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)

Although the cellular mechanisms controlling bile flow and biliary lipid secretion are unclear, morphologic data suggest that intracellular vesicles may be involved. Therefore, to investigate the role of hepatocyte lysosomes in bile flow and biliary lipid secretion, we studied the effect of cholestasis on biliary lipid output and on lysosomal enzyme activities and total protein concentration in liver and bile. Castrated male rats were treated with ethinyl estradiol at 0.5 or 5 mg/kg per day for 5 days; bile was collected through a complete bile fistula hourly for 4 hours, and then liver homogenates were prepared. Bile acids, cholesterol, and phospholipid were measured in bile, and three lysosomal glycosidases (beta-glucuronidase, beta-galactosidase, and N-acetyl-beta-glucosaminidase) and total protein were measured in bile and liver. Ethinyl estradiol inhibited bile flow in a dose-dependent fashion; it also inhibited bile acid and phospholipid outputs. In contrast, a marked and parallel increase in the biliary outputs of all three lysosomal hydrolases was observed after high-dose ethinyl estradiol; no change in the biliary concentration of total protein was found. Our data suggest that bile flow and biliary lipid secretion involve cellular mechanisms other than vesicular transport by lysosomes.
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PMID:Dissociation of bile flow and biliary lipid secretion from biliary lysosomal enzyme output in experimental cholestasis. 678 57

Post-transcriptional gene silencing (cosuppression) results in the degradation of RNA after transcription. A transgenic Arabidopsis line showing post-transcriptional silencing of a 35S-uidA transgene and uidA-specific methylation was mutagenized using ethyl methanesulfonate. Six independent plants were isolated in which uidA mRNA accumulation and beta-glucuronidase activity were increased up to 3500-fold, whereas the transcription rate of the 35S-uidA transgene was increased only up to threefold. These plants each carried a recessive monogenic mutation that is responsible for the release of silencing. These mutations defined two genetic loci, called sgs1 and sgs2 (for suppressor of gene silencing). Transgene methylation was distinctly modified in sgs1 and sgs2 mutants. However, methylation of centromeric repeats was not affected, indicating that sgs mutants differ from ddm (for decrease in DNA methylation) and som (for somniferous) mutants. Indeed, unlike ddm and som mutations, sgs mutations were not able to release transcriptional silencing of a 35S-hpt transgene. Conversely, both sgs1 and sgs2 mutations were able to release cosuppression of host Nia genes and 35S-Nia2 transgenes. These results therefore indicate that sgs mutations act in trans to impede specifically transgene-induced post-transcriptional gene silencing.
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PMID:Arabidopsis mutants impaired in cosuppression. 976