Genetic Control of Insulin Receptors

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 sp...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1981-10, Vol.78 (10), p.6359-6361
Main Authors: Goldfeld, Anne E., Rubin, Charles S., Siegel, Todd W., Shaw, Phyllis A., Schiffer, Susan G., Gluecksohn-Waelsch, Salome
Format: Article
Language:English
Subjects:
Albinism
Animals
Animals, Newborn
Cell Membrane - metabolism
Cell membranes
Female
Fetus
Genes, Lethal
genetic control
Hepatocytes
Heterozygote
Homozygote
Homozygotes
Insulin
Insulin - metabolism
Kidney cells
Kinetics
Liver
Liver - metabolism
Mice
mutants
Mutation
P branes
Pregnancy
Receptor, Insulin - genetics
Receptor, Insulin - metabolism
Receptors
String theory
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Summary: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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.78.10.6359