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)

1. Intact mouse neuroblastoma NS20 cells, in the presence of cyclic adenosine 3':5'-monophosphate (cAMP) phosphodiesterase inhibitor, responded to adenosine (200 muM) and 2-chloroadenosine (200 muM) with a 20-fold increase in intracellular cAMP levels. AMP (200 muM) additions caused only a 3.5-fold cAMP level elevation. ATP, ADP, guanosine, cytidine, uridine, and guanine, all at 200 muM, had no effect on the cAMP level of these cells. 2. Homogenate NS20 adenylate cyclase activity was increased 2.5- to 4-fold by addition of 200 muM adenosine, 2-chloroadenosine, 2-hydroxyadenosine, or 8-methylaminoadenosine. Prostaglandin E1 additions (1.4 muM) produced about an 8-fold stimulation of homogenate cyclase activity. The Km of homogenate cyclase activation by adenosine and 2-chloroadenosine was 67.6 and 6.7 muM, respectively. Addition of 7-deazaadenosine, tolazoline, yohimbine, guanosine, cytosine, guanine, 2-deoxy-AMP, and adenine 9-beta-D-xylopyranoside, all at 200 muM were found to be without effect on homogenate NS20 adenylate cyclase. Two classes of inhibitors of homogenate NS20 adenylate cyclase activity were observed. One class, which included AMP, adenine, and theophylline, blocked 2-chloroadenosine but not prostaglandin E1 stimulation of cyclase. Theophylline was shown to be a competitive inhibitor of 2-chloroadenosine, with a Ki of 35 muM. The second class of inhibitors, which included 2'- and 5'-deoxyadenosine, inhibited unstimulated, 2-chloroadenosine and prostaglandin E1-stimulated homogenate cyclase activity to about the same degree. 3. Activation of NS20 homogenate adenylate cyclase by adenosine appears to be noncooperative. 4. The inhibitory action of putative "purinergic" neurotransmitters is postulated to be due to their effects on adenylate cyclase activity.
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PMID:Mouse neuroblastoma adenylate cyclase. Adenosine and adenosine analogues as potent effectors of adenylate cyclase activity. 117 Oct 95

The mechanisms that control herpes simplex virus type 1 latency and reactivation are still poorly understood. We developed an in vitro murine neuroblastoma cell HSV-infected, acyclovir suppressed model to study the influence of different cyclic nucleotide mediators on the latency and reactivation of HSV-1. A positive cDNA 'in situ' hybridisation for HSV genome was used to prove the establishment of a viral-host cell nuclear relationship. An ABC-immunoperoxidase reaction to cell surface HSV mature glycoproteins was also performed to determine the time of viral reactivation with formation of mature virions. Supernates of cultured cells were placed on Vero cells for confirmation of reactivation by classic cytopathic effect. Theophylline (50 micrograms/ml) and dibutyryl-cAMP (0.1, 0.5, 1 mg/ml) produced the most pronounced response, accelerating HSV reactivation time by 150%. Epinephrine (10, 20 micrograms/ml) had an intermediate effect on accelerating viral reactivation; and verapamil (20, 50 micrograms/ml), theophylline and epinephrine at lower doses had a smaller effect. Carbamylcholine (10 micrograms/ml) prolonged the time to viral reactivation by 100%, 36 hours compared to control time of 18 hours. Insulin (0.1, 0.5, 1 mg/ml) also prolonged HSV 'latency' by six hours. Exogenous dibutyryl-cGMP and carbamylcholine at lower concentrations did not have an effect on viral reactivation. These findings suggest that there is a relationship between changes of intracellular concentration of cyclic nucleotides and HSV latency and reactivation.
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PMID:The role of cyclic nucleotide mediators in latency and reactivation of HSV-1 infected neuroblastoma cells. 166 22

Hormonal regulation of Mg2+ influx was examined in the neuroblastoma X glioma hybrid cell line NG108-15 and the skeletal muscle cell line G8 using 28Mg2+. Both cell lines express multiple classes of hormone receptors; in addition, G8 cells can be induced to differentiate from a single myoblast-like cell into fused myotube-like cells. In NG108-15 cells, 2-Cl-adenosine, an adenosine receptor agonist, stimulated Mg2+ influx by about 60%. This effect was not mimicked by norepinephrine or PGE1, agonists at alpha 2-adrenergic and prostaglandin receptors which NG108-15 cells also express. Carbachol, acting through a muscarinic receptor, gave minimal and variable stimulation of Mg2+ influx. The effect of 2-Cl-adenosine was not blocked by theophylline, an adenosine receptor antagonist, and was not mimicked by adenosine analogs selective for either A1 or A2 adenosine receptors, suggesting that a nonclassical adenosine receptor mediates the effect on Mg2+ influx. Theophylline slightly stimulated Mg2+ influx as did the permeable cyclic AMP analog, 8-Br-cyclic AMP. These results indicate that cyclic AMP may influence Mg2+ influx in NG108-15 cells unlike previous results in murine S49 lymphoma cells [Maguire and Erdos, J. biol. Chem. 255: 1030-1035, 1980] where receptor modulation of Mg2+ influx was independent of cyclic AMP. In G8 cells, the nicotinic cholinergic receptor agonist carbachol stimulated Mg2+ influx at the myoblast cell stage but had no effect on Mg2+ influx after cells had formed myotubes. The beta-adrenergic agonist isoproterenol had the opposite effect, stimulating Mg2+ influx in the myotube stage but not in the myoblast stage. Taken together, these results demonstrate that only a subset of receptors expressed by a cell may be coupled to Mg2+ influx, that the regulation of Mg2+ influx differs from cell type to cell type, and finally, that modulation of Mg2+ influx by hormone receptors may change with differentiation.
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PMID:Hormonal regulation of magnesium uptake: differential coupling of membrane receptors to magnesium uptake. 282 11

Adenosine causes an increase in the concentration of cyclic AMP in mouse neuroblastoma cells. The amount of increase observed in intracellular cyclic AMP levels due to exogenous adenosine depends greatly on the concentration of a specific cyclic AMP phosphodiesterase inhibitor, 4-(-3-butoxy-4-methoxybenzyl)-2-imidazolidinone. Unstimulated concentrations of cyclic AMP were 29-40 pmol/mg of protein, and concentrations after addition of 0.2 mM adenosine were usually twice as high. The presence of 0.7 mM inhibitor along with 0.2 mM adenosine caused an increase in cyclic AMP levels up to 1000-2000 pmol/mg of protein. In the presence of 0.7 mM inhibitor, 2 muM adenosine gives a half-maximal cyclic AMP elevation. Theophylline blocked the elevation of cyclic AMP concentrations caused by exogenous adenosine. The data show that the cyclic AMP system of mouse neuroblastoma has the necessary receptor components to respond positively to exogenous adenosine. The results presented support a direct effect of adenosine, mediated through its control of intracellular levels, on neuronal elements of the nervous system.
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PMID:Adenosine-mediated elevation of cyclic 3':5'-adenosine monophosphate concentrations in cultured mouse neuroblastoma cells. 436 76

The effect of three stable adenosine analogues, L-phenylisopropyl-adenosine (L-PIA), 2-chloroadenosine, and adenosine 5'-ethylcarboxamide (NECA), on cyclic AMP accumulation was studied in five different cell lines derived from the nervous system. In N18-neuroblastoma cells, with cholinergic properties, all three analogues caused an increased accumulation of cyclic AMP with the following relative order of potency: NECA greater than 2-chloroadenosine greater than L-PIA. The half maximal effect of NECA was obtained at close to 10(-8) M concentration. In the two other neuroblastoma cell lines, 41A3 with cholinergic and NIE115 with adrenergic properties, the two analogues NECA and PIA had similar effects. In glioma C6 and 138 MG cells NECA was also found to be more potent that PIA in elevating cyclic AMP levels. However, the absolute potency of NECA in these cell lines was almost 100 times lower. Phosphodiesterase (PDE) activity in crude homogenates of the five cell lines showed essentially similar Km and Vmax, with the exception that the three neuroblastoma cell lines showed biphasic, the glial cell lines monophasic Eadie-Hofstee plots. Theophylline was equally potent as an inhibitor of PDE in all cell lines, but the non-xanthine, inhibitor rolipram, was more potent against neuroblastoma than glial cell PDE. These results indicate that all five cell lines have adenosine receptors of the A2-subtype. However, the apparent affinity of the adenosine analogues to these receptors was markedly different between the neuroblastoma and glial cell lines. The absolute potency of adenosine analogues may be a poor criterion to classify adenosine receptors, into A1 and A2 subtypes, especially when intact cells are used.
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PMID:Adenosine analogues stimulate cyclic AMP-accumulation in cultured neuroblastoma and glioma cells. 609 94