Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.4.99.6 (sialyltransferase)
 1,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glycolipids in the thymus of mice after administration of dexamethasone were compared with those in control mice. In parallel with a decrease in the tissue weight due to the disappearance of immature thymocytes in the cortex, the amounts of GlcCer, Gg4Cer and GM1 decreased from 18 h after intraperitoneal administration of dexamethasone, but those of Gb4Cer and Forssman glycolipid did not change, indicating the differential distribution of ganglio- and globo-series glycolipids in the thymus, GlcCer, Gg4Cer and GM1 being on dexamethasone-sensitive cortical thymocytes, and Gb4Cer and Forssman glycolipid on dexamethasone-resistant cells including thymic stromal cells, respectively. At the same time, a characteristic increase in GM3, whose amount per thymus and concentration per mg of thymus were increased 4-fold and 13-fold compared to those in the control mice, respectively, was observed at the onset of the decrease in tissue weight and was due to the increased activity of LacCer sialyltransferase with the enhanced expression of its gene and the concomitant decrease in cytosolic sialidase activity. One can suggest that endogenous accumulation of GM3 is involved in the dexamethasone-induced apoptosis of cortical thymocytes. On radiolabeling of the thymus with CMP-[14C]-NeuAc, the incorporation of radioactivity into GM3 was preferentially observed in the thymuses of dexamethasone-administered mice, but not in those of control mice, suggesting the possible involvement of plasma membrane-associated sialytransferase in GM3 synthesis in the thymuses of dexamethasone-administered mice.
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PMID:Changes in the glycolipid composition and characteristic activation of GM3 synthase in the thymus of mouse after administration of dexamethasone. 1613 32

To determine how T cells of thymic origin regulate the intestinal mucous response induced by nematode infection, mucin production and goblet cell-specific secretory peptide expression were examined in euthymic rnu/+ and athymic rnu/rnu rats infected with the nematode Nippostrongylus brasiliensis. Euthymic rats showed transient goblet cell hyperplasia and upregulation of mucin production, which returned to preinfection levels by 21 days postinfection, when nematodes had been rejected from the intestine. In athymic rats, which failed to reject nematodes, goblet cell hyperplasia and accelerated mucin production continued at least until 21 days postinfection. Gene transcription of mucin-core peptide (MUC)-2 and -3 and trefoil factor (TFF)-2 and -3 in the jejunal epithelium was upregulated parallel to the levels of goblet cell hyperplasia in both euthymic and athymic rats. On the other hand, resistin-like molecule (Relm)beta, sialyltransferase Siat4c and sulfotransferase 3ST1 showed significantly higher transcription levels in euthymic than in athymic rats at 7 and/or 10 days postinfection. These results suggest that the induction of intestinal mucin production occurs without the activation of thymus-derived T cells, while the expression of Relmbeta, Siat4c and 3ST1 in the intestinal epithelial cells seems to be regulated at least partly by thymus-dependent mechanisms.
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PMID:T cell-dependent and -independent expression of intestinal epithelial cell-related molecules in rats infected with the nematode Nippostrongylus brasiliensis. 1736 66

In chicken, ST3 beta-galactoside alpha-2, 3-sialyltransferase III (ST3GAL III) is one of the key enzymes participating in the biosynthesis of avian influenza virus receptors. Knowledge about ST3Gal III could increase our understanding of its function in the occurrence and development of avian influenza. To date, no detailed data have been published about the expression pattern and histological distribution of ST3Gal III in chicken. This paper presents data on the nucleotide sequence, mRNA expression pattern and histological distribution of ST3Gal III protein in yellow chicken for the first time. The results show that the nucleotide homology of ST3Gal III among yellow chicken and turkey, chicken, cattle, humans, swine, mouse, rat and chimpanzee was 98%, 92%, 75%, 59%, 70%, 76% and 75%. The relative expression level of ST3Gal III in the heart, kidney and brain of yellow chicken was significantly higher than in other tissues examined for mRNA level (P < 0.05). The histological distribution of ST3Gal III in the heart, liver, spleen, lung, thymus and bursa of Fabricius was determined by immunohistochemical staining using rabbit anti-chicken ST3Gal III IgG prepared by us. Interestingly, the epithelial reticular cells in the immune organs proved to be positive, which may suggest that these cells are important immune cells playing a role in influenza virus infection. The results of this study provide basic data for further research on the functions of ST3Gal III in chicken.
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PMID:The expression pattern and histological distribution of sialyltransferases ST3Gal III in yellow chicken. 2394 96

T lymphocytes are important players in beneficial and detrimental immune responses. In contrast to other lymphocyte populations that develop in the bone marrow, T-cell precursors need to migrate to the thymus for further development. The interaction of P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1) is crucial for thymic entry of T-cell precursors during settings of T-cell lineage reconstitution. PSGL-1 has to be sialylated to function as a ligand for P-selectin, and the sialyltransferase ST3Gal-IV might play a critical role in this process. We therefore investigated the role of ST3Gal-IV for T-cell development using competitive mixed bone marrow chimeric mice. We found that ST3Gal-IV is dispensable for homing and engraftment of hematopoietic precursors in the bone marrow. However, ST3Gal-IV deficiency affects seeding of the thymus by early T-cell progenitors, leading to impaired restoration of the peripheral T-cell compartment. This defect could be restored by ectopic retroviral expression of ST3Gal-IV in hematopoietic stem cells derived from ST3Gal-IV-deficient donor mice. Our findings show that ST3Gal-IV plays a critical and nonredundant role for efficient T-cell lineage reconstitution after bone marrow transplantation.
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PMID:The sialyltransferase ST3Gal-IV guides murine T-cell progenitors to the thymus. 3238 May 39


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