Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The enzymic activity of acid alkaline phosphatases, of alanyl- and leucine-aminopeptidases, of beta-galactosidase and beta-glucuronidase, and of Tween-60-esterase was tested in the rabbit lung tissue during the following experimental processes: a) the sensitization with Freund adjuvant containing PPD and challenge of the delayed hypersensitivity reaction to PPD), b) the sensitization with gamma-globulin in Freund adjuvant, c) the pulmonary Arthus reaction, d) the lung granulomas induced by intravenous administration of Freund adjuvant containing heterologous lung proteins, e) the tuberculosis and silicotuberculosis under the influence of tuberculostatics. A metabolic intensification expressed by a marked increase of the tested hydrolytic enzymes was observed comparatively with controls in all these immune, granulomatous and inflammatory processes experimentally induced in the lung. The morphologic substrate of this behaviour was represented by the numerous cell proliferation and differentiations of the reticulomacrophagic type occurring during these experimental processes under the stimulation of antigenic elicitors. The latter also induced an increase of the lysosome-formation as submicroscopic site of these hydrolytic enzymes.
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PMID:Histoenzymology of the lung. II. The behaviour of lung hydrolytic enzymes during some experimental pulmonary processes. 14 Mar 19

To investigate the mechanisms that control expression of the gene for pyruvate, orthophosphate dikinase (PPDK) in maize, the 5' flanking region of the gene was analyzed for interactions with nuclear extracts. Gel retardation assays showed that there are several sites in the promoter region which bind to protein factors. In this report we describe further study of one of these sites, designated the PPD-1 binding site. The nuclear binding factor, PPD-1, is restricted to nuclear extracts from green leaves where the PPDK gene is expressed. No binding of PPD-1 was detected in tissues such as roots or etiolated leaves where the gene is not expressed in vivo. Gel retardation assays using deletion fragments from the promoter region and synthetic oligonucleotides, as well as exonuclease III protection assays, revealed that the site of PPD-1 binding lies between positions -301 and -296. To identify the functional role of the interaction between PPD-1 and its binding site, a deletion series of the promoter region was joined to a reporter gene, beta-glucuronidase. These constructs were introduced into green leaves of maize by microprojectile bombardment. Expression of the reporter gene occurred if the PPD-1 binding site remained in the promoter region of the chimeric genes but deletion of the binding site caused a drastic reduction in expression levels. These data indicate that interaction between PPD-1 and its binding site is essential for active transcription of the PPDK gene.
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PMID:Cis-acting elements in the pyruvate, orthophosphate dikinase gene from maize. 165 3

Bilateral hilar and mediastinal lymphadenopathy was observed in a 32-year-old man who had been engaged in asbestos spraying for 16 years. Lymph nodes obtained from Daniel's biopsy revealed tissue reaction compatible with sarcoidosis. On the other hand, a large number of asbestos particles were detected in the lung tissue from transbronchial lung biopsy and in bronchoalveolar lavage fluid, but no epithelioid granuloma was observed in the lung tissue. Various immunoserological findings such as PPD skin test, serum angiotensin converting enzyme activity, serum beta-glucuronidase and lysozyme level, serum antinuclear antibody, lymphocyte subset of blood and bronchoalveolar lavage fluid were inconsistent with sarcoidosis. However, lymph node enlargement and immunological abnormalities in this patient may be related to asbestos exposure and may not have occurred merely by chance.
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PMID:Sarcoid reaction observed in a worker with a history of asbestos exposure. 223 96

Experiments are reported dealing with the correlation between activities of lysosomal acid hydrolases and hyperreactivity to endotoxin induced by BCG infection. Acid hydrolases were determined quantitatively in peritoneal MP, liver homogenate, and plasma of normal and hyperreactive mice. Mice infected with BCG not only exhibited a hyperreactive state to lethal effect of endotoxin, but also responded to endotoxin by rapid increase of acid hydrolases, especially of beta-glucuronidase, in the plasma; whereas control mice responded to endotoxin by almost no change in plasma acid hydrolases. The extent of increase of beta-glucuronidase in plasma of hyperreactive mice was shown to correlate fairly well with the degree of hyperreactivity to the lethal effect of endotoxin. Desensitization of such animals with endotoxin was found to cause a decreased response of plasma beta-glucuronidase parallel with decreased mortality. A large amount of PPD exerted the similar effect to that of endotoxin in hyperreactive mice. Furthermore, the effect of PPD was decreased by desensitization of such animals with endotoxin, a fact which suggests contamination of PPD with endotoxin.
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PMID:LYSOSOMAL ACID HYDROLASES AND HYPERREACTIVITY TO ENDOTOXIN IN MICE INFECTED WITH BCG. 1427 28