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)

Mouse neuroblastoma clone NIE-115 contains two species of acetylcholinesterase (AChE) which sediment at 4S and 11S. The former is predominant in growing cells (70%), whereas the 11S is more abundant in cells with neurites (55--65%). When cell replication is arrested by sodium butyrate, there is an increase in AChE activity but no modification in the proportion of 4S:11S species. Inhibition of protein synthesis by cycloheximide provokes a slow increase in the 11S form and a parallel decrease in 4S. Neurite retraction in presence of colchicine or excess serum does not lead to a concomitant reversion in the high 11S proportion. We postulate that the 11S AChE is formed by a conversion of the 4S and that the shift in the S-value ratio of the enzyme reflects changes in membrane remodeling during neurite extension.
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PMID:Phenotypic modulation in mouse neuroblastoma cells: the case of acetylcholinesterase. 74 57

Differentiated mouse neuroblastoma cells (C 1300) were exposed to various mitosis-inhibitors (vinblastine, colchicine and griseofulvin) and substances with anesthetic action (lidocaine, tetracaine, chlorpromazine and sodium dodecyl sulphate). All the drugs caused rapid retraction of the neurites, which was reversible in all cases but for sodium dodecyl sulphate, and showed a sigmoid dose-response relationship. The two groups of substances caused morphologically similar effects in that the microtubules disappeared and the intracellular orientation was lost. The order of potency of the anesthetics corresponded to their efficiency to cause nerve-block and antihemolysis as reported by others. Colchicine, griseofulvin, lidocaine and chlorpromazine were tested for effects of agglutination of undiffentiated cells. They inhibited agglutination at doses that were only slightly higher than those causing neurite retraction. The possibility of a close relationship between the cell membrane and microtubule system will be considered.
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PMID:Reversal of morphological differentiation of mouse neuroblastoma cells by mitosis-inhibitors and anesthetics. 81 Sep 56

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

The adrenergic mouse neuroblastoma clone NIE 115 contains two species of AChE which sediment at 4S and 11S. These two species are found both in logarithmic growing phase cells (round neuroblast morphology) and in cells which have undergone morphological differentiation due to the elimination of serum. The 4S form is predominant in the growing cells (70 per cent) whereas the 11S form is more abundant (55 per cent to 65 per cent) in the cells with neurites. When protein synthesis is inhibited by cycloheximide, there is an increase states : we postulate that the 11S species is formed by a conversion of the 4S species. When cell division is blocked by sodium butyrate, there is an increase in AChE activity but no modification in the proportion of 4S/11S species as compared to the cells in growing phase. We were unable to associate temporally the increase in the 11S species with neurite outgrowth ; when cells were allowed to retract their neurites and were subsequently maintained in a GROWING state for 10 to 15 days, the 11s species still predominates. Although the presence of the 11S molecule cannot always be correlated with the state of morphological differentiation, the shift in sedimentation coefficient of AChE form 4S to 11S might eventually constitute a reference in the study of biochemical events leading to terminal differentiation in this system.
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PMID:Changes in the sedimentation properties of acetycholinesterase during neuroblastoma differentiation. 93 91

Four neurotoxins that activate the action potential Na+ionophore of electrically excitable neuroblastoma cells interact with two distinct classes of sites, one specific for the alkaloids veratridine, batrachotoxin, and aconitine, and the second specific for scorpion toxin. Positive heterotropic cooperativity is observed between toxins bound at these two classes of sites. Tetrodotoxin, a specific inhibitor of the action potential Na+ current, inhibits activation by each of these toxins in a noncompetitive manner (KI=4-8 nM). These results suggest the existence of three functionally separable components of the action potential Na+ionophore: two regulatory components which bind activating neurotoxins and interact allosterically in controlling the activity of a third ion-transport component, which binds tetrodotoxin. The dissociation constant for scorpion toxin binding is increased 10-fold by depolarization of the cells with K+, suggesting that the scorpion toxin binding site is located on a voltage-sensitive regulatory component of the ionophore.
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PMID:Interactions of neurotoxins with the action potential NA + ionophore. 102 23

Four neurotoxins that activate the action potential Na+ ionophore of electrically excitable neuroblastoma cells interact with two distinct classes of sites, one specific for the alkaloids veratridine, batrachotoxin, and aconitine, and the second specific for scorpion toxin. Positive heterotropic cooperativity is observed between toxins bound at these two classes of sites. Tetrodotoxin is a noncompetitive inhibitor of activation by each of these toxins (KI = 4-8 nM). These results suggest the existence of three functionally separable components of the action potential Na+ ionophore: two regulatroy components, which bind activating neurotoxins and interact allosterically in controlling the activity of a third ion-transport component, which binds tetrodotoxin.
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PMID:Cooperative activation of action potential Na+ ionophore by neurotoxins. 105 69

Tubulin from cultures of the rat glial cell clone C6 could be polymerized in vitro into intact microtubules. The polymerization was reversible and spontaneous, i.e., no addition of heterologous nucleation centers was necessary. Two cycles of polymerization/depolymerization yielded tubulin preparations of 95% purity as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Electron microscopy was used to show that the microtubules assembled in vitro by two cycles of polymerization/depolymerization were morphologically intact and temperature sensitive. In contrast, tubulin from neuroblastoma cells, clone Neuro-2A, could not be polymerized in a reversible fashion. The discovery of a cell line from which tubulin can be reversibly polymerized in vitro establishes a model system for studies of cell-cycle- and cell-type-dependent regulatory mechanisms controlling the assembly of microtubules.
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PMID:Reversible in vitro polymerization of tubulin from a cultured cell line (rat glial cell clone C6). 106 5

Depolarization of neuroblastoma cells causes a 70-fold increase in the apparent dissociation constant KD for scorpion toxin enhancement of activation of the action potential Na+ ionophore by veratridine and a large increase in the rate of reversal of scorpion toxin action. Depolarization also inhibits binding of 125I-labeled scorpion toxin to a small number of saturable binding sites on electrically excitable neuroblastoma cells and increases the rate of dissociation of scorpion toxin from these sites. The results suggest that scorpion toxin binds to a regulatory component of the action potential Na+ ionophore whose conformation changes on depolarization.
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PMID:Membrane potential dependent binding of scorpion toxin to action potential Na+ ionophore. 106 80

A kinetic analysis of the appearance of 14C-labelled proteins in the surface membranes isolated from exponentially growing neuroblastoma cells (N2a) showed that the total membrane proteins reached a steady-state specific radioactivity in 18-20 h. However, examination of individual protein bands resolved by sodium dodecyl sulphate-urea-polyacrylamide-gel electrophoresis illustrated that differences in the kinetics of specific surface-membrane proteins could be detected. Although most of the protein bands reached a steady-state specific radioactivity at a time similar to that for total membrane proteins, at least two bands (mol. wt. 180000 and 130000) attained the steady-state within 8-10 h. It was shown by the use of dual-labelling techniques that these two protein bands turned over in the surface membranes of neuroblastoma N2a cells at least 180 and 150% faster than the total membrane protein. These two proteins were glycosylated and located on the outer surface of the cells, since they were labelled with radioactive carbohydrates and readily removed by treatment of the intact neuroblastoma cell with proteinases.
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PMID:Synthesis and turnover of plasma-membrane proteins and glycoproteins in a neuroblastoma cell line. 127 13

Microspectrofluorometry was used to study the regulation of intracellular pH (pHi) in 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF)-loaded astrocytes and the neuroblastoma-glioma cells of the NG 108-15 line. The cells rapidly regulated pHi during an acid transient induced by an NH4+ prepulse. This regulation was blocked by removal of Na+, or by addition of 1 mM amiloride. The back regulation was also inhibited when extracellular pH (pHc) was lowered. Furthermore, when cells were exposed to buffer with reduced or increased pHc, pHi changed in parallel. Thus, although these cells possess at least one efficient H+ extrusion mechanism, which is likely to be the ubiquitous Na+/H+ antiporter, they fail to regulate pHi to a normal value unless pHc is held constant. The implications of these findings are discussed.
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PMID:The regulation of intracellular pH in cultured astrocytes and neuroblastoma cells, and its dependence on extracellular pH in a HCO3-free solution. 129 78


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