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. 2017 Jul 3;216(7):2151–2166. doi: 10.1083/jcb.201702099

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© 2017 Zhang et al.

This article is available under a Creative Commons License (Attribution 4.0 International, as described at https://creativecommons.org/licenses/by/4.0/).

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Figure 7. — Proposed model for BAIAP3 function. (Top) In resting cells, DCVs undergo maturation and slow spontaneous exocytosis. DCV membrane proteins are recycled to the TGN by retrograde trafficking with the basal activity of BAIAP3. Knockdown of BAIAP3 disrupts protein recycling and may deplete DCV membrane proteins, causing DCV maturation and trafficking defects that lead to immature DCV (iDCVs) accumulation in BON cells or DCV turnover in INS-1 cells. (Bottom) When cells are stimulated with Ca²⁺, increased BAIAP3 activity may stimulate retrograde trafficking to meet the increased demand for protein recycling during Ca²⁺-triggered DCV exocytosis.