Skip to main content
. 2014 Feb 10;124(3):1296–1308. doi: 10.1172/JCI72051

Figure 5. AXL and LRP-1 interact in DCs in vitro and in vivo.

Figure 5

(A) Representative immunofluorescent confocal microscopy of BMDCs stained at 4°C with anti–LRP-1 antibody followed by Alexa Fluor 488–labeled secondary antibody (green), and with anti-AXL antibody followed by Alexa Fluor 568–labeled secondary antibody (red). Points of AXL and LRP-1 colocalization are indicated by yellow staining in the merged image as well as in the mask of colocalization. Scale bar: 5 μm. (B) Endogenous AXL or LRP-1 was subjected to IP from whole-cell lysates of BMDCs, then probed by Western blotting for AXL, LRP-1, or RANBP9. Rabbit or rat IgG in the IP reaction was used as control. (C) Flow cytometric analysis of FRET (sensitized emission) in splenic DCs (CD11c+ gate) immunostained with fluorophore-conjugated antibody against AXL as donor and LRP-1 as acceptor (left) or vice versa (right). Other cells were stained singly with fluorophore-conjugated antibody against AXL (left) or LRP-1 (right) as donor. Cells stained with IgG conjugated to Alexa Fluor 546 were used as controls. (D) Donor fluorescence measurements in cells as in C. Data are representative of 3 independent experiments.