The structure and function of A1 and A2B adenosine receptors
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Cited by (45)
Adenosine metabolized from extracellular ATP promotes type 2 immunity through triggering A<inf>2B</inf>AR signaling in intestinal epithelial cells
2022, Cell ReportsCitation Excerpt :The upregulation of A2BAR in the intestinal epithelium has been shown to induce chloride secretion through a cyclic AMP (cAMP)-dependent pathway (Strohmeier et al., 1995), as well as increases in intracellular cAMP leading to activation of protein kinase A (PKA) (Kolachala et al., 2006), and the deletion of the A2BAR receptor leads to decreases in IL-10 expression, exacerbating colitis (Frick et al., 2009). The A2BAR receptor can also activate PLC via Gαq signaling, inducing Ca+ mobilization (Linden et al., 1998). As A2BAR signaling did not directly induce increased IL-33 production or bioactive cleavage products in the intestinal enteroids treated with the A2BAR agonist, other in vivo signals are likely needed.
Insulin/adenosine axis linked signalling
2017, Molecular Aspects of MedicineCitation Excerpt :A2AAR activate Gs and Golf (olfactory G protein, first identified in the olfactory epithelium) proteins (Hervé et al., 1993) increasing cAMP generation and protein kinase A (PKA) activity, and is mainly associated with NO-dependent vasodilation. A2BAR is coupled to Gq protein, activates mitogen-activated protein kinases (MAPKs) (Linden et al., 1998), and is involved in NO-dependent vasodilation. The Gi protein coupled-A3AR reduces AC activity and is depalmitoylated making this ARs subtype susceptible to desensitization (Gao et al., 1999; Palmer et al., 1996).
The resurgence of A2B adenosine receptor signaling
2011, Biochimica et Biophysica Acta - BiomembranesCitation Excerpt :More recently it was shown that the A2BAR can couple to the Gq family of G-proteins to activate phospholipase C (PLC) and increase intracellular calcium (Fig. 2) [92,93]. It appears the G protein coupling of the receptor is cell type dependent and coupling to Gs results in an anti-inflammatory response while coupling to Gq could potentially results in a pro-inflammatory response [94]. Finally, the A2BAR is the only adenosine receptor subtype that can activate ERK1/2, JNK and p38 map kinase signaling [29,95–97].
Normal and abnormal functions of adenosine receptors in the central nervous system revealed by genetic knockout studies
2011, Biochimica et Biophysica Acta - BiomembranesCitation Excerpt :Like A2ARs, A2BR signaling is coupled to the Gs protein-AC-cAMP-PKA pathway. In addition, A2BRs can couple with Gq/11 to activate phospholipase C [53,54], and some evidence also suggests that they can interact with the arachidonic acid pathway [55]. The A3R was the last subtype to be identified when it was first isolated as an orphan receptor in rat testis [56] and later cloned and expressed in other cell types [57].
Neurochemistry of somatosensory and pain processing
2011, Essentials of Pain MedicinePyrazolo[1′,5′:1,6]pyrimido[4,5-d]pyridazin-4(3H)-ones as selective human A<inf>1</inf> adenosine receptor ligands
2010, Bioorganic and Medicinal ChemistryCitation Excerpt :Selective antagonists of subtype A2A, which is present in high density in the striatum,13 but also in numerous peripheral tissue such as platelets, lymphocytes and neutrophils,16–18 are promising drugs for the treatment of Parkinson’s disease.19 A2B receptors are implicated in vascular tone, gene expression, cell growth, mast cell degranulation and hepatic glucose balance,20–22 and are proposed as antiasthmatic and antidiabetic drugs.23–25 Finally, antagonists of A3 receptors, which are particularly abundant in human lung and liver26 and seem also to be involved in cell survival regulation,27 could be useful in the treatment of inflammatory states,28 asthma,29 chronic obstructive pulmonary disease,30 cancer31 and glaucoma.32