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)

Identification of hexose transporter sites by cytochalasin B binding was conducted with a centrifugation assay. The determination of KD and Bmax values by LIGAND computer analysis provided binding data that are similar in primary astrocytes (238 nM and 14 pmol/mg protein) and neuroblastoma cells (179 nM and 13.6 pmol/mg protein). In contrast, only an insignificant number of transporter sites was detectable in C6 glioma cells, irrespective of whether membrane fractions were obtained by a two-phase polymer system or by a latex phagocytosis technique yielding inside-out plasma membranes. The latter membrane preparation was utilized to identify and quantitate the transporter molecules at the inner membrane surface of primary astrocytes, i.e., 160 nM (KD) and 5.8 pmol/mg protein (Bmax), respectively.
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PMID:Glucose transporter in plasma membranes of cultured neural cells, as characterized by cytochalasin B binding. 376 Aug 68

Insulin receptors were detected in a variety of rat neuroblastoma and glioma cell lines. The binding of 125I-insulin to B103 neuroblastoma cells had characteristics typical of insulin receptors in other tissues, including high affinity for insulin, low affinity for insulin-like growth factor I (IGF-I), and curvilinear Scatchard plots. Using photoaffinity labeling procedures and sodium dodecyl sulfate (SDS) gel electrophoresis to analyze the subunit structure of insulin receptors in B103 cells, the predominantly labeled protein had an apparent molecular weight of 125K and the mobility of this protein was shifted after removal of sialic acid residues. On the basis of size and susceptibility to neuraminidase, the insulin binding subunit in neuroblastoma cells was identical to the alpha-subunit of insulin receptors in adipocytes and different from the 115K subunit found in brain. The presence of an "adipocyte" form of the insulin receptor in clonal cells derived from brain is probably a consequence of transformation and results from more extensive oligosaccharide processing of the 115K receptor expressed in normal brain cells. The fully glycosylated receptors in neuroblastoma cells were capable of exerting functions typical of insulin receptors in adipocytes such as internalization of insulin and stimulation of glucose transport.
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PMID:Structural and functional characteristics of insulin receptors in rat neuroblastoma cells. 390 Feb 95

The resistance of cultured mouse neuroblastoma cells, primary cultures of rat cerebellar neurons, and rat brain astrocytes to a block of aerobic metabolism was studied. Parameters such as lactate production and ATP content were measured in the presence of antimycin A and under various conditions of glucose, oxygen, and serum supply. The following conclusions can be drawn: (1) All cell types studied were characterized by an active production of lactate; (2) Incubation of the various cell types in the absence of glucose at normal oxygen tension did not affect ATP levels; (3) Respiration blocked by antimycin led to a Pasteur effect; (4) Neuroblastoma cells, but not the other cell types, were fully resistant to inhibition of respiration provided that sufficient glucose was supplied; (5) In the absence of glucose no stores of energy or utilizable substrate were present in the cell types studied when respiration was blocked; (6) In the presence of fetal calf serum anoxic neurons showed irreversible signs of degeneration.
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PMID:Effects of antimycin, glucose deprivation, and serum on cultures of neurons, astrocytes, and neuroblastoma cells. 396 24

Neuroblastoma cells rapidly incorporate exogenous fatty acids into cellular triacylglycerol and relationships between triacylglycerol and phospholipid biosynthesis have been indicated by the relative time course of labeling of these lipids. To evaluate this further, neuroblastoma cells were labeled using potential precursors of phospholipid including radiolabeled triacyglycerol, glycerol, glucose, and fatty acid. With [2-3H]glycerol or a mixture of [2-3H]glycerol trioleate and glycerol tri[1-14C]oleate, phospholipids were labeled at very low levels (less than 0.1 and less than 0.5%, respectively). With [6-3H]glucose, labeling of lipids (0.5-3.5%) was greatest in medium containing 19 mM fructose, whereas labeling with [1-14C]18:2(n-6) was similar in media containing either 19 mM fructose or 25 mM glucose. Labeling of the glycerol moiety of triacylglycerol with [6-3H]glucose increased with 40-200 microM 18:2(n-6) present and occurred predominantly in 2 h. Some [6-3H]glucose label was in fatty acyl chains (chiefly 16:0) of triacylglycerol by 16 h, but was unaffected by exogenous 18:2(n-6). Triacylglycerol was the only lipid to increase in mass (threefold with 200 microM 18:2(n-6)). During the chase of cells pulsed with [6-3H]glucose, label in triacylglycerol declined within 0.5 h, whereas in phospholipid it increased transiently up to 2 h and then declined. Changes were inversely proportional to 18:2(n-6) levels in the chase medium and labeled acyl chains moved in parallel with the glycerol moiety. Thus, a major portion of acyl chain transfer from triacylglycerol was accompanied by glycerol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Triacylglycerol as a precursor in phospholipid biosynthesis in cultured neuroblastoma cells: studies with labeled glucose, fatty acid, and triacylglycerol. 407 30

The addition of norepinephrine to cultured glioblastoma cells results in an inhibition of uptake of radioactivity from D-[2-(3)H]glucose, D-[1-(14)C]glucose, D-[2-(14)C]glucose, and D-[6-(14)C]glucose. In addition, if the glioblastoma cells are previously labeled with these substrates, norepinephrine causes an increase in the release of radioactivity. These effects were not observed with cultured neuroblastoma cells. It is suggested that the breakdown of glycogen is activated by norepinephrine as a result of an increase in 3':5'-cyclic AMP.
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PMID:Effect of norepinephrine on glucose metabolism in glioblastoma and neuroblastoma cells in cell culture. 434 Jan 54

We have examined the metabolism of ketone bodies in neuroblastoma C1300 and glioma C6 cells, two established lines of neural origin. The three ketone body-metabolizing enzymes are present in cells of both lines in the relative proportions normally found in brain (D-3-hydroxybutyrate dehydrogenase less than acetoacetyl-CoA thiolase less than 3-ketoacid CoA-transferase), the activities of the first two are higher in glioma cells than in neuroblastoma, and that of the third is 2-fold higher in neuroblastoma cells than in glioma cells. The specific activity of 3-ketoacid CoA-transferase (EC 2.8.3.5) in both cell lines increased as the cultures achieved confluence, then decreased. Ketone bodies and especially acetoacetate are preferred substrates for synthesis of neural lipids in cells of both lines. The incorporation of glucose carbon into lipids is significantly reduced in cells of both lines in the presence of ketone bodies. Addition of acetoacetate but not DL-3-hydroxybutyrate to the culture medium resulted in a significant increase in the activity of 3-ketoacid CoA-transferase and also in the rate of acetoacetate oxidation in neuroblastoma cells but not glioma cells. These findings indicate that specific differences exist in the capacity of these two cell lines to metabolize ketone bodies and also that substrate-level regulation of the ketone body-metabolizing pathway exists. These two lines therefore provide a potentially useful system in which the mechanisms of regulation of these enzymes may be examined.
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PMID:Ketone-body metabolism in glioma and neuroblastoma cells. 611 69

Strain N2a neuroblastoma cells were grown in monolayer and in spinner culture in Coon's modified Hamms F12 medium, or in Dulbecco's modified Eagle Medium with either high (4.5 g/l) or low (1.0 g/l) glucose, and the specific binding of [3H]GABA and [3H]flunitrazepam were determined. GABA binding was highest in monolayer cells grown in low glucose Dulbecco's, and undetectable in monolayer or spinner cells grown in high glucose Dulbecco's. Binding of flunitrazepam was not sensitive to the medium or culture conditions. Flunitrazepam binding suggested the presence of a 'peripheral' benzodiazepine receptor, because: (a) binding was blocked by RO5-4864 but not clonazepam; (b) binding was not enhanced by 0.1 mM GABA or 50 mM Cl-; and (c) the Kd value was approximately 300 nM. Neither ethanol (100 mM) nor pentobarbital (0.2 mM) had any effect on the binding of GABA; flunitrazepam binding was not affected by ethanol but was decreased about 20% by pentobarbital. GABA, muscimol and veratridine did not alter the membrane potential of the cells, as measured by tetraphenylphosphonium accumulation. The data are discussed in terms of separate receptors for GABA and for benzodiazepines which are not incorporated into a GABA--benzodiazepine receptor--chloride ionophore complex.
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PMID:GABA and flunitrazepam binding to neuroblastoma cell membranes--effects of growth conditions, ethanol and pentobarbital. 612 16

The effects of the highly neurotoxic organophosphate pinacolyl methylphosphonofluoridate (soman) on several cellular processes of a homogeneous neuronal cell system, Neuroblastoma cells (NS 20), has been investigated. The protein biosynthesis was measured by [14C] L-Leucine uptake and incorporation into total protein. The glycolytic energy metabolism was measured by [14C] deoxy-D- Glucose [( 14C] DG) uptake and retention. The old method [14C] D-Glucose uptake was also performed. Exposure of cells in stationary growth phase for 24 h to 10(-6) M-soman, produced a statistically significant (P less than 0.001) decrease of the [14C] L-Leucine uptake and diminution of the incorporation of the amino acid into total protein. No changes were observed at lower concentrations. When energy metabolism was measured by uptake and retention of [14C] DG, the data indicate that both uptake and utilization of D-Glucose were unaffected by 10(-6) M-soman treatment. The results suggest that soman depress the rate of protein synthesis which may be responsible for neuronal degeneration. But no changes were observed on energy metabolism.
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PMID:[Effect of pinacolyl methylphosphonofluoridate on the metabolic activity of cultured neuroblastoma cells]. 623 88

Previous studies have revealed two different kinds of regulation of glucose utilization in cell lines derived from the nervous system (Keller et al., 1981). We found glucose metabolism of C-6 glioma cells to be limited and regulated by membrane transport. In contrast, glucose utilization of C-1300 neuroblastoma (N2A) cells was limited by the known regulatory enzymes of the Embden-Meyerhof pathway. Under the given experimental conditions the "membrane-limited" C-6 glioma cells were characterized by periodically changing glucose transport rates and very low intracellular glucose concentrations, which remained constant in spite of widely differing transport rates. These findings suggest the close functional coupling between transport and phosphorylation required for the regulation of glucose transport by cellular metabolic needs.
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PMID:Rapid cellular regulation of D-glucose transport in cultured neural cells. 629 65

The effect of dihydroergocristine on energy metabolism was studied in the isolated perfused rat brain affected by ischemia and in cultivated C-1300 neuroblastoma cells deprived of oxygen and glucose. Creatine phosphate, ATP, ADP, AMP, glucose, glucose-6-phosphate, fructose-6-phosphate, fructose-1,6-diphosphate, pyruvate, and lactate were measured enzymatically. After a perfusion period of 30 min, the cortex of the isolated perfused rat brain exhibited an energy state not different from that in vivo. Dihydroergocristine added to the perfusion medium (5 mumol/L) did not influence these substrate levels under normal perfusion conditions. However, this drug was able to retard the breakdown of high-energy phosphates during ischemia and to accelerate the restoration of the energy state during the postischemic reperfusion period. The perfusion rate was not changed by the drug, and therefore it was assumed that dihydroergocristine could act directly on cell metabolism. This view was supported by the results obtained from experiments using cultivated N-2a neuroblastoma cells. These cells were incubated in a buffered salt solution deprived of glucose and oxygen for 15 min. Under these conditions, dihydroergocristine (2 mumol/L) added to the incubation medium caused changes in the concentrations or the high-energy phosphates similar to those in the isolated brain preparation: It increased the ATP concentration and decreased the ADP concentration significantly.
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PMID:Effect of dihydroergocristine on energy metabolism studied in the isolated perfused rat brain affected by ischemia and in neuroblastoma cells deprived of oxygen and glucose. 643 25


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