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. 2012 Sep 15;23(18):3707–3721. doi: 10.1091/mbc.E12-01-0053

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© 2012 Sakuma et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 9: — A model for preventing excess degranulation via PKCα-mediated cofilin phosphorylation. The aggregation of FcεRI triggers PKCα activation, resulting in phosphorylation of cofilin at Ser-23 and/or Ser-24. The novel phosphorylation results in inactivation of cofilin, leading to an increase in cortical F-actin polymerization, which is necessary to prevent excess degranulation. Phosphorylation strengthens cofilin binding to 14-3-3ζ, contributing to the system. To simplify, cortical F-actin in the resting state and actin depolymerization at early phase are omitted in the model. Newly polymerized F-actin is indicated with red arrows.