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Endocrinology, Vol 135, 387-394, Copyright © 1994 by Endocrine Society
ARTICLES |
ME Gafvels, LG Paavola, CO Boyd, PM Nolan, F Wittmaack, A Chawla, MA Lazar, M Bucan, BO Angelin and JF Strauss 3rd
Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Philadelphia 19104.
We report the cloning of a complementary DNA for the mouse homolog of the very low density lipoprotein (VLDL)/apolipoprotein-E receptor (VLDLR), the deduced amino acid sequence of the protein, and the mapping of the gene encoding the receptor to mouse chromosome 19. Northern hybridization revealed that the VLDLR messenger RNA (mRNA) is most abundant in skeletal muscle, heart, kidney, and brain. It was also detected in lung and in low levels in liver, but it was not found in spleen or testes. Levels of VLDLR mRNA in mouse placenta increased from days 8-18 of gestation. The VLDLR mRNA was induced in 3T3-L1 cells undergoing differentiation into adipocytes. The increase in VLDLR mRNA paralleled the rise in lipoprotein lipase and hormone-sensitive lipase mRNAs. However, VLDLR and low density lipoprotein receptor-related protein were increased in the presence of retinoic acid, whereas the induction of lipoprotein lipase and hormone-sensitive lipase mRNAs was inhibited. Our observations demonstrate regulated expression of the VLDLR gene in placenta and adipocytes, where the receptor protein may play roles in the uptake of triglyceride-rich particles for storage of lipid (adipocytes) or for lipid transport to the fetus (placenta). The availability of a murine complementary DNA probe and the knowledge of the map position of the VLDLR gene in the mouse genome will facilitate studies on the function and regulation of this protein.
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