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Adenosine A1-A2A Receptor-Receptor Interaction: Contribution to Guanosine-Mediated Effects
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Focusing on Adenosine Receptors as a Potential Targeted Therapy in Human Diseases

1
Division of Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan
2
Department of Pulmonology and Respiratory Medicine, Medical Faculty of Airlangga University, Surabaya 60131, Indonesia
*
Author to whom correspondence should be addressed.
Cells 2020, 9(3), 785; https://doi.org/10.3390/cells9030785
Received: 20 February 2020 / Revised: 21 March 2020 / Accepted: 23 March 2020 / Published: 24 March 2020
(This article belongs to the Special Issue Adenosine Receptors: From Cell Biology to Human Diseases)
Adenosine is involved in a range of physiological and pathological effects through membrane-bound receptors linked to G proteins. There are four subtypes of adenosine receptors, described as A1AR, A2AAR, A2BAR, and A3AR, which are the center of cAMP signal pathway-based drug development. Several types of agonists, partial agonists or antagonists, and allosteric substances have been synthesized from these receptors as new therapeutic drug candidates. Research efforts surrounding A1AR and A2AAR are perhaps the most enticing because of their concentration and affinity; however, as a consequence of distressing conditions, both A2BAR and A3AR levels might accumulate. This review focuses on the biological features of each adenosine receptor as the basis of ligand production and describes clinical studies of adenosine receptor-associated pharmaceuticals in human diseases. View Full-Text
Keywords: adenosine; adenosine receptors; G protein-coupled receptors; agonists; antagonists; allosteric molecules adenosine; adenosine receptors; G protein-coupled receptors; agonists; antagonists; allosteric molecules
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Effendi, W.I.; Nagano, T.; Kobayashi, K.; Nishimura, Y. Focusing on Adenosine Receptors as a Potential Targeted Therapy in Human Diseases. Cells 2020, 9, 785.

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