GCC185 binds Rab6, and mutation of residues needed for Rab binding abolishes Golgi localization.
Mutation of residues implicated in zinc or phosphoethanolamine binding, or catalytic activity, restores colistin susceptibility of recombinant E. coli.
Mutation of residues critical to the inter-subunit lasso interaction abolishes CP polymerization.
Mutation of residues at the PCNA DNA interface has been shown to impair the initiation of DNA synthesis by polymerase δ (pol δ).
PLSCR family members contain a conserved calcium-binding motif, and Zhou, et al.59 found that mutation of residues in this region of PLSCR1 completely removed enzymatic activity.
We also analyzed the effect of mutation of residues Met208, Cys212 and Cys273 into Phe in all combinations.
Mutation of residues 846 and 883 to alanine and glycine, respectively, conferred novel inhibitor sensitivity onto PTPH1.
In three of these sera, mutation of residues at positions 876, 877, 878, 880, and/or residues 862 and 822 reduced antibody binding by more than 50%.
Mutation of glutamine 862 abolished binding in two of these sera, and mutation of residues 876, 877, 878, and 880 markedly reduced binding in two others.
Mutation of residues R619 and S433 demonstrates their importance in catalysis and suggests that R619 functions as a general acid in catalysis.
Furthermore, we demonstrated the requirement of the identified motifs for these interactions; mutation of residues in the first binding motif in USP17 reduced its ability to coimmunoprecipitate with TRAF2, and mutation of the second motif reduced its ability to coimmunoprecipitate with both of TRAF2 and TRAF3 (Fig. 6c, d).
