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• W2071451946 abstract "ATP-binding cassette transporter A-1 (ABCA1)-mediated lipid efflux to lipid-poor apolipoprotein A-I (apoA-I) results in the gradual lipidation of apoA-I. This leads to the formation of discoidal high-density lipoproteins (HDL), which are subsequently converted to spherical HDL by the action of lecithin:cholesterol acyltransferase (LCAT). We have investigated the effect of point mutations and deletions in the carboxy-terminal region of apoA-I on the biogenesis of HDL using adenovirus-mediated gene transfer in apoA-I-deficient mice. It was found that the plasma HDL levels were greatly reduced in mice expressing the carboxy-terminal deletion mutants apoA-I[Δ(185−243)] and apoA-I[Δ(220−243)], shown previously to diminish the ABCA1-mediated lipid efflux. The HDL levels were normal in mice expressing the WT apoA-I, the apoA-I[Δ(232−243)] deletion mutant, or the apoA-I[E191A/H193A/K195A] point mutant, which promote normal ABCA1-mediated lipid efflux. Electron microscopy and two-dimensional gel electrophoresis showed that the apoA-I[Δ(185−243)] and apoA-I[Δ(220−243)] mutants formed mainly preβ-HDL particles and few spherical particles enriched in apoE, while WT apoA-I, apoA-I[Δ(232−243)], and apoA-I[E191A/H193A/K195A] formed spherical α-HDL particles. The findings establish that (a) deletions that eliminate the 220−231 region of apoA-I prevent the synthesis of α-HDL but allow the synthesis of preβ-HDL particles in vivo, (b) the amino-terminal segment 1−184 of apoA-I can promote synthesis of preβ-HDL-type particles in an ABCA1-independent process, and (c) the charged residues in the 191−195 region of apoA-I do not influence the biogenesis of HDL." @default.
• W2071451946 created "2016-06-24" @default.
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• W2071451946 date "2007-04-21" @default.
• W2071451946 modified "2023-10-16" @default.
• W2071451946 title "The Carboxy-Terminal Region of apoA-I Is Required for the ABCA1-Dependent Formation of α-HDL But Not Preβ-HDL Particles in Vivo" @default.
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• W2071451946 doi "https://doi.org/10.1021/bi602354t" @default.
• W2071451946 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2528067" @default.
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