Abstract
Genetic defects in humans have greatly improved our insight in the function of genes controlling the lipoprotein metabolism. A good example is the apolipoprotein (APO) E gene, for which both dominant and recessive mutations have been observed. These findings have clearly established an important role for apoE in lipoprotein remnant metabolism1. In contrast, mutations within the APOCI gene have not been observed hampering insight in the in vivo function of apoC1.
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© 1995 Springer Science+Business Media New York
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Hofker, M.H. et al. (1995). Generation and Characterization of Apolipoprotein Cl-Deficient Mice. In: Gallo, L.L. (eds) Cardiovascular Disease. GWUMC Department of Biochemistry Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1959-1_39
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DOI: https://doi.org/10.1007/978-1-4615-1959-1_39
Publisher Name: Springer, Boston, MA
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