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)

We report quantitative data on beta-glucuronidase- and sulfatase-hydrolyzable conjugates of homovanillic acid, 3,4-dihydroxyphenylacetic acid, p-hydroxyphenylacetic acid, and vanillic acid in the urine of 20 apparently normal and healthy control persons and of three patients with neuroblastoma. We used organic solvent extraction and capillary gas chromatography. There was considerable person-to-person variation in the conjugation percentages calculated. Mean conjugated percentages of the four compounds for 16 normal healthy persons 2.5--40 years of age were, respectively, 12%, 33%, 14%, and 35%. For newborns and patients with neuroblastoma, these percentages were somewhat different. Increased amounts of vanillic acid were found in the urine of the patients with neuroblastoma, but results of a small metabolic study in rats suggest that this increase most probably is of dietary origin.
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PMID:Urinary excretion of conjugated homovanillic acid, 3,4-dihydroxyphenylacetic acid, p-hydroxyphenylacetic acid, and vanillic acid by persons on their usual diet and patients with neuroblastoma. 45 49

A subclone of NG108-15 neuroblastoma-glioma hybrid cells was used to study the intracellular distribution of opioid receptors. Subcellular organelles were separated on self-generating Percoll-sucrose gradients and the enzymes beta-glucuronidase, galactosyltransferase, 5'-nucleotidase, and glucose-6-phosphatase were used as markers to localize the various structures. Analysis of the receptor distribution from untreated cells shows that the plasma membranes contained the highest receptor density, but a significant portion of the opioid binding sites was unevenly distributed between the lysosomes, microsomes, and Golgi elements. The enzyme markers indicated that appearance of opioid receptors in these intracellular structures does not result merely from contamination with plasma membranes. About 11% of the receptors appeared in a fraction lighter than plasma membranes. The antilysosomal agent chloroquine altered the intracellular compartmentation of the receptors, possibly by blocking their translocation in the cells. Leu-enkephalin induced time-dependent loss of receptors from all four intracellular compartments examined, but a kinetic analysis showed that the rate of receptor loss in these fractions was not identical. Thus, the percent of receptors appearing in the lysosomal fraction that could still bind [3H]D-Ala2-D-Leu5-enkephalin in vitro was increased on treatment with Leu-enkephalin. As an additional approach to follow the intracellular fate of the receptors, cells were labeled with [3H]diprenorphine, chased with various unlabeled opiates, and the distribution of 3H-ligand-receptors in the cells was monitored. Leu-enkephalin and etorphine altered the distribution of receptor-bound [3H]diprenorphine between the plasma membranes, lysosomes, and Golgi elements, whereas morphine had no such effect. The study sheds light on the role of intracellular structures in the metabolism of opioid receptors in untreated and opioid-treated cells.
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PMID:Subcellular compartmentation of opioid receptors: modulation by enkephalin and alkaloids. 300 5

Rabbit polyclonal antibodies were raised against beta-glucuronidase purified from mouse liver. This antiserum immunoprecipitated the beta-glucuronidase secreted by mouse fibroblasts but did not cross-react with the same enzyme isolated from human tissue. The beta-glucuronidase present in mouse 3T3 fibroblasts and mouse peritoneal macrophages was clearly identified by indirect immunofluorescence, using the antiserum and an FITC-conjugated second antibody, while human fibroblasts with normal levels of beta-glucuronidase activity did not fluoresce when tested with the same reagents. A range of human fibroblasts, human neuroblastoma and rat glioma cells did not fluoresce when incubated with the antibody but did fluoresce after they had been co-cultured for 24 h with mouse macrophages, showing that mouse beta-glucuronidase had been transferred from adherent macrophages into adjacent recipient cells. Transfer took place even when receptor-mediated endocytosis was blocked with a suitable competitive ligand, the transferred enzyme being visible mainly as a bright punctate fluorescence with a lysosome-like distribution. Macrophages thus have the potential to act as donors of lysosomal enzymes to a wide range of recipient cells and to transfer enzymes to them during direct cell-to-cell contact.
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PMID:Direct transfer of beta-glucuronidase from mouse macrophages to other types of cell. 391 78

Astrocytes are a good candidate cell type for brain transplantation: They are endogenous to the CNS, they have efficient secretory machinery, and they play a major role in neuronal support. We assessed the potential of genetically modified primary adult human astrocytes as vehicles for the delivery of secreted molecules in the mammalian CNS. We report that such cells can be efficiently transduced by a recombinant adenoviral vector carrying the human beta-glucuronidase cDNA (Ad/CMV*beta-glu) and that the transduced astrocytes produce large amounts of the enzyme. Released beta-glucuronidase could be captured, in vitro, by primary neurons and astrocytes and by a neuroblastoma cell line and beta-glucuronidase-deficient fibroblasts. Following grafting into the mouse striatum, adult human astrocytes survived and expressed the transgene for at least 8 weeks. Moreover, the dosage of beta-glucuronidase activity within the grafted brains revealed high enzymatic levels at a long distance from the graft. These experiments document the grafting of engineered primary adult human astrocytes, allowing the release of a secreted therapeutic factor throughout the brain.
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PMID:Primary adult human astrocytes as an ex vivo vehicle for beta-glucuronidase delivery in the brain. 1140 1

Genome-wide analyses have identified a set of TIR-NBS-encoding genes in plants. However, the molecular mechanism underlying the expression of these genes is still unknown. In this study, we presented a TIR-NBS-encoding gene, PtDrl02, that displayed a low level of tissue-specific expression in a triploid white poplar [(Populus tomentosa x P. bolleana) x P. tomentosa], and analyzed the effects of the 5' untranslated region (UTR) on gene expression. The 5' UTR sequence repressed the reporter activity of beta-glucuronidase (GUS) gene under PtDrl02 promoter by 113.5-fold with a staining ratio of 2.97% in the transgenic tobacco plants. Quantitative RT-PCR assays revealed that the 5' UTR sequence decreased the transcript level of the GUS reporter gene by 13.3-fold, implying a regulatory role of 5' UTR in transcription and/or mRNA destabilization. The comparison of GUS activity with the transcript abundance indicated that the 5' UTR sequence decreased the translation efficiency of target gene by 88.3%. Additionally, the analysis of the transgenic P-985/UTRDelta/GUS plants showed that both the exon1 sequence and the leading intron within the 5' UTR region were responsible for the regulation of gene expression. Our results suggested a negative effect of the 5' UTR of PtDrl02 gene on gene expression.
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PMID:Functional analysis of 5' untranslated region of a TIR-NBS-encoding gene from triploid white poplar. 1961 15

The PtDrl02 gene belongs to the TIR-NBS gene family in triploid white poplar (Populus tomentosa x P. bolleana) x P. tomentosa. Its expression pattern displays tissue-specificity, and the transcript level can be induced by wounding, methyl jasmonate (MeJA), and salicylic acid (SA). To understand the regulatory mechanism controlling PtDrl02 gene expression, we functionally characterized the PtDrl02 promoter region. Using the beta-glucuronidase as a reporter, we found that the PtDrl02 promoter directed gene expression mainly in the aerial parts of the plants and was confined to the cortex tissues of leaf veins, petioles, stems, and stem piths, showing a typical tissue-specific expression pattern. Deletion analysis revealed two positive regulatory regions (-985 to -669 and -669 to -467) responsible for the basal activity of the PtDrl02 promoter. Impressively, the sequence from -669 to -467 was shown to contain cis-element (s) responding to wounding and MeJA, while the promoter region between -244 and 0 could individually display wounding-responsiveness, and the fragment from -467 to -244 was required for SA- and NaCl-inducible expression of the PtDrl02 promoter. Additionally, it was found that the -985 to -669 sequence was the ABA-responding promoter fragment. These results suggested that the PtDrl02 promoter was modulated by multiple cis-regulatory elements in distinct and complex patterns to regulate PtDrl02 gene expression. Our study also suggested that the PtDrl02 gene 5' untranslated region, as well as a Populus WRKY transcription factor, PtWRKY1, was involved in the regulation of PtDrl02 promoter activities.
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PMID:Functional identification and regulation of the PtDrl02 gene promoter from triploid white poplar. 2017 34