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. Author manuscript; available in PMC: 2021 Apr 22.
Published in final edited form as: J Mol Biol. 2019 Dec 19;432(5):1310–1325. doi: 10.1016/j.jmb.2019.12.012

Fig. 4. Functional and dysfunctional responses to disruptions in stoichiometry.

Fig. 4.

(A) An overabundance of STX4 in the β-cell increases the amplitude of both phases of GSIS and enhances glucose homeostasis in vivo. STX4 binds directly to F-actin and indirectly via association with the actin binding protein gelsolin. Additional units of STX4 increase the abundance of STX4-based SNARE complexes. (B) An overabundance of STX1A decreases VDCC and Kv channel activity/gating, linked to STX1A’s ability to bind to the channels and reduce function, which in vivo decreases GSIS and disrupts glucose homeostasis.