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Evidence for Coordinated Induction and Repression of Ecto-5'-Nucleotidase (CD73) and the A2a Adenosine Receptor in a Human B Cell Line
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R. Napieralski
Published/Copyright:
June 1, 2005
Abstract
In the human B cell line P493-6 two mitogenic signals, the Epstein-Barr virus nuclear antigen 2 (EBNA2) and myc, can be independently regulated by means of an estrogen receptor fusion construct or an inducible expression vector, respectively. Shut off of EBNA2, either in the presence or absence of myc, leads to a significant increase in enzymatic activity and surface expression of ecto-5'nucleotidase (CD73) as well as an increased adenosine receptor response in cyclic AMP formation. Shut off of myc expression has a small additional positive effect on CD73 activity. Among the four different subtypes of adenosine receptors, the A2a receptor exclusively is subject to regulation in this system, which is substantiated by pharmacologic data (specific agonists and inhibitors), as well as on the mRNA level. With upregulated CD73 and A2a, cells also respond to 5'-AMP with increased cyclic AMP formation. Turn on of EBNA2 has the reverse effect of repression of CD73 and A2a expression. The time course of both induction and repression of CD73 and A2a is rather slow.
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Published Online: 2005-06-01
Published in Print: 2003-03-14
Copyright © 2003 by Walter de Gruyter GmbH & Co. KG
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- HIV-1 TAR as Anchoring Site for Optimized Catalytic RNAs
- Transcription of Different Exons 1 of the Human Neuronal Nitric Oxide Synthase Gene Is Dynamically Regulated in a Cell- and Stimulus- Specific Manner
- Hepatitis B Virus Core Antigen: Enhancement of Its Production in Escherichia coli, and Interaction of the Core Particles with the Viral Surface Antigen
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- In vitro Uptake and Stability Study of pVEC and Its All-D Analog
- Calpastatin Exon 1B-Derived Peptide, a Selective Inhibitor of Calpain: Enhancing Cell Permeability by Conjugation with Penetratin
- Structure-Activity Relationships of Glucose-Dependent Insulinotropic Polypeptide (GIP)
- Interleukin-6 N-Terminal Peptides Modulate the Expression of junB Protooncogene and the Production of Fibrinogen in HepG2 Cells
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