Abstract

Nuclear pore complexes mediate the exchange of macromolecules between cytoplasm and nuclear interior. These complexes assemble from more than 500 individual nucleoporins and integrate into the double membrane structure of the nuclear envelope at the end of mitosis and in interphase via different pathways. Despite their universal function in all nucleated cells mutations in nucleoporins cause tissue specific disease phenotypes but the underlying molecular mechanisms are often unclear.

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