Extracellular vesicles are proposed as novel, non-cell-autonomous mediators of neuronal atrophy in Parkinson's disease.

Cationic cell-penetrating peptides (CPPs) enter cells through ~2 (–5)-nm-wide water pores induced by the strong negative plasma membrane potential that CPPs and the activity of potassium channels generate.

Unconventional secretion of a plasma membrane purine transporter via Golgi-bypass is established at an early ER-associated secretory compartment revealing that specific cargoes define alternative trafficking routes.

The SH3 domain of BIN1 mediates an unexpectedly large array of interactions, which is perturbed by missense variants.

By controlling the SUMOylation of the protein CAR-1, the aging-regulating pathways downstream of the Insulin/IGF signaling cascade and of the germ cells of the nematode Caenorhabditis elegans are integrated.

A gene network for heart versus head muscle specification has been identified in the tunicate Ciona.

By measuring the impacts of thousands of mutations on potassium channel trafficking and function, we illuminate the molecular basis of folding, structure–function relationships, and how these are altered in disease.

Vascular endothelial cells in the brain, heart and lung exhibit tissue-specific heterogeneity and plasticity, expressing genes that were traditionally thought to be only expressed by the surrounding parenchymal tissue cells.

With monoubiquitination sites of Rab5 identified and structural and biochemical studies using chemically synthesized ubiquitinated Rab5, Rab5 monoubiquitination is found to downregulate the function of Rab5 in a site-dependent manner.