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 time of appearance of a lysosomal enzyme, beta-glucuronidase, in the medium of cells infected with either measles virus or echovirus 6 varied with the host cell system. Replication and release of virus preceded leakage of beta-glucuronidase from green monkey kidney cells. In contrast, extracellular enzyme appeared before replication and release of virus in human amnion cells. Hydrocortisone depressed enzyme leakage but did not retard replication of measles virus or viral-induced cytopathology. The intracellular distribution of beta-glucuronidase in uninfected and measles virus-infected cells was also studied. Measles virus infection altered the position of particulate-bound beta-glucuronidase in linear sucrose gradients prior to substantial release of this enzyme intra- and extracellularly. At early stages in infection, most of the cell-associated virus banded with particulate-bound enzyme in the middle of the gradient. As infection progressed, separation of measles virus infectivity from enzyme activity occurred, and intracellular virus was recovered near the meniscus of sucrose gradients.
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PMID:Effect of host cell on distribution of a lysosomal enzyme during virus infection. 500 Jan 15

We used Ficoll-Hypaque isolated peripheral lymphocytes and PMNs to investigate the relationship between viral exposure and beta-adrenergic responses in target cells. Lymphocyte E-rosette formation with sheep red blood cells and PMN beta-glucuronidase release in response to opsonized zymosan particles are two cell activities regulated by beta-adrenergic agonists. After incubation with influenza or measles virus, the treated cells have decreased response to isoproterenol, a beta-adrenergic agonist. The in vitro viral exposure causes a decreased beta-adrenergic response in target cells.
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PMID:Virus exposure diminishes beta-adrenergic response in human leukocytes. 626 87