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Synaptotagmin-13 is a single-pass transmembrane protein distinguished from classic synaptotagmins by being Ca²⁺-independent. Its cytoplasmic C2A and C2B domains interact with membrane phospholipids and proteins involved in vesicle trafficking, facilitating both docking and fusion processes at target membranes. SYT13 plays an essential role in modulating cell-matrix adhesion and orchestrating endocrine cell egression during pancreatic islet morphogenesis. It is highly expressed in neuroendocrine cells in the brain, intestine, and pancreas, and upregulated in several cancers. The protein is evolutionarily conserved and participates in key processes of hormone secretion and cell migration. Loss-of-function models reveal major developmental and endocrine defects, underscoring its importance in cell polarity and tissue morphogenesis
Antisense oligonucleotide-mediated inhibition reduces cancer cell metastasis and progression. Impaired SYT13 function affects endocrine cell migration and pancreatic islet formation.
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