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. 2016 Oct 30;16(8):fow095. doi: 10.1093/femsyr/fow095

Figure 2.

Figure 2.

Summary of lesions found to relocate to the nuclear pore, some sumoylated proteins expected to bind them and observed functional outcomes of relocation. At top is a model for the function of relocation of persistent DNA lesions to the nuclear pore. The dashed line between Slx5/Slx8 STUbL and the Y-shaped Nup84 complex indicates interaction between Nup84 and Slx8 shown by Nagai et al. (2008). The isopeptidase Ulp1 that can cleave SUMO from modified proteins interacts with the nuclear basket. Three types of persistent DNA lesions that have been studied are illustrated at left. Only a few key proteins are shown; other proteins that have been shown to interact with these lesions and/or play a role in mediating interaction with the nuclear pore or NE are listed in Tables 1 and 2. The small blue circles represent SUMO (either mono-SUMO or poly-SUMO chains). TBP stands for telomere binding proteins. On the right are listed the known outcomes of interaction with the nuclear pore for each type of lesion (black arrows), or alternative outcomes that occur when NPC interaction is defective (gray arrows).