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J. Biol. Chem., Vol. 276, Issue 16, 12624-12628, April 20, 2001

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Asialoglycoprotein Receptor Deficiency in Mice Lacking the Major Receptor Subunit
ITS OBLIGATE REQUIREMENT FOR THE STABLE EXPRESSION OF OLIGOMERIC RECEPTOR^*

Ryu-ichi Tozawa, Shun Ishibashi^§, Jun-ichi Osuga, Kazuo Yamamoto^¶, Hiroaki Yagyu, Ken Ohashi, Yoshiaki Tamura, Naoya Yahagi, Yoko Iizuka, Hiroaki Okazaki, Kenji Harada, Takanari Gotoda, Hitoshi Shimano, Satoshi Kimura^**, Ryozo Nagai, and Nobuhiro Yamada

From the Departments of  Metabolic Diseases,  Cardiovascular Medicine, and ^** Infectious Diseases, Faculty of Medicine and ^¶ Department of Integrated Biosciences, Graduate School of Frontier Sciences, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655 and  Metabolism, Endocrinology, and Atherosclerosis, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan

The asialoglycoprotein receptor is an abundant hetero-oligomeric endocytic receptor that is predominantly expressed on the sinusoidal surface of the hepatocytes. A number of physiological and pathophysiological functions have been ascribed to this hepatic lectin (HL), the removal of desialylated serum glycoproteins and apoptotic cells, clearance of lipoproteins, and the sites of entry for hepatotropic viruses. The assembly of two homologous subunits, HL-1 and HL-2, is required to form functional, high affinity receptors on the cell surface. However, the importance of the individual subunits for receptor transport to the cell surface is controversial. We have previously generated HL-2-deficient mice and showed that the expression of HL-1 was significantly reduced, and the functional activity as the asialoglycoprotein receptor was virtually eliminated. However, we failed to detect phenotypic abnormalities. To explore the significance of the major HL-1 subunit for receptor expression and function in vivo, we have disrupted the HL-1 gene in mice. Homozygous HL-1-deficient animals are superficially normal. HL-2 expression in the liver is virtually abrogated, indicating that HL-1 is strictly required for the stable expression of HL-2. Although these mice are almost unable to clear asialo-orosomucoid, a high affinity ligand for asialoglycoprotein receptor, they do not accumulate desialylated glycoproteins or lipoproteins in the plasma.

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