We here provide a set of data showing that, unlike in rejuvenated iPSCs and their derivatives, human aging can be modeled through direct cell type conversion into iNs that preserve transcriptomic features of their donors age. Based on transcriptome profiling of aging fibroblasts, derived iNs, and the aging human cortex, we identified the nuclear pore-associated transport protein RanBP17 as a significant factor in cell aging that goes along with an impairment of protein localization between the nucleus and cytoplasm in different human somatic cell types, including neurons.
