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cc by-nc-nd (c) Llinàs del Torrent, Clàudia et al., 2024
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/229517

Allosterism in the adenosine A2A and cannabinoid CB2 heteromer

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Background and Purpose Allosterism is a regulatory mechanism for GPCRs that can be attained by ligand-binding or protein–protein interactions with another GPCR. We have studied the influence of the dimer interface on the allosteric properties of the A2A receptor and CB2 receptor heteromer. Experimental Approach We have evaluated cAMP production, phosphorylation of signal-regulated kinases (pERK1/2), label-free dynamic mass redistribution, β-arrestin 2 recruitment and bimolecular fluorescence complementation assays in the absence and presence of synthetic peptides that disrupt the formation of the heteromer. Molecular dynamic simulations provided converging evidence that the heteromeric interface influences the allosteric properties of the A2AR–CB2R heteromer. Key Results Apo A2AR blocks agonist-induced signalling of CB2R. The disruptive peptides, with the amino acid sequence of transmembrane (TM) 6 of A2AR or CB2R, facilitate CB2R activation, suggesting that A2AR allosterically prevents the outward movement of TM 6 of CB2R for G protein binding. Significantly, binding of the selective antagonist SCH 58261 to A2AR also facilitated agonist-induced activation of CB2R.

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LLINÀS DEL TORRENT, Clàudia, et al. Allosterism in the adenosine A2A and cannabinoid CB2 heteromer. British Journal of Pharmacology. 2024. Vol. 182, num. 14, pags. 3371-3384. ISSN 0007-1188. [consulted: 4 of June of 2026]. Available at: https://hdl.handle.net/2445/229517

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