Skip to main content
U.S. Department of Energy
Office of Scientific and Technical Information

Insulin-induced surface redistribution regulates internalization of the insulin receptor and requires its autophosphorylation

Journal Article · · Proceedings of the National Academy of Sciences of the United States of America; (United States)
; ;  [1];  [2];  [3]
  1. Univ. of Geneva (Switzerland)
  2. National Inst. of Health, Bethesda, MD (United States)
  3. Univ. of California, San Francisco (United States)

The role of insulin-induced receptor autophosphorylation in its internalization was analyzed by comparing {sup 125}I-labeled insulin ({sup 125}I-insulin) internalization in Chinese hamster ovary (CHO) cell lines transfected with normal (CHO.T) or mutated insulin receptors. In four cell lines with a defect of insulin-induced autophosphorylation, {sup 125}I-insulin internalization was impaired. By contrast, in CHO.T cells and in two other CHO cell lines with amino acid deletions or insertions that do not perturb autophosphorylation, {sup 125}I-insulin internalization was not affected. A morphological analysis showed that the inhibition is linked to the ligand-specific surface redistribution in which the insulin-receptor complexes leave microvilli and concentrate on nonvillous segments of the membrane where endocytosis occurs.

OSTI ID:
5618004
Journal Information:
Proceedings of the National Academy of Sciences of the United States of America; (United States), Journal Name: Proceedings of the National Academy of Sciences of the United States of America; (United States) Vol. 89:1; ISSN 0027-8424; ISSN PNASA
Country of Publication:
United States
Language:
English