Fig. 5

The extent of APP, APLP1, APLP2 dimers in N2a cells versus mouse brains. A APP F1 was heterologously expressed in N2a cells and treated either with 100 nM AP20187 over night to induce dimerization or with the same volume of ethanol as a control. One year old WT mouse cortices and APP KO mouse cortices were homogenized. All samples were prepared under semi-denaturing conditions for analysis on Blue Native gels. Western blot detection of APP followed with the primary α-APP C-terminal antibody Y188. B Quantification of data shown in A. Bars represent mean values ± SEM of the ratio dimer/total of FKBP-rapamycin induced APP dimer in N2a cells and endogenous APP dimer in mouse brains. n = 3. C APLP1 F1 was heterologously expressed in N2a cells and treated either with 100 nM AP20187 over night to induce dimerization or with ethanol as a control. In parallel, 1 year old WT mouse cortices and APLP1 KO mouse cortices were analyzed. Analysis of Blue Native gel samples was followed by Western blot detection of APLP1 with the primary α-APLP1 antibody 57. D Quantification of data shown in C. Bars represent mean values ± SEM of the ratio dimer/total of FKBP-rapamycin induced APLP1 dimer in N2a cells and endogenous APLP1 dimer in mouse brains. n = 3. E APLP2 F1 was heterologously expressed in N2a cells and treated either with 100 nM AP20187 over night to induce dimerization or with ethanol as a control. Those samples were compared to 1 year old WT mouse cortices and APLP2 KO mouse cortices. Analysis via Blue Native gels was followed by Western blot detection of APLP2 with the primary α-APLP2 antibody D2-II. F Quantification of data shown in E. Bars represent mean values ± SEM of the ratio dimer/total of FKBP-rapamycin induced APLP2 dimer in N2a cells and endogenous APLP2 dimer in mouse brains. n = 3