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)

The non-permissivity of C1300 mouse neuroblastoma cells for herpes simplex virus (HSV) infection is due to a failure of such cells to transcribe the immediate-early (IE) genes following viral infection. We have transfected both C1300 cells and permissive cells with constructs in which each of the 5 IE promoters drives expression of the readily assayable chloramphenicol acetyl transferase (CAT) gene. These experiments show that the lack of IE gene transcription in C1300 cells is due to the weak activity of the five IE promoters in these cells compared to that observed in a range of permissive cell types. This effect is mediated both by up-stream elements and by sequences present in the minimal promoter. The different effects of DNA concentration on the activities of the minimal and complete promoters suggests that the up-stream sequences act by binding a repressor factor present in C1300 cells whilst the weak activity of the minimal promoter results from the absence of a positive factor in such cells.
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PMID:Regulation of herpes simplex virus immediate-early gene promoters in mouse neuroblastoma cells. 217 73

The effect in vitro of some cytoplasmic structure and function inhibitors on the different stages of rabies virus infection was investigated. Treatment of fibroblasts (CER) and human neuroblastoma cells (IMR-32) with substances acting on low pH intracellular compartments (methylamine and monensin) prevented rabies virus genome delivery in the cytosol. An early inhibition of viral infection was also obtained in the presence of B and D cytochalasins and trifluoperazine which interact with microfilament structures. Treatment with colchicine and vinblastine did not affect rabies multiplication, suggesting that microtubules are not involved in this process. However, the multiplication of prebound virions did not take place in the presence of inhibitors of oxidative phosphorylation (sodium azide and CCCP) and of glycolysis (2-deoxy-D-glucose) indicating that rabies virus replication is largely energy-dependent in both host cells examined.
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PMID:Effect of inhibitors of cytoplasmic structures and functions on rabies virus infection in vitro. 229 83

Evidence is presented that LDH virus infection of mice results in drastic changes in several immune activities. Serum IFN titer and splenic NK activity are increased during the acute phase of infection. NK stimulation is mediated by IFN-alpha,beta since injection of an antibody against murine IFN-alpha,beta is able to abolish the effect. IL-2 production is inhibited throughout the study period following injection of LDH virus (14 days), although a partial recovery is observed during the second week. Similarly, IL-2 receptor expression and MLC responsiveness are suppressed. This suppression lasts for 2 and 7 days respectively after injection. Addition of recombinant IL-2, but not of indomethacin, to the MLC cultures restores the proliferation rate. Not only proliferation but also cytotoxic cell generation in MLC is diminished during the first week after LDH virus injection. Again, this response is normalized at day 14. Additional observations indicate that LDH virus is present in murine neuroblastoma. This explains some of the previously described effects of this tumor on the cellular immune system of the host.
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PMID:Cellular immunity changes caused by LDH virus: analogy with observations of neuroblastoma-bearing mice. 244 3

The effect of persistent measles virus infection on c-fos protooncogene and protein kinase C (PKC-I) gene expression in a murine neuroblastoma cell line was studied. Overexpression of c-fos protooncogene by infected NS20Y/MS cells was detected when compared with uninfected NS20Y cells. The level of PKC-I-specific mRNA was increased in infected NS20Y/MS cells. In addition, the level of total PKC activity in these cells was also enhanced. We conclude that persistent measles virus infection can alter both protooncogene expression and signal transduction in cells of neuronal origin.
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PMID:Effect of persistent measles virus infection on protein kinase C activity and c-fos protooncogene expression in neuroblastoma cells. 250 30

Opsoclonus is a very rare ocular dyskinesia associated to a viral infection or neoplasms, being neuroblastoma in children or carcinoma in adults. A case of opsoclonus as a paraneoplastic symptom preceding the diagnosis of breast carcinoma is presented. The abnormal movements had a complete response to the administration of chlormethiazole.
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PMID:[Opsoclonic cerebellar disease. A paraneoplastic syndrome sensitive to chlormethiazole]. 256 74

The ability of a neurotropic virus, mouse hepatitis virus type 3 (MHV3), to invade the central nervous system (CNS) and to recognize cells selectively within the brain was investigated in vivo and in vitro. In vivo, MHV3 induced in C3H mice a genetically controlled infection of meningeal cells, ependymal cells, and neurons. In vitro, purified MHV3 bound to the surface of isolated ependymal cells and cultured cortical neurons but not to oligodendrocytes or cultured astrocytes. MHV3 replicated within cultured cortical neurons and neuroblastoma cells (NIE 115); infected cultured neurons nonetheless survived and matured normally for a 7-day period postinfection. On the other hand, MHV3 had a low affinity for cortical glial cells or glioma cells (C6 line), both of which appear to be morphologically unaltered by viral infection. Finally, MHV3 infected and disrupted cultured meningeal cells. This suggests that differences in the affinity of cells for MHV3 are determinants of the selective vulnerability of cellular subpopulations within the CNS. In vivo, a higher titer of virus was needed for CNS penetration in the genetically resistant (A/Jx) mice than in the susceptible (C57/BL6) mouse strain. However, in spite of viral invasion, no neuropathological lesions developed. In vitro viral binding to adult ependymal cells of susceptible and resistant strains of mice was identical. Genetic resistance to MHV3-CNS infection appeared to be mediated both by a peripheral mechanism limiting viral penetration into the CNS and by intra-CNS mechanisms, presumably at a stage after viral attachment to target cells.
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PMID:Selective tropism of a neurotropic coronavirus for ependymal cells, neurons, and meningeal cells. 302 91

Opsoclonus-myoclonus (OM) is a neurological disorder usually occurring in infancy, clinically manifested by various involuntary movements. The pathogenesis of OM is unknown, but since the disease often is associated with viral infection or with neuroblastoma, an immunologic basis for OM has been postulated. We have studied two children with OM whose serum contained antibodies directed against the 210 kDa neurofilament protein; these antibodies were not seen in the serum of 21 children with other neurological disorders. Neurofilament proteins, which are found only in neurons, may be of prime importance in neuronal function, especially during development of the nervous system. Our findings suggest that generation of antibodies to the neurofilament proteins can occur in patients with opsoclonus-myoclonus; the role of the anti-NF210K antibodies in the pathogenesis of OM, however, is uncertain.
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PMID:Anti-neurofilament protein antibodies in opsoclonus-myoclonus. 329 94

This paper describes the inhibitory effect of a normal rat brain solubilized membrane preparation (RBSM-liposomes) on rabies virus infection. Rabies virus was incubated with RBSM-liposomes or their separated components (proteins, phospholipids, gangliosides) before infection of CER or neuroblastoma cells. In addition, both RBSM-liposomes and target cells were treated with enzymes prior to the infection step. All these experimental procedures showed that the active components were mainly lipids.
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PMID:Inhibition of rabies virus infection by a soluble membrane fraction from the rat central nervous system. 334 23

Acute and persistent rabies virus infection of mouse neuroblastoma-rat glioma hybrid cells (NG-108-15) results in a loss of the normal inhibiting function of opiates via the opiate receptor on hormone-stimulated adenylate cyclase activity. Previous studies of these persistently infected cells have shown a decrease in the affinity of the opiate receptors for agonists without any change in the number of these receptors. We now demonstrate that persistently infected cells are unable to couple the opiate receptors to the inhibitory regulatory protein Ni of the adenylate cyclase, as measured by the loss of stimulation of the GTPase activity of this protein. However, the unstimulated basal GTPase activities of the regulatory components Ni and Ns are unchanged in the persistently infected cells. These studies also reveal a disorder of the stimulation of the adenylate cyclase by GTP or fluoride via the stimulating regulatory G/F protein (Ns) in persistently infected cells, whereas direct stimulation of the catalytic subunit of the adenylate cyclase by forskolin remains unchanged. Therefore, there are different points of dysfunction caused by the persistent rabies infection in the signal pathway from the opiate receptor to the adenylate cyclase and from the stimulating Ns protein to the enzyme: (i) opiate receptor binding is reduced by a decrease of agonist affinity (previously published data), (ii) the stimulation of GTPase activity of the inhibiting regulatory component Ni of the adenylate cyclase system is inhibited, and (iii) the signal pathway from the stimulating regulatory component of the adenylate cyclase system to the unchanged activity of the catalytic subunit is defective.
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PMID:Inhibition of opiate receptor-mediated signal transmission by rabies virus in persistently infected NG-108-15 mouse neuroblastoma-rat glioma hybrid cells. 614 55

A potent interferon (IFN) inducer, 2-amino-5-bromo-6-phenyl-4-pyrimidinone (ABPP), induced hyporeactivity in mice, and so IFN induced by subsequently administered ABPP was reduced even 120 hr after the first administration of ABPP. This hyporeactivity was counteracted by the injection of IFN (10,000 IU or more) 3 hr before the subsequent administrations of ABPP. Since the injection of more than 5,000 IU/mouse of IFN 3 hr before an administration of ABPP enhanced the circulating IFN titer, the priming effect in vivo by IFN may result in the reduction of hyporeactivity. Administrations of ABPP (200 mg/kg or 500 mg/kg) at intervals of 2 days and the injection of IFN (25,000 IU/mouse) 3 hr before each administration of ABPP to neuroblastoma-bearing A/J mice reduced the mortality and completely cured 40% of the mice in each combined therapy group. These results suggest that the combined use of the IFN inducer with IFN may be available for patients with neoplasm or viral infection.
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PMID:Interferon counteracts pyrimidinone-induced hyporeactivity and the combined treatment has antitumor effect in mice. 620 30


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