Transcriptional regulation of the liver beta-galactoside alpha 2,6-sialyltransferase by glucocorticoids.
作者： X C Wang , T J Smith , J T Lau
DOI: 10.1016/S0021-9258(18)38241-3
关键词: Internal medicine 、 Glucocorticoid receptor 、 Messenger RNA 、 Transcription (biology) 、 Glucocorticoid 、 Cell biology 、 Promoter 、 Sialyltransferase 、 Biology 、 Transcriptional regulation 、 Chloramphenicol acetyltransferase 、 Endocrinology
摘要: Hepatic expression of the beta-galactoside alpha 2,6-sialyltransferase is at least in part specified by circulatory glucocorticoids. In this report we use glucocorticoid agonist, RU362, and antagonist, RU486, to demonstrate participation receptor pathway regulation. The existing pool sialyltransferase mRNA turned over with an approximate half-life 13 h, presence dexamethasone does not alter rate degradation. By means nuclear run-off assays measurement unprocessed transcripts that induction rat Reuber H35 cells mediated a transcriptional enhancement mechanism. same initiation site utilized for transcription both basal- hormone-stimulated synthesis. Sialyltransferase sequences residing upstream point are used control chloramphenicol acetyltransferase fusion constructs following transient transfection into functional promoter. Although no element similarity known GRE consensus sequence resides within promoter region, under subject low (1.6-fold) but reproducible response dexamethasone. Implications observation regulation discussed.
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