Fig. 4.
Fig. 4. Possible modes by which extracellular mutations in hβc , indicated by a star in each panel, lead to constitutive receptor activity. (A) The extracellular mutation induces constitutive heterodimerization with a putative γ signalling subunit. (B) The extracellular mutation leads to hβc homodimerization. (C) In this model, hβc normally associates with an inhibitory membrane-spanning molecule (I); the extracellular mutations disrupt this association and thus lead to activation. For simplicity, only a single β subunit is shown; however, the inhibitory molecule might normally function in suppressing the activity of a low level of spontaneously forming homodimers or heterodimers.

Possible modes by which extracellular mutations in hβc , indicated by a star in each panel, lead to constitutive receptor activity. (A) The extracellular mutation induces constitutive heterodimerization with a putative γ signalling subunit. (B) The extracellular mutation leads to hβc homodimerization. (C) In this model, hβc normally associates with an inhibitory membrane-spanning molecule (I); the extracellular mutations disrupt this association and thus lead to activation. For simplicity, only a single β subunit is shown; however, the inhibitory molecule might normally function in suppressing the activity of a low level of spontaneously forming homodimers or heterodimers.

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