Abstract
Background and Aims: Previous studies in patients have identified STAP1 as candidate gene for familial hypercholesterolemia (FH). In this light, we generated whole-body Stap1-/- mice, which did not differ from wild-type littermates in plasma lipid levels, on chow or high fat cholesterol diet. Since STAP1 is mainly expressed in immune tissues, we subsequently performed a bone marrow (BM) transplantation experiment into Ldlr-/- mice. This atherosclerosis prone animal model carries – like humans - a large fraction of cholesterol in low-density lipoprotein (LDL) and allows for atherosclerosis assessment.
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