The function and distribution of kinesin motors on exocytotic vesicles is dissected and visualized through a combination of gene knockout experiments, high-resolution microscopy and advanced data analysis.

Evidence that certain proteins can be transported between Golgi via structures that resemble COPI vesicles suggests that these vesicles could also be involved in the transport of proteins from the cis to the trans face of the Golgi.

A structure of the complete, membrane bound, COPII coat solved by sub-tomogram averaging reveals the arrangement of all protein subunits on the membrane and suggests a mechanism for coating heterogeneously-shaped carriers.

In mammals, the vesicular glutamate transporter 1 acquired a proline-rich sequence that negatively regulates the spontaneous release of glutamate by reducing the exchange of synaptic vesicles along the axon.

Components of a Spir:MyoV:Rab11 complex are recruited synergistically to coordinate actin tracks generation and myosin motor activity in vesicle transport processes.

The golgin GMAP-210 captures vesicles at the cis Golgi by merely recognizing the high curvature and lipid unsaturation level of transport vesicles.

Identification of novel vesicular transporters will shed light on to expanding the chemical diversity of neurotransmitters or neuromodulators.

The COPII coat protein, in association with p24 machinery molecules, actively excludes misfolded and resident proteins from endoplasmic reticulum-derived transport vesicles.

A fear conditioning-induced miRNA acts in a negative feedback loop that targets vesicle exocytosis and neurotransmitter receptor trafficking, and inhibits memory formation.

Mature axons lose the ability to regenerate because key growth molecules are excluded through changes in vesicle transport, and restoring transport can restore regeneration.