Whole-cell abundance profiling and interaction analysis of UBQLN2

To address whether expression of ALS/FTD-associated UBQLN2 mutant variants changes the cellular proteome, we performed label-free quantification-based global protein abundance profiling of patient-derived LCLs and CRISPR engineered HeLa cells. UBQLN2 mutant in both cell lines carried the mutation T487I or P497S both of which were reported to cause ALS (Deng et al., 2011; Williams et al, 2012). In addition, HeLa cells stably expressing HA-tagged MAP1B (HA-MAP1B) were subjected to HA immunoprecipitation (IP) followed by mass spectrometry to identify MAP1B interacting proteins.