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The goal of this study was to understand the molecular basis of how the amino acid substitution C112R that distinguishes human apolipoprotein (apo) E4 from apoE3 causes the more proatherogenic plasma lipoprotein-cholesterol distribution that is known to be associated with the expression of apoE4.

Molecular Mechanisms Responsible for the Differential Effects of ApoE3 and ApoE4 on Plasma Lipoprotein–Cholesterol Levels