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. Author manuscript; available in PMC: 2021 Jan 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2019 Oct 17;40(1):112–127. doi: 10.1161/ATVBAHA.119.312976

Fig.7. Model for the AIP1 isoform switch in vascular disease.

Fig.7.

Cytosolic AIP1A forms a complex with NOX2 via its PH domain to block the formation of an active NOX2 complex. In contrast, AIP1B localizes to the mitochondria and enhances TNF-induced mitoROS generation. CVD risk factors and inflammation reduce AIP1A through Smurf1-mediated proteolytic degradation. AIP1B is normally suppressed by RIF1/H3K9me3, but this suppression is released by inflammation, which leads to a shift from an AIP1A to an AIP1B dominated-state in endothelial cells. A shift from AIP1A to AIP1B under chronic inflammation promotes enhanced ROS production and CVD progression.