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.

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.

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.

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.

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

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

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.

The in-depth structural and functional work provide a deeper understanding as to how the epithelial sodium channel is a heteromeric ion channel that is regulated by Na⁺ and proteolysis.

A phage-encoded protein inhibits a bacterial replicative helicase loading factor by exploiting an internal site that auto-regulates loader self-assembly and ATPase activity.

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