![]() ![]() G protein-dependent activation of phospholipase C by adenosine A3 receptors in rat brain. ![]() Molecular cloning and characterization of an adenosine receptor: the A3 adenosine receptor. A2B adenosine receptor mediates human chorionic vasoconstriction and signals through the arachidonic acid cascade. Characterization of human A2B adenosine receptors: radioligand binding, western blotting, and coupling to Gq in human embryonic kidney 293 cells and HMC-1 mast cells. Linden, J., Thai, T., Figler, H., Jin, X. Cross-talk between cyclic AMP and protein kinase C pathways. A2B adenosine and P2Y2 receptors stimulate mitogen-activated protein kinase in human embryonic kidney-293 cells. An enprofylline-sensitive mechanism with implications for asthma. Adenosine A2B receptors evoke interleukin-8 secretion in human mast cells. Adenosine A2B-receptor-mediated cyclic AMP accumulation in primary rat astrocytes. Functional characterization of the A2B adenosine receptor in NIH 3T3 fibroblasts. Subclasses of adenosine receptors in the central nervous system: interaction with caffeine and related methylxanthines. Gα 15 and Gα 16 couple a wide variety of receptors to phospholipase C. Facilitation of noradrenaline release by activation of adenosine A2A receptors triggers both phospholipase C and adenylate cyclase pathways in rat tail artery. Adenosine A2A receptors are colocalized with and activate Golf in rat striatum. In vivo adenosine receptor preconditioning reduces myocardial infarct size via subcellular ERK signalling. Ionic basis of the electrophysiological actions of adenosine on cardiomyocytes. Phospholipase C is involved in the adenosine-activated signal transduction pathway conferring protection against iodoacetic acid-induced injury in primary rat neuronal cultures. Role of A1 adenosine receptors in the regulation of vascular tone. Subclasses of external adenosine receptors. Adenosine regulates via two different types of receptors, the accumulation of cyclic AMP in cultured brain cells. Allosteric modulation of the adenosine family of receptors. Astrocytes and neurons: different roles in regulating adenosine levels. Astrocytic purinergic signalling coordinates synaptic networks. Extracellular metabolism of ATP and other nucleotides. Anticonvulsant and antinociceptive actions of novel adenosine kinase inhibitors. Summarizes four modes of adenosine's tissue protective action. Adenosine in tissue protection and tissue regeneration. A publication on AR nomenclature, structure, function and regulation by members of NC-IUPHAR subcommittee. Nomenclature and classification of adenosine receptors. Highly selective agonists of the different ARs have been designed through both empirical approaches and a semi-rational approach based on molecular modelling.įredholm, B. Modification of adenosine has been the key strategy for discovering AR agonists and the structure–activity relationships of adenosine at ARs have been extensively probed. ![]() However, it is now apparent that other pathways, such as phospholipase C, Ca 2+ and mitogen-activated protein kinases, are also relevant. All four subtypes are members of the superfamily of G-protein-coupled receptors, and each of these ARs has a unique pharmacological profile, tissue distribution and effector coupling.Ĭlassically, AR signalling is thought to occur through inhibition or stimulation of adenylyl cyclase (also known as adenylate cyclase). The A 1, A 2A, A 2B and A 3 are the four known subtypes of adenosine receptors (ARs). However, there has been a recent impetus towards novel clinical targets, stimulated by the discovery and elucidation of the roles of the various AR subtypes and adenosine. Modulation of adenosine receptors (ARs) using selective agonists and antagonists is a promising therapeutic strategy for the treatment of diseases and disorders of the cardiovascular, renal and nervous systems, as well as endocrine and pulmonary disorders.Īlthough the development of novel AR ligands has therefore been the focus of much research, so far none has been approved for clinical use, in part owing to the ubiquity of ARs and the consequent possibility of side effects. ![]()
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