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Blood, Vol. 94 No. 10 (November 15), 1999:
pp. 3604-3606
Genetic Evidence of an Accessory Activity Required Specifically for
Cubilin Brush-Border Expression and Intrinsic Factor-Cobalamin
Absorption
Danbin Xu,
Renata Kozyraki,
Thomas C. Newman, and
John C. Fyfe
From the Department of Microbiology, College of Veterinary Medicine,
and MSU-DOE Plant Research Laboratory, Michigan State University, East
Lansing, MI; and the Institut National de la Santé et de la
Recherche Médicale, U489, Hôpital Tenon, Paris, France.
Cubilin is a high molecular weight multiligand receptor that
mediates intestinal absorption of intrinsic factor-cobalamin and
selective protein reabsorption in renal tubules. The genetic basis of
selective intestinal cobalamin malabsorption with proteinuria was
investigated in a canine model closely resembling human
Imerslund-Gräsbeck syndrome caused by cubilin mutations. Canine
CUBN cDNA was cloned and sequenced, showing high identity with
human and rat CUBN cDNAs. An intragenic CUBN marker was
identified in the canine family and used to test the hypothesis of
genetic linkage of the disease and CUBN loci. Linkage was
rejected, indicating that the canine disorder resembling
Imerslund-Gräsbeck syndrome is caused by defect of a gene product
other than cubilin. These results imply that there may be locus
heterogeneity among human kindreds with selective intestinal cobalamin
malabsorption and proteinuria and that normal brush-border expression
of cubilin requires the activity of an accessory protein.
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