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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Cells, Cultured, Coculture Techniques, Embryo, Mammalian, Enhancer Elements, Genetic, Epithelial Cells, Gene Expression Regulation, Glutamate-Ammonia Ligase, Hepatocytes, Liver, Mice, Mice, Transgenic, Promoter Regions, Genetic, Rats.
user
Does the RL-ET-14 cell line mediate expression of glutamine synthetase through the upstream enhancer/promoter region? Context: The expression of glutamine synthetase (GS) in the mammalian liver is confined to the hepatocytes surrounding the central vein and can be induced in cultures of periportal hepatocytes by co-cultivation with the rat-liver epithelial cell line RL-ET-14. We exploited these observations to identify the regulatory regions of the GS gene and the responsible signal-transduction pathway that mediates this effect. Fetal hepatocytes of wild-type or GS-transgenic mice were co-cultured with RL-ET-14 cells to induce GS expression. Small-interfering RNA was employed to silence beta-catenin expression in the fetal hepatocytes prior to co-culture. Co-cultivation of RL-ET-14 cells with fetal mouse hepatocytes induced GS expression 4.2-fold. The expression of another pericentral enzyme, ornithine aminotransferase and a periportal enzyme, carbamoylphosphate synthetase, were not affected. Co-culture of RL-ET-14 cells with transgenic fetal mouse hepatocytes demonstrated that GS expression was induced via its upstream enhancer located at -2.5 kb and that the signal mediator required a functional beta-catenin pathway.
assistant
The 'RL-ET-14' factor specifically induces GS expression, working via its upstream enhancer in a beta-catenin-dependent fashion. Final Decision: yes