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

Rabbit alveolar macrophages were exposed in culture medium to asbestos, beryllium sulfate, and beryllium oxide. The specific activities of the lysosomal hydrolases, acid phosphatase beta-N-acetylglucosaminidase and beta-glucuronidase plus the glycolytic enzyme, phosphohexose isomerase were determined in the medium, whole-cell homogenates, mitochondrial fractions, and supernatant. These hydrolases increased significantly in the medium but not in the mitochondrial fraction of cells exposed to dusts. Asbestos and beryllium sulfate were highly cytotoxic for alveolar macrophages in vitro and the data suggested that these agents were not associated with an increase in enzyme synthesis but rather a direct cytotoxic effect at the macrophage membrane level. For induction of enzyme release in vitro, a higher concentration of beryllium oxide was needed when compared with asbestos and beryllium sulfate. The cytotoxicity and enzyme release induced by these agents may represent an important nonspecific mechanism by which they induce inflammation and perhaps local proliferation of fibroblasts.
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PMID:Effects of asbestos and beryllium on release of alveolar macrophage enzymes. 45 20

Serum concentrations of lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBD), phosphohexose isomerase (PHI), leucine aminopeptidase (LAP), beta-glucuronidase (beta-gluc) and angiotensin-converting enzyme (ACE), were measured in 107 cases of untreated acute myeloid leukaemia which were classified by morphological, immunological and cytochemical criteria. The results show that serum LDH was increased in most cases, irrespective of leukaemic subtype, serum PHI and LAP were significantly higher in monocytic variants and serum beta-gluc and ACE levels were generally within normal limits. In addition, significant (p less than 0.05) relationships were found between serum LDH, PHI, LAP and beta-gluc concentrations and the numbers of circulating leucocytes.
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PMID:Serum enzyme concentrations in untreated acute myeloid leukaemia. 301 Nov 55

Enzyme activity changes in reagent and neoplastic glia are examined. In the case of reagent glia, considerably increased ADPase, ATPase and AMPase values have been observed in experimental elective parenchymal necrosis in the rat, in hypertrophic astrocytes from recent plaques in multiple necrosis, in demyelinisation associated with cyanide encephalopathy, and in reagent astrocytes surrounding tumours and arteriosclerosis sites. Depressed ATPase values have been observed in experimental oedema, as compared with increased TPPase in human oedema. BuChE and ChE activity disappears in both oligodendro- and astroglia near old cerebral infarct sites, whereas there is marked BuChE activity peripherally to multiple sclerosis plaques and in areas of phenylpyruvic oligophrenia demyelinisation. In neoplastic glia, ADPase is clearly evident in malignant gliomas, ATPase is related to the extent of the cell body, AMPase is positive in medulloblastoma cell cytoplasm and beta-glucuronidase increases in anaplasia. Above-normal ChE activity has been observed in astrocyte tumors, while BuChE is greater than that of AChE. Phosphorylase reaction is intense in astrocytoma and in glioblastoma giant cells. Phosphoglucomutase values are below-normal in tumours, except in the case of ependymoma, while both phosphohexoisomerase and hexokinase display increased activity in atypical forms.
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PMID:[Histochemical demonstration of glial enzyme activity. II. Reagent and neoplastic glia]. 1734 Aug 8

In the K/BxN mouse model of rheumatoid arthritis, autoantibodies specific for glucose-6-phosphate isomerase (GPI) can transfer joint-specific inflammation to most strains of normal mice. Binding of GPI and autoantibody to the joint surface is a prerequisite for joint-specific inflammation. However, how GPI localizes to the joint remains unclear. We show that glycosaminoglycans (GAGs) are the high affinity (83 nm) joint receptors for GPI. The binding affinity and structural differences between mouse paw/ankle GAGs and elbows/knee GAGs correlated with the distal to proximal disease severity in these joints. We found that cartilage surface GPI binding was greatly reduced by either chondroitinase ABC or beta-glucuronidase treatment. We also identified several inhibitors that inhibit both GPI/GAG interaction and GPI enzymatic activities, which suggests that the GPI GAG-binding domain overlaps with the active site of GPI enzyme. Our studies raise the possibility that GAGs are the receptors for other autoantigens involved in joint-specific inflammatory responses.
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PMID:High affinity glycosaminoglycan and autoantigen interaction explains joint specificity in a mouse model of rheumatoid arthritis. 1894 58

Starch synthesis and degradation require the participation of many enzymes, occur in both photosynthetic and nonphotosynthetic tissues, and are subject to environmental and developmental regulation. We examine the distribution of starch in vegetative tissues of Arabidopsis (Arabidopsis thaliana) and the expression of genes encoding core enzymes for starch synthesis. Starch is accumulated in plastids of epidermal, mesophyll, vascular, and root cap cells but not in root proper cells. We also identify cells that can synthesize starch heterotrophically in albino mutants. Starch synthesis in leaves is regulated by developmental stage and light. Expression of gene promoter-beta-glucuronidase fusion constructs in transgenic seedlings shows that starch synthesis genes are transcriptionally active in cells with starch synthesis and are inactive in root proper cells except the plastidial phosphoglucose isomerase. In addition, ADG2 (for ADPG PYROPHOSPHORYLASE2) is not required for starch synthesis in root cap cells. Expression profile analysis reveals that starch metabolism genes can be clustered into two sets based on their tissue-specific expression patterns. Starch distribution and expression pattern of core starch synthesis genes are common in Arabidopsis and rice (Oryza sativa), suggesting that the regulatory mechanism for starch metabolism genes may be conserved evolutionarily. We conclude that starch synthesis in Arabidopsis is achieved by spatial coexpression of core starch metabolism genes regulated by their promoter activities and is fine-tuned by cell-specific endogenous and environmental controls.
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PMID:Starch synthesis in Arabidopsis is achieved by spatial cotranscription of core starch metabolism genes. 1975 45