Insulin-binding activity was measured in hepatocyte suspensions and liver membrane preparations from newborn mice homozygous for a perinatal-lethal deletion at and around the albino locus in chromosome 7. Cell suspensions and membrane preparations from the mutant mice exhibited only 20-25% of the specific hormone-binding activity observed in comparable preparations from their homozygous normal and heterozygous littermates. The decrease in insulin-binding activity appears to be attributable to a decrease in the number of insulin receptor sites per cell rather than to a change in receptor affinity. Gene sequences deleted at and around the albino locus are therefore instrumental in the regulation of insulin receptor concentration rather than in coding for the insulin receptor itself. The results of the present studies extend the identification of the regulatory functions exerted by the genes around the albino locus of the mouse.
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