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. 2017 Jan 15;28(2):285–295. doi: 10.1091/mbc.E16-07-0526

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© 2017 Szíber 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 7: — RIN1 signaling pathways in motile dendritic filopodia (A) and established spines (B). (A) S292 phosphorylation of RIN1 enhances the phosphorylation of the Y36 site by Abl kinases and leads to Abl/Arg activation via disengaged autoinhibition. In turn, Abl kinase activity increases actin remodeling and/or alters integrin signaling. (B) In mature spines, RIN1 is sequestered in the cytoplasm by 14-3-3 proteins through binding to the phosphorylated S351 site, thereby blocking the downstream activation of Rab5. The E574 site of RIN1 is responsible for the Rab5 GEF activity and controls the conversion of Rab5 GDP to Rab5 GTP, leading to enhanced clathrin-mediated endocytosis of AMPA receptors. Both of these pathways counteract the stabilization of synaptic connections and decrease synaptic efficacy. PSD, postsynaptic density.