid cells (NG108-15) in suspension accumulate the permeant lipophilic cation [(3)H]tetraphenylphosphonium (TPP(+)) against a concentration gradient. The steady-state level of TPP(+) accumulation is about twice as great in physiological media of low K(+) concentration (i.e., 5 mM K(+)/135 mM Na(+)) than in a medium of high K(+) concentration (i.e., 121 mM K(+)/13.5 mM Na(+)). The latter manipulation depolarizes the NG108-15 plasma membrane and indicates that the resting membrane potential (DeltaPsi) is due primarily to a K(+) diffusion gradient (K(in) (+) --> K(out) (+)). TPP(+) accumulation is time and temperature dependent, achieving a steady state in 15-20 min at 37 degrees C, and is a linear function of cell number and TPP(+) concentration (i.e., the concentration gradient is constant). The difference in TPP(+) accumulation in low and high K(+) media under various conditions has been used to calculate mean (+/-SD) DeltaPsi values of -56 +/- 3, -63 +/- 4, and -66 +/- 5 mV at 26, 33, and 37 degrees C, respectively. Importantly, these values are virtually identical to those obtained by direct electrophysiological measurements made under the same conditions. TPP(+) accumulation is abolished by the protonophore carbonylcyanide-m-chlorophenylhydrazone, whereas the neurotoxic alkaloid veratridine diminishes uptake to the same level as that observed in high K(+) media. In addition, the effect of veratridine is dependent upon the presence of external Na(+) and is blocked by tetrodotoxin. The steady-state level of TPP(+) accumulation is enhanced by monensin, indicating that this ionophore induces hyperpolarization under appropriate conditions. Finally, ouabain has essentially no effect on the steady-state level of TPP(+) accumulation in short-term experiments, suggesting that Na(+),K(+)-ATPase activity makes little contribution to the resting potential in these cells. Because many of these observations are corroborated by intracellular recording techniques, it is concluded that TPP(+) distribution measurements can provide a biochemical method for determining membrane potentials in populations of cultured neuronal cells.
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PMID:Use of a lipophilic cation for determination of membrane potential in neuroblastoma-glioma hybrid cell suspensions. 28 90

Addition of the ionophore monensin to mouse neuroblastoma-rat glioma hybrid NG108-15 cells leads to a 20 to 30-mV increase in the electrical potential across the plasma membrane as shown by direct intracellular recording techniques and by distribution studies with the lipophilic cation [3H]-tetraphenylphosphonium+ (TPP+) [Lichtshtein, D., Kaback, H.R. & Blume, A.J. (1979) Proc. Natl. Acad. Sci. USA 76, 650-654]. The effect is not observed with cells suspended in high K+ medium, is dependent upon the presence of Na+ externally, and the concentration of monensin that induces half-maximal stimulation of TPP+ accumulation is approximately 1 microM. The ionophore also causes rapid influx of Na+, a transient increase in intracellular pH, and a decrease in extracellular pH, all of which are consistent with the known ability of monensin to catalyze the transmembrane exchange of H+ for Na+. Although ouabain has no immediate effect on the membrane potential, the cardiac glycoside completely blocks the increase in TPP+ accumulation observed in the presence of monensin. Thus, the hyperpolarizing effect of monensin is mediated apparently by an increase in intracellular Na+ that acts to stimulate the electrogenic activity of the Na+,K+-ATPase. Because monensin stimulates TPP+ accumulation in a number of other cultured cell lines in addition to NG108-15, the techniques described may be of general use for studying the Na+,K+ pump and its regulation in situ.
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PMID:Mechanism of monensin-induced hyperpolarization of neuroblastoma-glioma hybrid NG108-15. 28 48

It has been proposed that abnormal myo-inositol metabolism may be a factor in the development of diabetic complications. Studies with animal models of diabetes and cultured cells have suggested that hyperglycemia by an unknown mechanism may alter myo-inositol metabolism and content. Recently, we have shown that L-fucose, a 6-deoxy sugar whose content has been reported to be increased in diabetes, is a potent inhibitor of myo-inositol transport. To examine the effect of L-fucose on myo-inositol metabolism, neuroblastoma cells were cultured in medium supplemented with L-fucose. L-Fucose is a competitive inhibitor of Na(+)-dependent, high-affinity myo-inositol transport. The Ki for inhibition of myo-inositol transport by L-fucose is about 3 mM. L-Fucose is taken up and accumulates in neuroblastoma cells. The uptake of L-fucose is inhibited by Na+ depletion, D-glucose, glucose analogues, phloridzin, and cytochalasin B. In contrast, neither myo-inositol nor L-glucose inhibits L-fucose uptake. Chronic exposure of neuroblastoma cells to 1-30 mM L-fucose causes a decrease in myo-inositol accumulation and incorporation into inositol phospholipids, intracellular free myo-inositol content, and phosphatidylinositol levels. Na+,K(+)-ATPase transport activity is decreased by about 15% by acute or chronic exposure of neuroblastoma cells to L-fucose. Similar defects occur when neuroblastoma cells are exposed chronically to 30 mM glucose. Cell myo-inositol metabolism and Na+/K(+)-pump activity are maintained when 250 microM myo-inositol is added to the L-fucose-supplemented medium. Unlike the effect of chronic exposure of neuroblastoma cells to medium containing 30 mM glucose, the resting membrane potential of neuroblastoma cells is not altered by chronic exposure of the cells to 30 mM L-fucose. The effect of L-fucose on cultured neuroblastoma cell properties occurs at concentrations of L-fucose which may exist in the diabetic milieu. These data suggest that increased concentrations of L-fucose may have a role in myo-inositol-related defects in mammalian cells.
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PMID:L-fucose is a potent inhibitor of myo-inositol transport and metabolism in cultured neuroblastoma cells. 131 50

Endothelin-1 (ET-1) produced a dose-dependent increase of intracellular Ca++ concentrations [Ca++]i characterized by an early peak phase and a delayed plateau in LAN-1 human neuroblastoma cells. The ET-1 receptor showed a rapid desensitization since a second pulse application of ET-1 did not elicit a further [Ca++]i increase. Furthermore thapsigargin, an endoplasmic reticulum Ca(++)-ATPase inhibitor, completely abolished the ET-1 induced intracellular Ca++ elevation.
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PMID:LAN-1 human neuroblastoma cells are provided of endothelin-1 receptors linked to [Ca++]i elevation. 132 9

Morphological rearrangements, such as synapse number changes, have been observed in the adult mammalian brain after various experimental paradigms of learning and behavioral experience. The role of axonal transport in the physical translocation of material during this form of brain plasticity has not been fully appreciated. We show here by quantitative video microscopy that sabeluzole (R58735), a new memory-enhancing drug in humans, effectively increases fast axonal transport in rat neuronal cell cultures. Long-term incubation (24 hr) with sabeluzole in the concentration range between 0.1 and 1 microM increases both velocity and jump length of saltatory movements maximally by 20-30% in embryonic hippocampal neurons. Acute treatment only increases the velocity by 15-20%. Furthermore, the inhibition of axonal transport by 0.1 mM vanadate in N4 neuroblastoma cells is reversed by 1 microM sabeluzole. Observations on the kinesin-induced microtubule mobility in a reconstituted system show a 10% enhancement by sabeluzole at an optimal concentration of 2 microM, but no increase in kinesin ATPase activity. To our knowledge, this is the first pharmacological compound shown to increase fast axonal transport. The mechanism of fast axonal transport enhancement is discussed as a rationale for new therapeutic treatment in neuropathology.
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PMID:Sabeluzole, a memory-enhancing molecule, increases fast axonal transport in neuronal cell cultures. 137 35

Continuous superfusion of rat glioma cells with medium containing bradykinin (from 0.2 nM) induced a transient hyperpolarization followed by regular hyperpolarizing oscillations of the membrane potential. Similar repetitive hyperpolarizing oscillations were caused by extracellularly applied bradykinin or muscarine or by intracellularly injected GTP-gamma-S. The frequency of the oscillations was 1 per minute at bradykinin concentrations ranging from 0.2 nM to 2 microM, but the amplitude and duration increased with rising peptide concentration. The muscarine-induced oscillations were blocked by atropine. In the presence of extracellular Ca2+, the substances thapsigargin, 2,5-di(tert-butyl)-1,4-benzohydroquinone (tBuBHQ), and ionomycin reversibly suppressed the bradykinin-induced oscillations. Thapsigargin and tBuBHA, which are known to block the Ca2+ ATPase of endoplasmic reticulum, caused a transient rise in cytosolic Ca2+ activity, monitored with Fura-2, in suspensions of rat glioma cells or of mouse neuroblastoma-rat glioma hybrid cells. After a transient Ca2+ rise caused by thapsigargin, tBuBHQ, or ionomycin, the Ca2+ response to bradykinin which is known to be due to release of Ca2+ from internal stores was suppressed. This indicates that thapsigargin and tBuBHQ deplete internal Ca2+ stores as already seen previously for ionomycin. Thus, the inhibition of the membrane potential oscillations by thapsigargin, tBuBHQ, and ionomycin indicates that the oscillations are associated with activation of InsP3-sensitive Ca2+ stores. In some cells composite oscillation patterns which consisted of two independent oscillations with different amplitudes that overlapped additively were seen. We discuss that this pattern and the concentration dependency of the oscillations could be due to "quantal" Ca2+ release from stores with different inositol 1,4,5-triphosphate sensitivities. Subsidence of the oscillations after omission of extracellular Ca2+ seems to be due to a lack of replenishment of the intracellular stores with Ca2+, which comes from the extracellular compartment.
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PMID:Bradykinin and muscarine induce Ca(2+)-dependent oscillations of membrane potential in rat glioma cells indicating a rhythmic Ca2+ release from internal stores: thapsigargin and 2,5-di(tert-butyl)-1, 4-benzohydroquinone deplete InsP3-sensitive Ca2+ stores in glioma and in neuroblastoma-glioma hybrid cells. 139 96


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