The nucleus is enclosed in a double-membraned nuclear envelope, that houses nuclear pore complexes, which serve as the permeability barrier that orchestrates the passage of macromolecules (proteins, nucleic acids) across the nuclear envelope; this transport, between the nucleus and cytoplasm, is precisely regulated and plays a critical role in maintaining cellular homeostasis. Dysfunction of nuclear-cytoplasmic transport has been associated with multiple disorders, including age-related neurodegenerative diseases, ageing, viral infections, certain genetic diseases and cancer. Yet, the molecular mechanisms underlying impaired nucleocytoplasmic transport and the pathogenesis leading to these diseases remain to be deciphered. Proteins that mediate the shuttling of components across the nuclear envelope, such as nuclear transport receptors, have gained attention as possible biomarkers and therapeutic targets, given their implication in disrupted nucleocytoplasmic transport that underlies pathologies.
This collection will gather articles that shed light on the mechanisms of nucleocytoplasmic transport, research that presents links between dysregulation in the nucleocytoplasmic interface and diseases, and work that highlights the diagnostic and therapeutic potential of players.