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Influence of retinoic acid and of cyclic AMP on the expression of choline acetyltransferase and of vesicular acetylcholine transporter in NG108-15 cells
Institution:3. Minerva Max Planck Research Group, Molecular Physiology, Center of Advanced European Studies and Research (caesar), 53175 Bonn, Germany;4. Department of Molecular Sensory Systems, Center of Advanced European Studies and Research (caesar), 53175 Bonn, Germany;5. Department of Cell Biology of Lipids, LIMES Institute, University of Bonn, Bonn, Germany;6. LIMES Institute, c/o Kekulé-Institute, University of Bonn, 53115 Bonn, Germany;12. Proteomic Core Facility, EMBL Heidelberg, 69117 Heidelberg, Germany;8. Biochemie-Zentrum (BZH), Ruprecht-Karls-University Heidelberg, 69120 Heidelberg, Germany;9. Department of Biomolecular Sciences, Weizmann Institute of Science, Rehovot 76100, Israel;10. Institute of Innate Immunity, University Hospital, University of Bonn, 53127 Bonn, Germany;1. College of Engineering and Technology, American University of the Middle East, Kuwait;2. International Centre for Neurotherapeutics, Dublin City University, Glasnevin, Dublin 9, Ireland;3. School of Chemical Sciences, Dublin City University, Glasnevin, Dublin 9, Ireland;4. School of Food Science and Environmental Health, College of Sciences and Health, Technological University Dublin, Cathal Brugha Street, Dublin 1, Ireland;1. Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles CA 90048, USA;2. Department of Pathology, Cedars-Sinai Medical Center, Los Angeles CA 90048, USA;1. Institute of Management Research, Radboud University, Postbus 9108, 6500 HK, Nijmegen, The Netherlands;2. Documentation Centre Dutch Political Parties, University of Groningen, Broerstraat 4, 9712 CP Groningen, The Netherlands
Abstract:Treatment of the cholinergic cell line NG108-15 with retinoic acid or cAMP results in an increase of choline acetyltransferase activity (ChAT) whereas none of these agents influences the amount of the vesicular acetylcholine transporter (VAChT) as judged from vesamicol binding and immunoblot studies. We suggest that immaturity of posttranslational events controlling the expression of VAChT protein is responsible for the apparent absence of coregulation of ChAT and VAChT protein expression.
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