Abstract
1. A functional study of cell surface A(2b) adenosine receptors was performed on the T cell leukaemia line, Jurkat. 2. A(2b) receptors were coupled both to the adenylate cyclase system and to intracellular calcium channels. In fact, the agonist of A(2b) receptors, 5'-N-ethylcarboxamidoadenosine (NECA), led to a transient accumulation of intracellular calcium by an inositol phosphate-independent mechanism. 3. The NECA-induced accumulation of cGMP was not responsible for the calcium mobilization via A(2b) receptors. 4. The calcium response elicited by activation of A(2b) receptors was independent of that evoked by activation of the T cell receptor. 5. These findings not only delineate a novel transduction mechanism for adenosine but also support a specific role for adenosine in modulating signals elicited via the T cell receptor.
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Mirabet, M., Mallol, J., Lluis, C., & Franco, R. (1997). Calcium mobilization in Jurkat cells via A(2b) adenosine receptors. British Journal of Pharmacology, 122(6), 1075–1082. https://doi.org/10.1038/sj.bjp.0701495
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