Summary
The adenosine transport in bovine chromaffin cells is highly regulated by different extracellular signals, both at short and long-term. The short-term regulation by extracellular signals such as secretagogues or direct activation of protein kinases A and C inhibit the adenosine transport capacity. Binding studies with nitrobenzylthioinosine show that the inhibition of the transport runs in parallel with a decrease in the number of binding sites for this ligand. The adenosine transport inhibition is mediated by a phosphorylation-dephosphorylation process. Extracellular signals that bind o nuclear receptors are responsible for the long-term regulation. Thyroid hormones increase the adenosine transport by increasing the number of adenosine transporters at the plasma membrane level. This transport activation requires the protein-synthesizing mchanism. On the contrary, dexamethasone and retinoic acid inhibit the adenosine transpor capacity and revert the action of thyroid hormones.
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Delicado, E.G., Sen, R.P., Casillas, T., Fideu, M.D., Miras-Portugal, M.T. (1994). Extracellular Signals and Transduction Mechanisms Controlling the Adenosine Transport in Neural Cells. In: Municio, A.M., Miras-Portugal, M.T. (eds) Cell Signal Transduction, Second Messengers, and Protein Phosphorylation in Health and Disease. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1879-2_21
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DOI: https://doi.org/10.1007/978-1-4615-1879-2_21
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