Extended Data Fig. 6: Structural comparison of in active and inactive state of GPCRs.
From: Molecular mechanism of allosteric modulation for the cannabinoid receptor CB1
Structural comparison of TM2 conformation in active and inactive GPCRs. (a)The comparison reveals that there is less obvious conformational rearrangement of TM2 in most GPCRs, including aminergic receptors β2AR (active PDB: 6NI3, inactive PDB: 5D5A), M2 (active PDB: 6OIK, inactive PDB: 5ZKC), D2 (active PDB: 6VMS, inactive PDB: 7DFP), 5-HT2B (active PDB: 5TUD, intermedia: 6DRY) and H1 (active PDB: 7DFL, inactive PDB: 3RDZ); Nucleotide receptors A1R (active PDB: 6D9H, inactive PDB: 5N2S), Lipid receptors CB2 (active PDB: 6KPF, inactive PDB: 5ZTY) and EP4 (active PDB: 7D7M, inactive PDB: 5YWY); Chemokine receptor CXCR2 (active PDB: 6LFM, inactive PDB: 6LFL); Peptide receptors OPRD (active PDB: 6PT2, inactive PDB: 4RWD), AT1R (active PDB: 6OS0, inactive PDB: 4ZUD) and MC4 (active PDB: 7AUE, inactive PDB: 6W25). (b) The comparison reveals that there is more obvious conformational rearrangement of TM2 in most GPCRs, including OX2R (active PDB: 7L1V, inactive PDB: 6TPN), 5-HT2A (active PDB: 6WHA, inactive PDB: 6A94), A2A (active PDB: 6GDG, inactive PDB: 6ZDV), OPRM (active PDB: 6DDE, inactive PDB: 4DKL), OPRK (active PDB: 6B73, inactive PDB: 6VI4).
