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Baseline mucin secretion (BMS) is independent of external agonists and controlled by a small calcium binding protein named KChIP3. KChIP3 hosting mucin granules are not released until intracellular cytosolic calcium oscillations reach a threshold, KChIP3 binds calcium and detaches from granules, allowing their fusion to plasma membrane. Loss of KChIP3 or blocking its membrane attachment causes mucin hypersecretion. How is KChIP3 recruited to mucin granules? We show here that zDHHCdoi:10.1101/2020.12.15.422936 fatcat:v4c3y2yul5fvtg7g5nzj3cutne