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. Recent data suggesting that the human neuroblastoma SH-SY5Y is a suitable cell line in which to study the effect of second messengers on NA release are discussed in the context of current views on exocytosis. 2. Release of NA is evoked by depolarization, as well as activation of muscarinic (M3) and bradykinin (B2) receptors in SH-SY5Y cells which have not been differentiated by the addition of growth factors. 3. Evoked release is enhanced by activation of protein kinase C. 4. Activation of protein kinase C decreases the changes in intracellular calcium evoked by carbachol, bradykinin and 100 mM K+. 5. SH-SY5Y express N-type and L-type voltage sensitive Ca2+ channels. L-Type Ca(2+)-channels are coupled to NA release under conditions of weak depolarization. However with strong depolarization (100 mM K+) both L-type and N-type channels are involved. 6. Muscarinic- and neuropeptide Y receptors are coupled to the inhibition of Ca2+ channel activity.
Gen Pharmacol 1995 Oct
PMID:The use of the human neuroblastoma SH-SY5Y to study the effect of second messengers on noradrenaline release. 759 Jan 7

In many eukaryotic cell types, receptor activation leads to the formation of inositol 1,4,5-trisphosphate (IP3) which causes calcium ions (Ca) to be released from internal stores. Ca release was observed in response to the muscarinic agonist carbachol by fura-2 imaging of N1E-115 neuroblastoma cells. Ca release followed receptor activation after a latency of 0.4 to 20 s. Latency was not caused by Ca feedback on IP3 receptors, but rather by IP3 accumulation to a threshold for release. The dependence of latency on carbachol dose was fitted to a model in which IP3 synthesis and degradation compete, resulting in gradual accumulation to a threshold level at which Ca release becomes regenerative. This analysis gave degradation rate constants of IP3 in single cells ranging from 0 to 0.284 s-1 (0.058 +/- 0.067 s-1 SD, 53 cells) and a mean IP3 lifetime of 9.2 +/- 2.2 s. IP3 degradation was also measured directly with biochemical methods. This gave a half life of 9 +/- 2 s. The rate of IP3 degradation sets the time frame over which IP3 accumulations are integrated as input signals. IP3 levels are also filtered over time, and on average, large-amplitude oscillations in IP3 in these cells cannot occur with period < 10 s.
J Gen Physiol 1995 Jan
PMID:The lifetime of inositol 1,4,5-trisphosphate in single cells. 773 Jul 88

Uptake of catechol isoquinolines to dopamine cells was studied using human dopaminergic neuroblastoma SH-SY5Y cells. Only (R)-1,2-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline [(R)-1,2-DiMeDHTIQ] was transported by dopamine uptake system, while (S)-1,2-DiMeDHTIQ, (R)- and (S)-1-methyl-6,7-dihydroxy-tetrahydroisoquinoline, and 1,2-dimethyl-6,7-dihydroxyisoquinolinum ion were not. Kinetical study showed that the uptake of (R)-1,2-DiMeDHTIQ followed the Michaelis-Menten equation, and the values of the Michaelis constant and the maximal velocity were obtained to be 102.6 +/- 36.9 microM and 66.0 +/- 2.8 pmol/min/mg protein. Dopamine was found to inhibit (R)-1,2-DiMeDHTIQ uptake competitively. These results suggest that the selective uptake by dopamine transporter may account for the specific neurotoxicity of (R)-1,2-DiMeDHTIQ to dopamine neurons.
J Neural Transm Gen Sect 1994
PMID:Uptake of a neurotoxin-candidate, (R)-1,2-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline into human dopaminergic neuroblastoma SH-SY5Y cells by dopamine transport system. 773 8

1. Cultured human SH-SY5Y neuroblastoma cells were used to determine whether 17-beta-estradiol affects the metabolism of microtubular tau protein. 2. After 24-hr treatment 17-beta-estradiol (10(-7) M) increased 50 kDa tau protein in the cytoplasmic (supernatant) fraction and decreased it in the membrane (pellet) fraction. 3. The increase in cytoplasmic tau was accompanied by increases in total protein in both cytoplasmic and membrane fractions, 50 and 70%, respectively. 4. The estrogen (10(-7) M) also caused a 31% reduction in the total number of cells.
Gen Pharmacol 1993 Nov
PMID:Changes in microtubular tau protein after estrogen in a cultured human neuroblastoma cell line. 790 61

The activation of muscarinic receptors in N1E-115 neuroblastoma cells elicits a voltage-independent calcium current. The current turns on slowly, reaches its maximum value approximately 45 s after applying the agonist, is sustained as long as agonist is present, and recovers by one half in approximately 10 s after washing the agonist away. The current density is 0.11 +/- 0.08 pA/pF (mean +/- SD; n = 12). It is absent in zero-Ca++ saline and reduced by Mn++ and Ba++. The I(V) curve characterizing the current has an extrapolated reversal potential > +40 mV. The calcium current is observed in cells heavily loaded with BAPTA indicating that the calcium entry pathway is not directly gated by calcium. In fura-2 experiments, we find that muscarinic activation causes an elevation of intracellular Ca++ that is due to both intracellular calcium release and calcium influx. The component of the signal that requires external Ca++ has the same time course as the receptor operated calcium current. Calcium influx measured in this way elevates (Ca++)i by 89 +/- 41 nM (n = 7). Thapsigargin, an inhibitor of Ca++/ATPase associated with the endoplasmic reticulum (ER), activates a calcium current with similar properties. The current density is 0.22 +/- 0.20 pA/pF (n = 6). Thapsigargin activated current is reduced by Mn++ and Ba++ and increased by elevated external Ca++. Calcium influx activated by thapsigargin elevates (Ca++)i by 82 +/- 35 nM. The Ca++ currents due to agonist and due to thapsigargin do not sum, indicating that these procedures activate the same process. Carbachol and thapsigargin both cause calcium release from internal stores and the calcium current bears strong similarity to calcium-release-activated calcium currents in nonexcitable cells (Hoth, M., and R. Penner. 1993. Journal of Physiology. 465:359-386; Zweifach, A., and R. S. Lewis, 1993. Proceedings of the National Academy of Sciences, USA. 90:6295-6299).
J Gen Physiol 1994 Jul
PMID:Calcium current activated by muscarinic receptors and thapsigargin in neuronal cells. 796 92

We have studied human immunodeficiency virus type 1 (HIV-1) infection in human SH-SY5Y neuroblastoma cells at various stages of morphological differentiation. Two days' treatment of the cells with retinoic acid (RA) or dibutyryl cAMP (db-cAMP) resulted in the appearance of elongated neurites and enhanced production of 160K to 200K neurofilament proteins as shown by indirect immunofluorescence. DNA synthesis was reduced only in RA-treated cells as detected by 5-bromo-2'-deoxyuridine incorporation. The cells were infected with two T-lymphotropic virus strains (IIIB and NDK) and two fresh isolates (39001 and 46001) from bronchoalveolar lavage samples of AIDS patients. The latter two isolates were unable to form syncytia in infected CD4-positive T-lymphoblastoid C8166 cells which was in contrast to our T-lymphotropic virus strains. Interphase in situ hybridization showed that 14 to 16% of SH-SY5Y cells become positive for HIV-1 DNA. Regardless of the virus strain, morphological differentiation of the cells with RA or db-cAMP inhibited infection by 50% at a single cell in situ resolution. Nested PCR confirmed the presence of proviral DNA in the infected cells. These results show that human neuroblastoma cells, tumour cells of neuroectodermal origin, can be infected by different HIV-1 isolates and that the infection is inhibited by neurotypic cell differentiation.
J Gen Virol 1994 Jan
PMID:Morphological differentiation of human SH-SY5Y neuroblastoma cells inhibits human immunodeficiency virus type 1 infection. 811 28

We describe the analysis of the herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) promoter using an HSV-1-based vector system. Sequences under investigation for LAT promoter activity were analysed for their ability to direct chloramphenicol acetyltransferase gene expression, either in transfection assays or following their insertion into an HSV-1 vector from which the endogenous LAT promoter sequences had been removed. The analysis mapped the main determinants of LAT promoter activity during lytic infection of tissue culture cells to a 277 bp region between -279 and -2 relative to the recognized 5' end of the primary 8.3 kb transcript. The LAT promoter constructs behaved similarly in the context of the virus genome and in the plasmid-based transfection assays. Comparison of the relative activities following infection of fibroblast and neuroblastoma cell lines indicates that sequences upstream from -279 are important for LAT promoter activity in neurons.
J Gen Virol 1994 Feb
PMID:Analysis of sequences important for herpes simplex virus type 1 latency-associated transcript promoter activity during lytic infection of tissue culture cells. 811 52

Several H-2 defined cell lines were examined for their ability to support infection and replication of Japanese encephalitis virus (JEV) before their use in in vitro and in vivo stimulation protocols for generating cytotoxic T lymphocytes (CTLs) against JEV. Among 11 different cell lines tested, two H-2d macrophage tumour lines (P388D1, RAW 264.7), an H-2d hybridoma (Sp2/0), an H-2KkDd neuroblastoma (Neuro 2a), and H-2k fibroblast cell line (L929) were found to support JEV infection and replication. These cell lines were used to generate anti-JEV CTLs by using in vivo immunization followed by in vitro stimulation of BALB/c mice. We observed that not only syngeneic and allogeneic infected cells but also JEV-infected xenogeneic cells could prime BALB/c mice for the generation of JEV-specific CTLs upon subsequent in vitro stimulation of splenocytes with JEV-infected syngeneic cells. Although infected xenogeneic cells were used for immunization, the anti-JEV effectors that were generated lysed infected syngeneic targets but not JEV-infected xenogeneic or allogeneic target cells in a 5 h 51Cr release assay. These anti-JEV effectors recognized syngeneic target cells infected with West Nile virus to a lesser extent and were shown to be Lyt-2.2+ T cells. The results of unlabelled cold target competition studies suggested alterations in the cell surface expression of viral antigenic determinants recognized by these CTLs. We further demonstrate that the JEV-specific CTLs generated could virtually block the release of infectious virus particles from infected P388D1 and Neuro 2a cells in vitro.
J Gen Virol 1994 Apr
PMID:Cytotoxic T lymphocytes raised against Japanese encephalitis virus: effector cell phenotype, target specificity and in vitro virus clearance. 815 Dec 96

To investigate the effect of persistent measles virus infection on signal transduction in cells of neuronal origin, the mouse neuroblastoma cell line NS20Y/MS, which is persistently infected with measles virus, was used. The results demonstrate an approximate 50% increase in total phosphorylation and a similar increase in protein kinase C (PKC) activity. Western blot analysis with anti-total PKC or anti-PKC-alpha antibodies revealed a significant increase in the level of an 80K immunoreactive PKC in NS20Y/MS cells. Following incubation of NS20Y/MS cells with polyclonal anti-measles virus antibodies, which down-regulate the level of measles virus proteins, total and PKC-mediated phosphorylation returned to the basal level of uninfected cells. This effect was reversible and removal of the antibodies resulted in restoration of the high level of total and PKC-mediated phosphorylation. The release of infectious measles virus was strongly inhibited by incubation of NS20Y/MS cells with the PKC inhibitor, 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine (H-7). These results demonstrate that measles virus induces elevation in cellular phosphorylation which is essential for measles virus production.
J Gen Virol 1994 Apr
PMID:Reversal of the measles virus-mediated increase of phosphorylating activity in persistently infected mouse neuroblastoma cells by anti-measles virus antibodies. 815 Dec 98

There are major differences between tumors in children and adults, viz. the incidence of tumor types, the predisposition of certain organs and tissues (e.g. sympathetic nervous tissue, kidney, and soft tissues) to develop tumors, problems related to tumor classification, and the biologic behavior of childhood malignancies, which are usually characterized by high rates of proliferation activity. A large number of new entities, especially in soft tissue tumors, have been published over the past years, including nodular mesothelial hyperplasia, which is a tumor-like lesion derived from peritoneal macrophages; infantile myofibromatosis, which can mimic leiomyosarcoma; intermediate grade fibrohistiocytic tumors, like dermatofibrosarcoma protuberans-related giant-cell fibroblastoma, plexiform fibrohistiocytic tumor and angiomatoid malignant fibrous histiocytoma displaying evidence of myogeneous differentiation; finally, the high-grade intraabdominal desmoplastic small cell tumor. With modern methods we can gain better insights into the biology of tumors. For example, tumors of the Ewing's sarcoma family have in common a characteristic t(11; 22) chromosomal translocation, the Ewing's sarcoma (EWS) (22q12) gene rearrangement, and the MIC2 gene. The EWS gene rearrangement is not restricted to tumors of the Ewing's sarcoma family (classic Ewing's sarcoma and malignant peripheral neuroectodermal tumor), however, but occurs in malignant melanoma of the soft tissue and in intraabdominal desmoplastic small cell tumor. Rhabdomyosarcomas (RMS) can be divided into two basic types with different prognoses: embryonal RMS, including botryoid and spindle-cell variants, and alveolar RMS, including the solid variant. The prognosis of alveolar RMS is poorer than that of classic embryonal RMS, mainly due to early tumor dissemination in alveolar RMS. The prognosis of neuroblastoma is mainly based on chromosomal and molecular biologic findings. Structural chromosome 1 abnormalities, double minute chromosomes, homogeneously staining regions, N-myc amplifications, and DNA diploidy are indications for an unfavorable outcome. Despite progress in childhood solid tumor pathology, many questions remain open, including those relating to basic chromosomal defects in germ cell tumors and the obscure nature of tumor heterogeneity.
Gen Diagn Pathol 1995 May
PMID:New entities, concepts, and questions in childhood tumor pathology. 854 1


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