Established NBEA as a brake on regulated secretion rather than a positive trafficking factor, defining the directionality of its role in dense-core vesicle release.
Evidence siRNA silencing and overexpression in mouse beta-TC3 cells with stimulated LDCV secretion measurement, plus platelet dense-core granule ultrastructure in haploinsufficient patients
- Molecular partners mediating the secretory brake not identified
- Whether the effect is exocytic, biogenesis-related, or both is unresolved
- No structural basis for the regulatory activity