Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.2.1.31 (
beta-glucuronidase
)
7,680
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The activation of macrophages by exposure to the polyribonucleotide, poly [I:C], is accompanied by a large stimulation of the synthesis of the C components factor B and C3, and a concomitant inhibition of the synthesis of the lysosomal enzyme
beta-glucuronidase
. Northern blot analysis of poly [A+] RNA extracted from poly [I:C]-stimulated cells revealed that the changes in the synthesis of factor B and C3 were related to changes in the levels of their respective mRNA and hence the expression of these proteins appeared to be regulated at a pre-translational level. The down-regulation of the synthesis of
beta-glucuronidase
appeared to be regulated at both translational and pre-translational levels. In view of the proposed role of macrophage-derived IFN in the regulation of macrophage activation, we investigated the possible role of IFN-alpha/beta in the regulation of the synthesis of factor B, C3, and
beta-glucuronidase
. Exposure of macrophages to mouse IFN-alpha and
IFN-beta
induced limited changes in the synthesis of factor B, C3, and
beta-glucuronidase
. However, pretreatment of macrophages with only 500 U/ml of
IFN-beta
primed the cells thereby increasing their sensitivity to poly [I:C]. IFN-alpha was less effective as a priming agent. When macrophages were exposed to poly [I:C] in the presence of an anti-mouse IFN-alpha/beta antiserum, the changes in the synthesis of factor B, C3, and
beta-glucuronidase
were partially inhibited. Collectively, these data indicate first, that exposure of mouse bone marrow-derived macrophages to poly [I:C] differentially regulates the expression of the products of the genes for factor B, C3, and
beta-glucuronidase
. Second, IFN-alpha and
IFN-beta
prime macrophages to increase the sensitivity of macrophages to poly [I:C]. Third, in the absence of exogenous IFN, macrophage-derived IFN appears to participate in priming the cells in an autocrine or paracrine fashion.
...
PMID:Differential regulation of gene expression during macrophage activation with a polyribonucleotide. The role of endogenously derived IFN. 337 3
The degradation of 32P-labelled E. coli and the activity of three lysosomal enzymes, acid phosphatase, cathepsin D and
beta-glucuronidase
, in mouse peritoneal macrophages (MPM) were tested after cultivation of the cells for 24 or 48 hours with 10(1) - 10(4.7) U per ml of a homologous beta-interferon preparation (
IFN-beta
). Low to moderate concentrations of
IFN-beta
did not influence bacterial degradation in MPM. However, a reduction in bacterial degradation by 20 per cent or more was seen when the MPM were pre-treated with 10(4.7) U per ml for 24 hours or 10(3) U per ml of
IFN-beta
for 48 hours. Cultivation of the MPM with 10(2) U per ml of
IFN-beta
suppressed the activities of the lysosomal enzymes, provided that the cells were treated for 48 hours. The beta--glucuronidase activity was significantly reduced also after 24 hours. Increased release of
beta-glucuronidase
from MPM to the medium during cultivation with 10(2) U per ml of
IFN-beta
was also observed. Specific anti-
IFN-beta
globulin abolished the suppression by
IFN-beta
on the lysosomal enzyme activities. A human IFN-alpha preparation did not influence bacterial degradation or lysosomal enzyme activities in MPM.
...
PMID:Effect of a homologous beta-interferon preparation on degradation of Escherichia coli and on lysosomal enzyme activities in mouse peritoneal macrophages. 617 90
