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. 2019 Oct 1;34(1):1–13. doi: 10.1097/QAD.0000000000002385

Fig. 1.

Schematic representation of the effects of Nef extracellular vesicles on target cells.

Fig. 1

The cell plasma membrane is shown in light green, and membrane lipid rafts – in blue. Endoplasmic reticulum is shown in olive green around the cell nucleus. Nef, ABCA1, and calnexin are represented by their scaled down three-dimensional structures. (a) Cell not treated with Nef extracellular vesicles. In the endoplasmic reticulum, calnexin interacts with ABCA1 supporting ABCA1 maturation and transport to plasma membrane. ABCA1 is recycled from the cell membrane, and some is internalized to the proteasomes and degraded. (b) Cell treated with Nef extracellular vesicles. Extracellular vesicles carrying Nef molecules surround the cell and deliver Nef into the cell. Nef interacts with cytoplasmic domain of calnexin, which ostensibly causes changes in the calnexin structure, disrupting interaction of its intraendoplasmic reticulum domain with ABCA1. As a result, maturation of ABCA1 is impaired and it is targeted to proteasomes reducing cholesterol efflux. This increases cell's cholesterol content and changes abundance and properties of lipid rafts, leading to decreased recycling of the plasma membrane ABCA1 and its preferential targeting to proteasomes [63,69,73,76].