The BRCT domain of the AMD contains numerous possible automodification sites (9/15 glutamates found in the AMD are in the BRCT domain) and has been implicated in protein-protein interactions of PARP-1, including its homodimerization (which is thought to be important for catalytic activity and automodification [41]), recruitment of XRCC1, and recruitment of PARG (necessary for PAR turnover [10]). Here, XRCC1 is linked to age-related macular degeneration.