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 effect of estradiol-17 beta on the activities of glycolytic enzymes from female rat brain was studied. The following enzymes were examined: hexokinase (HK, EC 2.7.1.1), phosphofructokinase (PFK, EC 2.7.1.11), aldolase (EC 4.1.2.13), glyceraldehyde-3-phosphate dehydrogenase (EC 1.2.1.12), phosphoglycerate kinase (EC 2.7.2.3), phosphoglycerate mutase (EC 2.7.5.3), enolase (EC 4.2.1.11) and pyruvate kinase (PK, EC 2.7.1.40). The activities of HK (soluble and membrane-bound), PFK and PK were increased after 4 h of hormone treatment, while the others remained constant. The changes in activity were not seen in the presence of actinomycin D. The significant rise of the activities of the key glycolytic enzymes was also observed in the cell culture of mouse neuroblastoma C1300 treated with hormone. Only three of the studied isozymes, namely, HKII, B4 and K4 were found to be estradiol-sensitive for HK, PFK and PK, respectively. The results obtained suggest that rat brain glycolysis regulation by estradiol is carried out in neurons due to definite isozymes induction.
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PMID:Rat brain glycolysis regulation by estradiol-17 beta. 153 2

Inherited variations in monoamine oxidase (MAO) activity are thought to affect human behavior and expression of disease. The present study has established the chromosomal location of one of the structural genes coding for this enzyme. Mapping was carried out by somatic cell hybridization between normal human skin fibroblasts and mouse neuroblastoma cells. Selective media for growth of cells with or without hypoxanthine phosphoribosyltransferase (HPRT) activity were used to obtain hybrid lines which had retained or lost the human X chromosome, respectively. Cytogenetic techniques, isozyme analysis, and limited proteolysis and peptide mapping of [3H]pargyline-labeled MAO were used to characterize hybrid lines. With one exception, only lines containing the human X chromosome and human forms of two X-linked enzymes (phosphoglycerate kinase and glucose-6-phosphate dehydrogenase) expressed the human form of the flavin polypeptide of type A MAO. The exceptional hybrid line contained a putative translocation of part of the human X chromosome, since it expressed human forms of both MAO and phosphoglycerate kinase but neither the human form of glucose-6-phosphate dehydrogenase nor HPRT activity. This evidence indicates that the structural gene for the flavin polypeptide of MAO-A is on the human X chromosome. This represents the first chromosomal assignment of a human gene coding for an enzyme of neurotransmitter metabolism. This information will help to elucidate the structure of MAO and modes of its inheritance in the human population.
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PMID:Gene for monoamine oxidase type A assigned to the human X chromosome. 719 39

Prion diseases are induced by pathologically misfolded prion protein (PrPSc), which recruit normal sialoglycoprotein PrPC by a template-directed process. In this study, we investigated the expression of PrPC in a rat model of cerebral ischemia to more fully understand its physiological role. Immunohistochemical analysis demonstrated that PrPC-immunoreactive cells increased significantly in the penumbra of ischemic rat brain compared with the untreated brain. Western blot analysis showed that PrPC protein expression increased in ischemic brain tissue in a time-dependent manner. In addition, PrPC protein expression was seen to colocalize with neuron, glial, and vascular endothelial cells in the penumbric region of the ischemic brain. Overexpression of PrPC by injection of rAd (replication-defective recombinant adenoviral)-PGK (phosphoglycerate kinase)-PrPC-Flag into ischemic rat brain improved neurological behavior and reduced the volume of cerebral infarction, which is supportive of a role for PrPC in the neuroprotective adaptive cellular response to ischemic lesions. Concomitant upregulation of PrPC and activated extracellular signal-regulated kinase (ERK1/2) under hypoxia-reoxygenation in primary cortical cultures was shown to be dependent on ERK1/2 phosphorylation. During hypoxia-reoxygenation, mouse neuroblastoma cell line N18 cells transfected with luciferase rat PrPC promoter reporter constructs, containing the heat shock element (HSE), expressed higher luciferase activities (3- to 10-fold) than those cells transfected with constructs not containing HSE. We propose that HSTF-1 (hypoxia-activated transcription factor), phosphorylated by ERK1/2, may in turn interact with HSE in the promoter of PrPC resulting in gene expression of the prion gene. In summary, we conclude that upregulation of PrPC expression after cerebral ischemia and hypoxia exerts a neuroprotective effect on injured neural tissue. This study suggests that PrPC has physiological relevance to cerebral ischemic injury and could be useful as a therapeutic target for the treatment of cerebral ischemia.
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PMID:Overexpression of PrPC by adenovirus-mediated gene targeting reduces ischemic injury in a stroke rat model. 1619 87

Lentiviral vectors transduce both dividing and non-dividing cells and can support sustained expression of transgenes. These properties make them attractive for the transduction of neurons and other neural cell types in vitro and in vivo. Lentiviral vectors can be targeted to specific cell types by using different promoters in the lentiviral shuttle vector. Even with identical constructs, however, levels of expression can vary significantly in different types of neurons and different culture preparations; expression levels in the same neuronal subtypes can be very different in primary cell culture and in vivo. We systematically assessed the ability of different promoters to direct expression of foreign transgenes in primary murine neocortical neurons, cerebellar granule cells and in undifferentiated and differentiated neuroblastoma cells. In primary cortical neurons, constructs using the ubiquitin C promoter directed the highest level of transgene expression; the phosphoglycerate kinase (PGK) promoter also directed robust transgene expression, while the cytomegalovirus (CMV) and MND (a synthetic promoter that contains the U3 region of a modified MoMuLV LTR with myeloproliferative sarcoma virus enhancer) promoters resulted in the expression of the transgenes in only limited number of neurons. In contrast, in cerebellar granule cells and in differentiated SH-SY5Y neuroblastoma cultures, the CMV promoter directed the most robust transgene expression. There was similar variability in transgene expression directed by these promoters in primary cultures of oligodendrocytes and astrocytes. These findings may prove useful in the design of lentiviral vectors for use in cell culture models of the nervous system.
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PMID:Optimal promoter usage for lentiviral vector-mediated transduction of cultured central nervous system cells. 2034 73