a role in transducing NLS-containing damage signals back from the injured axon to the nucleus (Hanz et al., 2003). Together with our data, all these findings point to NCC as potentially a key process in the age-related loss of neuronal performance and stress resistance in the old brain. Given that RanBP17 decrease appears in different tissues, NCC defects may also be present in other aging cell types, contributing to a range of age-related phenotypes in different organs. However, the functional relationship, if any, of age-related NCC impairment with potential downstream effectors, including the ones mentioned above, needs to be determined.
