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)

Sequential phenotypic changes in hyperplastic areas of rat liver during N-2-fluorenylacetamide feeding were studied by enzyme and immunohistochemical methods combined with radioautography. Hyperplastic area showed a marked deficiency of beta-glucuronidase and serine dehydratase during their developing phase, the 6th through the 9th experimental weeks, and were fairly specifically labeled by injections of tritiated thymidine after partial hepatectomy performed at the 9th week. A sequential observation on these labeled hyperplastic areas revealed a considerable elevation of the levels of these marker enzymes in the majority of the labeled areas in 3 to 18 weeks after labeling. On the other hand, there was a small group of hyperplastic areas in which the enzyme deficiency persisted during the observation period. This type of lesion was generally larger than those showing enzymic maturation. Labeled cells were not detectable either in distinct hyperplastic nodules at late phase or in carcinomas. The metabolic regulation in the cells comprising hyperplastic areas was studied by checking the induction and repression of serine dehydratase after dietary stimuli. Serine dehydratase was not inducible in hyperplastic areas during the developing phase or in areas with persistent enzyme deficiency, but it was clearly induced and repressed in areas where there was an elevation of the endogenous enzyme level. The areas of hyperplasia with persistent enzyme deficiency and growth appeared to be more important than the ones of phenotypic maturation in relation to the later development of carcinoma. The phenotypic maturation in hyperplastic areas might represent reversion of altered cells towards normalcy from the condition related with neoplastic transformation.
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PMID:Sequential phenotypic changes in hyperplastic areas during hepatocarcinogenesis in the rat. 127 64

Circulating human neutrophils from patients with severe inflammatory disorders such as erysipelas and sepsis are specifically desensitized to complement factor C5a stimulation but not to stimulation with other stimuli like N-formyl-methionyl-leucyl-phenylalanine (FMLP), interleukin-8 (IL-8), leukotriene B4 (LTB4), or platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine). In this study, we raised the question whether factors released from polymorphonuclear leukocytes (PMNs) can specifically down-regulate C5a-dependent neutrophil functions. When neutrophils were preincubated with either neutrophil lysates or neutrophil degranulation supernatants, a complete inhibition of C5a-stimulated beta-glucuronidase release and chemotaxis could be observed, whereas FMLP-, IL-8-, LTB4- or PAF-dependent functions were not affected. Serine protease inhibitors like phenylmethylsulfonyl fluoride, antileukoprotease, or elafin abolished this effect. High-performance liquid chromatography of neutrophil degranulation supernatants revealed pronounced inhibition of C5a-dependent neutrophil functions in fractions exerting elastase or cathepsin G activity, but not in fractions exerting proteinase 3 activity. Using purified human leukocyte elastase (HLE), C5a responses like intracellular calcium influx, beta-glucuronidase release, and chemotaxis were also specifically inhibited. Our experiments show that the release of HLE or cathepsin G from neutrophils specifically down-regulates the responsiveness of neutrophils to C5a. Elastase and cathepsin G may therefore play an important role in the down-regulation of acute inflammation.
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PMID:Human leukocyte elastase and cathepsin G are specific inhibitors of C5a-dependent neutrophil enzyme release and chemotaxis. 1514 22

From a T-DNA tagged Arabidopsis population, a line, M-57 showing GUS (beta-glucuronidase) expression in the vascular regions of young roots was identified. Southern analysis revealed presence of a single T-DNA insert. Using inverse PCR, the plant sequence flanking the T-DNA insertion was cloned. The insertion was identified to be in the intergenic area between loci At4G13940 and At4G13930, coding for SAHH (S-Adenosyl-l-Homocysteine Hydrolase) and SHMT (Serine Hydroxy Methyl Transferase) genes, respectively. A 452-bp fragment immediately upstream of the T-DNA insertion when cloned and mobilized as a GUS fusion was capable of driving a similar root-specific expression of reporter gene in transgenic Arabidopsis plants and their progenies. This cryptic promoter element does not show the presence of any known root-specific promoter element.
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PMID:T-DNA tagging and characterization of a cryptic root-specific promoter in Arabidopsis. 1630 4