Clathrin-coated vesicles can be made to form on intracellular membranes using a minimal molecular system, which defines the core vesicle budding machinery.

The Ca²⁺-dependence of vesicle priming, fusion, and replenishment at cerebellar mossy fiber boutons show a prominent Ca²⁺-dependent priming step, a shallow non-saturating dose-response curve up to 50 µM, and little Ca²⁺-dependence of sustained vesicle replenishment.

Ultrasound promotes release of extracellular vesicles from cultured myotubes and elicits anti-inflammatory effects on macrophages, indicating the potential of ultrasound stimulation to muscle for anti-inflammatory purposes.

A synaptic F-actin network tightly controls the flow of synaptic vesicles during exocytosis at the inner hair cell ribbons.

Lumen extension in intracellular tubes relies on a molecular pathway involving Rho GTPase signaling, cell polarity, and vesicle-tethering proteins.

Studies of Lowe syndrome patient cells, which lack the inositol 5-phosphatase OCRL, suggest that a defect in endocytosis plays a role in the pathological manifestations of the disease.

Prominin 1 and Tweety Homology 1, two proteins that regulate membrane shape in neural and neuroepithelial cells, have shared evolutionary history and both cause cells to secrete extracellular vesicles.

Neuronal Calcium Sensor-1 (NCS1) is a protein that captures the preciliary vesicle in the early step of the cilium formation.

QuantEv is a fully automatic and semi-parametric method that allows quantitative analysis of the spatio-temporal distribution of complex molecular trafficking objects at the scale of the whole cell.

Chemical labelling of all primary endocytic vesicles allows the contribution of different endocytic mechanisms to the total endocytic uptake in cultured mammalian cells to be quantified.