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 interaction of cytochalasin B-treated human neutrophils with the synthetic tripeptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP) results in a time- and concentration-dependent generation of superoxide anion (O2-) by an extracellular release of granule-associated beta-glucuronidase and lysozyme from these cells. Granule exocytosis was not accompanied by significant cytoplasmic lactate dehydrogenase extrusion. FMLP-stimulated O2- production occurs but is significantly curtailed in the absence of extracellular calcium. Nevertheless, incubation of neutrophils with EGTA in calcium-free medium had no effect on the O2- -generating system. Trifluoperazine (TFP), an inhibitor of calmodulin (a calcium-binding protein), caused a dose-related inhibition of FMLP-elicited degranulation and O2- production in the presence of absence of extracellular calcium. This effect TFP could be reversed by washing the cells before contact with FMLP. These data suggest that TFP represents a useful tool for defining the relevance of calmodulin and calcium to neutrophil function.
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PMID:Effects of trifluoperazine on human neutrophil function. 627 92

1-O-Hexadecyl-2-O-acetyl-sn-glyceryl-3-phosphorylcholine (C16-AGEPC) and 1-O-octadecyl-2-O-acetyl-sn-glyceryl-3-phosphorylcholine (C18-AGEPC) stimulated a time- and concentration-dependent release of granule-associated lysozyme and beta-glucuronidase from human neutrophils. Maximum discharge of granule enzymes occurred between 30 and 60 sec after neutrophil exposure to C16- or C18-AGEPC (0.01-10 microM). Less than 10% of total enzyme activity is released when cells are not preincubated with cytochalasin B prior to interaction with the AGEPC analogs. A time-dependent desensitization for granule exocytosis was observed in neutrophils which were stimulated with C18-AGEPC prior to contact with cytochalasin B. The rate and amount of enzyme released by C16- and C18-AGEPC activated neutrophils was significantly enhanced in the presence of extracellular calcium. Trifluoperazine, an inhibitor of calmodulin, caused a dose-related suppression of C18-AGEPC-induced degranulation. Granule enzyme extrusion from C18-AGEPC-treated neutrophils was inhibited by the sulfhydryl reagents, N-ethylmaleimide and iodoacetic acid, and by the glycolytic inhibitor, 2-deoxy-D-glucose. Sodium cyanide was inactive. Pretreatment of neutrophils with C16- or C18-AGEPC rendered the cells unresponsive to subsequent exposure to either AGEPC analog. C18-AGEPC-induced desensitization of neutrophil degranulation appears to be stimulus specific in that serum-treated zymosan and N-formyl-methionyl-leucyl-phenylalanine were capable of eliciting granule enzyme release from C18-AGEPC-pretreated cells.
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PMID:Characteristics of 1-O-hexadecyl- and 1-O-octadecyl-2-O-acetyl-sn-glyceryl-3-phosphorylcholine-stimulated granule enzyme release from human neutrophils. 687 58