Importin subunit alpha (importin-α) and Importin subunit beta-1 (importin-β1) (Importin-α/β (also known as KPNA/KPNB1 system))

Importin alpha and importin beta function as essential nuclear transport receptors, together enabling the energy-dependent import of proteins containing a classical nuclear localization signal (NLS) into the nucleus. Importin-α serves as the adaptor that directly binds the NLS cargo, while importin-β interacts with both importin-α (via the importin-β binding [IBB] domain) and the nuclear pore complex (via FG-nucleoporins)[1][3][5][6][7][9]. This system is central to regulating nuclear-cytoplasmic transport, is vital for cell cycle progression and spindle assembly, and plays key roles in diseases where nuclear import is dysregulated[8]. Increased expression or dysregulation of importin-α and β (especially KPNA2) is associated with cancer progression and poor patient outcomes, making them of keen therapeutic interest[5][8]. Several antiviral and anticancer agents target the importin α/β pathway either directly or indirectly. However, therapeutic modulation carries risks due to the fundamental cellular role of these transporters.

Other names

karyopherin alphakaryopherin betaKPNAKPNB1importin alphaimportin beta

Competitive inhibition of nuclear localization signal (NLS) binding. Disruption of importin–cargo interaction to block nuclear import (e.g., prevent viral protein entry). Interference with nuclear pore complex translocation.