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The Journal of Lipid Research, Vol. 40, 814-823, May 1999
Copyright © 1999 by Lipid Research, Inc.

Original Article

Compensated endocytosis of LDL by hamster cells co-expressing the two distinct mutant LDL receptors defective in endocytosis and ligand binding

Hiroyuki Yoshidaa, Masayuki Yokodea, Akitsugu Yamamotob, Ryuichi Masakib, Toshinori Murayamaa, Hisanori Horiuchia, and Toru Kitaa
a Department of Geriatric Medicine, Graduate School of Medicine, Kyoto University, 54 Shogoinkawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan
b Department of Physiology, Kansai Medical University, Humizono-cho, Moriguchi, Osaka 570-8506, Japan

Correspondence to: Masayuki Yokode

The low density lipoprotein receptor (LDLR) regulates the plasma cholesterol level by mediating endocytosis of LDL. We established stable hamster cell lines expressing two LDLRs with distinct functional defects, i.e., endocytosis and ligand binding. In the cell line expressing only I189D h/r (human-rat chimeric) LDLR, defective in LDL binding, very little amount of LDL was internalized, although the receptor was endocytosed efficiently. In the cell line expressing Y807C LDLR solely, very few receptors were located in coated pits or endocytosed, while LDL binding to the receptor was not disrupted. In striking contrast, in the cells co-expressing both receptors, a much larger number of Y807C LDLR were internalized and co-located with I189D h/r LDLR in the perinuclear region. In these cells, LDL was bound exclusively to Y807C LDLR and its uptake was enhanced by 80% as compared to the cell expressing Y807C LDLR solely, whereas LDL binding affinity was not changed.

These results suggest that a defect of the essential motif for endocytosis, cysteine 807, could be compensated by co-expression of I189D h/r LDLR, but the LDL binding was not affected.—Yoshida, H., M. Yokode, A. Yamamoto, R. Masaki, T. Murayama, H. Horiuchi, and T. Kita. Compensated LDL receptors defective in endocytosis and ligand binding. J. Lipid Res. 1999. 40: 814–823.

Supplementary key words: LDL receptor, co-expression, endocytosis, familial hypercholesterolemia


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