Skip to main content
. Author manuscript; available in PMC: 2015 Oct 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2014 Aug 14;34(10):2254–2260. doi: 10.1161/ATVBAHA.114.304027

Figure 5. Model depicting opposing fates of G162C apoA-V in plasma.

Figure 5

Left) Upon secretion from hepatocytes, WT apoA-V associates with VLDL and HDL and remains 100 % lipoprotein bound. Right) In addition to lipoprotein association, G162C apoA-V forms disulfide bonds with extraneous plasma proteins, thereby abrogating its lipoprotein interaction capability (depicted by the X). As such, hetero-disulfide bonded G162C apoA-V constitutes a nonfunctional pool of apoA-V in terms of TG modulation.