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. 2010 Feb;135(2):81–97. doi: 10.1085/jgp.200910344

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© 2010 Falkenburger et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jgp.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 4. — Outline of the kinetic model. Model species are depicted with Roman letters, and reactions are in italics. For reversible reactions (double arrows), forward reactions are in the direction of association. Note that most species and some reactions occur in several places in the schema. (A) Binding of agonist ligand (L) and G protein heterotrimers (G) to the M₁R (R) are implemented as an allosteric (ternary complex) model (blue), where ligand binding increases the affinity for G proteins and G protein binding increases the affinity for ligand. It is assumed that after NX, Gα_q-GTP dissociates from the receptor, leaving behind Gβγ (gray). (B) G protein activation by NX (includes G protein dissociation; orange) and G protein deactivation by GTPase activity (green). Activated G proteins (Gα-GTP) deactivate slowly through their own GTPase activity (GTPase1) or much faster (GTPase2) when bound to PLC.