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)

A membrane glycoprotein, Mr = 20,000, has been purified from human neuroblastoma cells (IMR-5) with the use of monoclonal antibody selected for binding capacity to human neuroblastoma cell lines. The antigen was extracted with 0.5% Nonidet P-40 from cells metabolically labeled with L-[3H]fucose or D-[3H]glucosamine. A double antibody affinity column was used to purify the membrane glycoprotein. Goat anti-mouse IgM was coupled to cyanogen bromide-activated Sepharose 4B. The absorption of the monoclonal antibody contained in ascites fluid completed the affinity column. Appropriate controls of similar material from other cell types and another monoclonal antibody demonstrated the specificity of the affinity column. Glycopeptides from the surface of human neuroblastoma cells, IMR-5 and CHP-134, had antigenic activity, as radioactive pronase-digested material bound to the affinity column and inhibited complement-mediated cytolysis. Glycolipids extracted from the cells had no antigenic activity. It was concluded that the carbohydrate residues of the glycoprotein conferred the antigenic specificity. Three methods were devised to aid in detection and purification of the antigen. These were: 1) an assay for the detection of complement-mediated cytolysis by measuring the enzyme creatine phosphokinase in the nonlysed target cells; 2) precipitation of the antigen . antibody complex with 4% polyethylene glycol; and 3) removal of the antibody by a wheat germ agglutinin-agarose column.
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PMID:A membrane glycoprotein from human neuroblastoma cells isolated with the use of a monoclonal antibody. 616 Jan 55

1. Binding of a purified scorpion toxin to membrane fragments isolated from electroplaque of an electric eel Electrophorus electricus was studied using a radio-iodinated toxin.2. A scorpion toxin was purified from the venom of Leiurus quinquestriatus and iodinated with (125)I in a lactoperoxidase-catalysed reaction. Monoiodinated toxin, isolated by an ion exchange chromatography, retarded the inactivation kinetics of Na current to a similar extent as the native toxin, indicating that radioiodination did not appreciably affect physiological and binding properties of the native toxin.3. Analyses of binding properties by Scatchard plots showed the presence of two classes of binding sites (with low and high affinities) in the membrane preparation from eel electroplaque; similar preparation from an electric skate, of which the electroplaque is known to be devoid of Na channels, possessed only the low affinity sites.4. The number of high affinity sites in the eel preparation was 41.8 +/- 10.5 p-mole/g tissue; the value was within the range reported for tetrodotoxin binding to similar preparations (15-148 p-mole/g tissue).5. A variety of cations (Na(+), Mn(2+) and La(3+)) inhibited the high affinity scorpion toxin binding, as indicated for the toxin binding to Na channels by a previous electrophysiological study. K(D) value in the presence of 120 mM-Na(+) (approx. 8 nM) agreed reasonably with that (approx. 10nM) reported for the scorpion toxin binding to excitable neuroblastoma cells or synaptic nerve ending particles under conditions where membrane potential was depolarized by the addition of 135 mM-KCl.6. Pretreatment of the eel membrane preparation with beta-bungarotoxin (7-44 ng/ml.) in the presence of Ca ions (10-200 muM) resulted in a substantial loss of high affinity binding of scorpion toxin. When phospholipase A(2) activity of the beta-toxin was inactivated by a chemical modification with p-bromophenacyl bromide, the inhibitory action of the beta-bungarotoxin was abolished.7. It is concluded that a high affinity binding of scorpion toxin to the eel electroplaque membrane fragments represents the binding to Na channels in vitro, and that phospholipase A(2) activity of beta-bungarotoxin interferes with the binding of scorpion toxin to Na channels.
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PMID:Binding of scorpion toxin to sodium channels in vitro and its modification by beta-bungarotoxin. 624 82

Differentiated C1300 mouse neuroblastoma cells were treated with 10(-4)-10(6) M gamma-aminobutyric acid (GABA) and/or sodium bromide (NaBr) for 2 days and then fixed. Quantitative studies revealed an increase in the length and branching of the processes, as well as an increase in the number of cells when compared to the controls. It is suggested that the above changes contribute to the augmentation of specialized contacts between cells and processes as well as the further maturation of the primitive stages of synaptogenesis as discussed.
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PMID:GABA or sodium-bromide-induced plasticity of neurites of mouse neuroblastoma cells in culture. A quantitative study. 685 Jul 57

Sodium bromide was applied in vitro to mouse neuroblastoma cells of different ages for short and long periods (2 h to 10 days). The changes observed light-and-electron microscopically were similar to those described earlier after GABA treatment. Coated vesicles proliferated and originated by pinching off from the Golgi complex and from the rough endoplasmic reticulum. Numerous coated vesicles were continuous with the plasma membrane, especially near zones in which electron-dense material aggregated at the inner aspect of the plasmalemma. Small invaginations, similar in ultrastructure to coated vesicles, were also formed. It is unclear whether the coated vesicles or the dense plasmalemma invaginations contribute to the "undercoating" by fusing with the adjacent electron-dense plasma membrane. There was a distinct increase in the number and area of specialized contacts (intermediate junctions and zonulae adhaerentes) between cells and their processes. A floccular or filamentous electron-dense substance varying in amount and appearance was occasionally seen between the contacting membranes. Varicosities of terminal swellings of cell processes contained vesicles of variable size, shape and density, and also profiles of the smooth endoplasmic reticulum. Under the influence of sodium bromide, similar to the effect of GABA, mitochondria appeared within the varicosities, and primitive contacts (intermediate junctions) were formed between the terminal swellings and potential postsynaptic elements, which were absent in controls. Additionally, dense-core vesicles proliferated and aggregated at the cell periphery. They were often arranged linearly below the plasma membranes of perikarya and processes, and surrounded by a highly electron-dense substance. The similarity of the present findings to those obtained after GABA treatment and their relation to synaptogenesis are discussed.
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PMID:Morphological changes induced by sodium bromide in murine neuroblastoma cells in vitro. 708 7

Partially purified extracts from neuroblastoma x glioma hybrid cells inhibit via opioid receptors the PGE1-elicited formation of cyclic AMP in the same hybrid cell system. The purification of extracts reveals two active fractions very similar to Met- and Leu-enkephalin by several criteria including treatment with cyanogen bromide. On an average, the intracellular concentration of opioids in hybrid cells is 0.1 pmol per mg protein. The concentration is strongly dependent on the cell density. Furthermore, the content in the hybrids of enkephalin-like peptides is specifically elevated by glucocorticoids.
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PMID:Production and regulation of enkephalin-like peptides in neuroblastoma x glioma cells. 712

Growth cones of differentiated neuroblastoma cells in monolayer cultures were studied by electron microscopy. Morphological differentiation of the growth cone formation was induced by sodium bromide. Upon prolonged application of 10(-4) to 10(-5) M sodium bromide to the cultures, a peculiar or modified formation of the growth cone occurred. Growth cones lengthened gradually. The ultrastructure of the growth cone in contrast to the control was typified by a round to oval structure, midway being electron-dense and carrying laterally denser cytoplasmic protrusions. Bundles of microtubules, aggregates of many dense-cored vesicles, 70-150 nm in diameter, a few less electron-dense, as well as some agranular vesicles were present. Comparing the findings with previous ultrastructural accounts of growth cones of cultured ganglion cells or neuroblastoma cells, differences outnumbered similarities. The organization of the microtubule bundles and the abundance of dense-cored vesicles, sometimes extending distally was remarkable. The presence of an electron-dense substance, of unknown origin, extending laterally with the cytoplasmic protrusions has not been describe as yet.
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PMID:Modified growth cones in mouse neuroblastoma cultures; an electron microscopic study. 713 Jun 78

The ATP signaling mechanism in neuroblastoma x glioma hybrid NG108-15 cells differentiated by exposure to dibutyryl-cAMP was characterized. In cells loaded with fura-2, ATP rapidly raised the cytosolic Ca2+ concentration ([Ca2+]i); the magnitude of the rise was inversely proportional to the extracellular Na+ concentration. Large increases in cytosolic Na+ concentration, measured with the fluorescent Na+ indicator sodium-binding benzofuran isophthalate, were dose-dependently elicited by ATP. ATP also evoked the entry of ethidium bromide into cells, and this process was inhibited by Mg2+. Inositol-1,4,5-trisphosphate (IP3) generation induced by ATP was totally blocked by removal of extracellular Ca2+, but residual IP3 generation still remained in nondifferentiated cells. In addition, ATP produced a concentration-, time-, and Mg(2+)-dependent biphasic uptake of 45Ca2+. A range of nucleotides and ATP analogues, including CTP, UTP, and GTP, induced only 9-29% of the ATP response. However, adenosine 5'-thiotriphosphate evoked 79% of ATP-induced 45Ca2+ uptake. 45Ca2+ uptake elicited by ATP could be potently blocked by purinoceptor antagonists, but other tested reagents less effectively blocked the action of ATP. When bradykinin was used as an agonist, the [Ca2+]i rise was transient and was insensitive to the extracellular Na+ concentration. Na+ influx, entry of ethidium bromide, and 45Ca2+ uptake were unaffected by bradykinin. Furthermore, bradykinin-evoked IP3 generation was insensitive to extracellular Ca2+. Neither ATP nor bradykinin had any effect on cAMP levels within cells. These data suggest that ATP induces a [Ca2+]i rise in differentiated NG108-15 cells via two distinct Ca2+ influx mechanisms, i.e., a receptor-operated cation channel and pores formed by ATP4-. These mechanisms are distinct from those elicited by bradykinin.
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PMID:Two distinct ATP signaling mechanisms in differentiated neuroblastoma x glioma hybrid NG108-15 cells. 751 80

Amplification of the oncogene MYCN is a genetic change frequently observed in neuroblastoma and is an indicator of poor prognosis. MYCN copy number is currently determined by Southern blot hybridization. This technique takes 2 to 3 weeks, is labor-intensive, is sensitive to DNA degradation, and requires large quantities of DNA. We have evaluated a new, semiquantitative method of estimating gene copy number that uses differential polymerase chain reaction (PCR). The procedure can be performed in 1 day, is highly reproducible, and requires only nanogram quantities of DNA. It employs a semiquantitative, nonisotopic PCR technique based on differential competition for PCR substrates. MYCN gene primers are amplified together with primers from a single-copy internal control gene. Following electrophoretic separation, the ratio of the two PCR products is determined visually and by densitometric analysis of ethidium bromide-stained agarose gels. This differential ratio is then compared to a series of ratios generated from standards of known MYCN gene copy number. We compared the results obtained by this differential PCR method with those obtained by conventional Southern blotting in 16 cases of primary neuroblastoma. All amplified tumors were detected by differential PCR, and no false positives were observed. We confirmed that differential PCR is a rapid and reliable alternative to Southern blotting for MYCN copy number assessment and is highly suited to the analysis of DNA derived from needle biopsies.
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PMID:Assessment of MYCN amplification in neuroblastoma biopsies by differential polymerase chain reaction. 780 81

Spontaneously transformed Chinese hamster lung cells with high levels of resistance (approximately 100-fold to 70,000-fold) to actinomycin D, daunorubicin, or vincristine exhibit morphology and growth patterns characteristic of normal cells in vitro and reduced tumorigenicity in vivo. These reverse transformed, multidrug-resistant cells amplify and highly overexpress one or more genes encoding P-glycoprotein. Similarly, hydrocarbon-induced mouse sarcoma cells selected with actinomycin D, vincristine, or ethidium bromide developed high levels of resistance associated with reduced drug accumulation and suppression of malignancy. To determine whether human tumor cells would undergo similar changes and whether reverse transformation reflected an altered state of differentiation, nine multidrug-resistant sublines were selected with four agents from human neuroblastoma cells with well defined pathways of differentiation. Those five with resistance levels above about 125-fold showed a reduced tumor frequency as compared to control cells. All resistant sublines showed altered differentiation. The changes in transformation phenotype appear to be intrinsic and not the result of altered immunogenicity. Two additional consequences of high level multidrug resistance have been observed: change in ganglioside composition in the Chinese hamster cells, manifested as a block in higher ganglioside biosynthesis and/or a relative increase in GM3, and increase in epidermal growth factor receptor in all three cell systems. A tentative hypothesis links ganglioside and growth factor receptor changes to the change in transformation phenotype. The basis of the reverse transformation phenomenon is not known, but the major alterations in expression of P-glycoprotein, gangliosides, and the epidermal growth factor receptor implicate, in some way, the plasma membrane.
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PMID:Reverse transformation of multidrug-resistant cells. 792 50

Both mu and delta opioid receptors are expressed in undifferentiated human neuroblastoma SHSY5Y cells and are negatively coupled to adenylate cyclase. The ability of various mu opioid, delta opioid and alpha-2 adrenergic agonists to inhibit acutely forskolin-stimulated adenylate cyclase activity in undifferentiated SHSY5Y cells after chronic administration with the selective mu opioid agonist [N-MePhe3,D-Pro4]morphiceptin (PLO17) or delta opioid agonist, [D-Pen2,D-Pen5]enkephalin (DPDPE) was assessed. In control cells, both PLO17 and DPDPE inhibited cyclic AMP (cAMP) formation with equal maximal inhibition, i.e., 60 +/- 3 and 66 +/- 2%, having IC50 values of 51.1 +/- 1.3 and 3.7 +/- 1.0 nM, respectively. The inhibition of intracellular cAMP formation by both agonists could be blocked by pertussis toxin pretreatment. After 24 hr of chronic administration of PLO17 (50 nM to 10 microM), a concentration-dependent loss of the ability of mu opioid agonists PLO17 and DAMGO, but not the delta opioid agonists DPDPE, nor alpha-2 adrenergic agonist UK-14304 (5-Bromo-N-(4,5,-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine) to inhibit adenylate cyclase activity was observed. In contrast, chronic administration of DPDPE (0.1 nM to 0.3 microM) resulted in a concentration-dependent reduction in the inhibition of cAMP formation produced by delta opioid agonists DPDPE and DSLET, but not mu opioid, nor alpha-2 adrenergic agonists tested. The observed homologous desensitization was also time-dependent. In addition, antagonist-induced increases in adenylate cyclase activity were observed only after chronic PLO17 administration.2+ Finally, chronic pretreatment of cells with PLO17 (10 microM) resulted in a significant decrease in mu opioid, but not delta opioid receptor, binding, whereas treatment with DPDPE (0.3 microM) resulted in a significant decrease in delta opioid, but not mu opioid receptor binding. Therefore, undifferentiated SHSY5Y cells may provide an excellent model system to study not only the signal transduction mechanisms of mu and/or delta opioid receptors, but also the cellular adaptations of specific opioid receptors.
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PMID:Mu and delta opioid receptor desensitization in undifferentiated human neuroblastoma SHSY5Y cells. 803 14


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