Ena/VASP proteins act as positive regulators of cell motility and are required for the formation of microspikes, as opposed to filopodia that can arise from distinct molecular mechanisms.

SARS-CoV-2 has evolved to cleverly mimic the FURIN-cleavage site in human ENaC-α, unlike any prior coronavirus strain, shedding new light on the Acute Respiratory Distress Syndrome (ARDS) in COVID-19 patients.

Dysfunction and overexpression of ENaC-mediated sodium influx exacerbates activation of NLRP3-inflammasome mediated inflammation in cells with CF-associated mutations and is modulated by inhibition of these amiloride-sensitive sodium (Na⁺) channels.

Lamellipodin, an important regulator of cytoskeletal and assembly cell migration, enhances the activity of Ena/VASP family actin polymerases by clustering them on leading-edge membranes and tethering them to actin filaments.

Signalling and metabolic interactions of the plant energy organelles, chloroplasts and mitochondria, depend on the nuclear regulatory protein RCD1.

The protein UNC-8 is a neuronal activity sensor that triggers the elimination of synapses during development of the nervous system.

A reconstituted system has been developed that self-organizes into dynamic actin cortices capable of spontaneous polarization, similar to the initial cortical polarization observed in cells during embryogenesis and development.

The use of advanced 3D culture systems with engineered quiescent human T-cells, mimicking in vivo cellular dynamics, paves the way to a new era of much needed pre-clinical research tools.

Methods that use puromycin to localize active translation do not actually detect the site of translation.

The mRNA that encodes a Drosophila sodium channel enables neurons to adapt to acute temperature changes, via a mechanism independent of its protein-coding role.