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)

Hepatic expression of the beta-galactoside alpha 2,6-sialyltransferase is at least in part specified by circulatory glucocorticoids. In this report we use the glucocorticoid agonist, RU362, and the antagonist, RU486, to demonstrate the participation of the glucocorticoid receptor pathway in beta-galactoside alpha 2,6-sialyltransferase regulation. The existing pool of sialyltransferase mRNA is turned over with an approximate half-life of 13 h, and presence of dexamethasone does not alter this rate of degradation. By means of nuclear run-off assays and measurement of nuclear unprocessed transcripts we demonstrate that dexamethasone induction of beta-galactoside alpha 2,6-sialyltransferase mRNA in rat Reuber H35 cells is mediated by a transcriptional enhancement mechanism. The same initiation site is utilized for sialyltransferase transcription in both basal- and hormone-stimulated synthesis. Sialyltransferase sequences residing upstream of this transcriptional initiation point are used to control chloramphenicol acetyltransferase expression in fusion constructs following transient transfection into H35 cells to demonstrate the presence of a functional promoter. Although no element with similarity to the known GRE consensus sequence resides within this promoter region, chloramphenicol acetyltransferase expression under the control of the sialyltransferase promoter is subject to a low (1.6-fold) but reproducible induction in response to dexamethasone. Implications of this observation to glucocorticoid regulation are discussed.
 ...
PMID:Transcriptional regulation of the liver beta-galactoside alpha 2,6-sialyltransferase by glucocorticoids. 221 65

A dysfunction in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis, possibly attributed to a change in glucocorticoid receptor (GR) functionality, has been implicated in depression. We have measured both lymphocyte GR receptor binding parameters and plasma sialyltransferase activity, as a biochemical marker of GR function, in two groups of patients suffering from depression or schizophrenia and in a group of age- and sex-matched controls. While there was a significant increase in plasma cortisol levels in the depressed group, there were no changes in the lymphocyte GR binding parameters (K(m) and Bmax). There was, however, a significant decrease in the plasma sialyltransferase: cortisol ratio in the depressed group suggesting an inability of the raised cortisol levels to induce enzyme expression and this ratio may provide a useful biochemical marker of cortisol receptor function. Although there was an increase in the plasma activity of the alpha 2,6 sialyltransferase isozyme in the schizophrenic group, no other changes were determined. Therefore, while the total plasma sialyltransferase:cortisol ratio reflects HPA axis function, alterations in specific isozyme activity may also be associated with other CNS disease states.
 ...
PMID:Plasma sialyltransferase levels in psychiatric disorders as a possible indicator of HPA axis function. 914 24