A new type of mRNAs-loaded CD133⁺ vesicles, named intercellsome, mediate cell-cell communications to compensate intracellular proliferative signal deficit, representing a previously unrecognized mechanism of cell proliferation under stress.

A lack of ADAM10-mediated shedding increases prion protein levels at the plasma membrane and promotes the generation of pathological prion proteins, which accelerates prion disease in mice.

Understanding communication mechanisms between unicellular parasites is crucial in the development of novel therapies, as they rely on diverse modes of communication (like extracellular vesicle release, cytoneme, and filopodia formation) to regulate their behavior and survival.

Prion-like transfer of mutant huntingtin aggregates from presynaptic to postsynaptic neurons is enhanced by neuronal silencing and requires passage through the cytoplasm of Draper-expressing phagocytic glia in adult Drosophila brains.

Live intracellular bacterial pathogens can transfer from infected cells to uninfected macrophages upon cell-to-cell contact.

A newly discovered membrane structure associates with one of the centrioles and affects two important centrosomal events in epidermal cells – ciliary positioning and spindle orientation – through a physical interaction.

Adult muscle precursors (AMP) cells in Drosophila send out filopodia to interact with neighbouring muscles, which drive the reactivation of AMPs via an Insulin-Notch-Myc cascade.

Filopodia driven by class X myosin promote the fusion of mammalian myoblasts in the development of skeletal muscle and are important for the regeneration of skeletal muscle following muscle injury.

Caveolin-1 controls the width of transendothelial cell tunnels via a direct or indirect effect on membrane bending rigidity.