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The receptor for insulin‐like growth factor II mediates an insulin‐like response.
Author(s) -
Hari J.,
Pierce S. B.,
Morgan D. O.,
Sara V.,
Smith M. C.,
Roth R. A.
Publication year - 1987
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1987.tb02658.x
Subject(s) - medicine
Insulin‐like growth factor II (IGF‐II) shares sequence homology and predicted three‐dimensional structure with insulin and IGF‐I. IGF‐II can bind, therefore, to a limited extent with the receptors for these two other hormones, as well as to a distinct receptor for IGF‐II. Previous studies have been unable to attribute a particular response of IGF‐II through its own receptor. In the present studies, the IGF‐II receptor is shown to mediate the stimulation of glycogen synthesis in human hepatoma cells since: (i) IGF‐II is found to be capable of stimulating a response at concentrations in which it would primarily interact with its own receptor; (ii) the response to IGF‐II was not blocked by monoclonal antibodies which inhibit the responses of cells through the insulin and IGF‐I receptors; and (iii) polyclonal antibodies to the IGF‐II receptor were found to mimic the ability of IGF‐II to stimulate glycogen synthesis. These results indicate that the IGF‐II receptor mediates a particular biological response–stimulation of glycogen synthesis in hepatoma cells. Furthermore, a monovalent Fab fragment of the polyclonal antibody to the IGF‐II receptor was also shown to stimulate glycogen synthesis in these cells. These data indicate that clustering of the IGF‐II receptor is not required to stimulate a biological response.

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