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. 2016 Jan 29;5:e12813. doi: 10.7554/eLife.12813

Figure 6. PD pathogenic LRRK2 mutations interfere with Rab-GDI1/2 association.

(A) Fold changes (T73A/T73E, n=3) of indicated MS-quantified Rab10 interactors. (B) Same as (A) but S106A-Rab12 and S106E-Rab12 (n=4). (C) Different LRRK2 versions were co-expressed with Rab8a in HEK293 cells, lysates subjected to immunoblot analysis or immunoprecipitation using α-HA antibodies and indicated signals quantified (D). (E) and (F) Same as (C) with Rab12 expression. (G) Scheme for analyzing T72A-Rab8a and T72E-Rab8a subcellular protein distributions in a SILAC experiment. (H) SILAC ratios (Log2) of T72E-Rab8a/T72A-Rab8a proteins in the cytosolic and membrane fraction of HEK293 cells. PD, Parkinson's disease.

DOI: http://dx.doi.org/10.7554/eLife.12813.016

Figure 6.

Figure 6—figure supplement 1. Rab10/12-GDI interactions.

Figure 6—figure supplement 1.

(A) HA-Rab10 constructs (wt, T73A, T73E) were expressed in HEK293 cells and lysates subjected to α-HA immunoprecipitation before western blotting. (B) Same as (A) using HA-Rab12 (wt, S106A, S106E). wt, wild type.