Abstract
Most of the biological actions of insulin-like growth factor I (IGF-I)/somatomedin C are initiated by its binding to the IGF-I receptor, a heterotetrameric glycoprotein structurally related to the insulin receptor1. The presence of IGF-I receptors in most body tissues suggests that it mediates many different effects. Indeed, IGF-I has been shown to be involved not only in endocrine functions, such as the mediation of growth hormone’s effect on longitudinal growth, but it is also involved in many autocrine/paracrine systems at the local tissue level2,3. These biological actions include both short-term, metabolic effects (similar in nature to those stimulated by insulin) as well as long term, growth promoting actions. It is not surprising then, that the IGF- I receptor should be able to respond to various tissue — and development- specific stimuli. To study the expression of the IGF-I receptor gene in both physiological and pathological conditions in a convenient animal model, we undertook the cloning of rat IGF-I receptor cDNAs.
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© 1991 Plenum Press, New York
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Werner, H., Stannard, B., Bach, M.A., Roberts, C.T., LeRoith, D. (1991). Regulation of Insulin-Like Growth Factor I Receptor Gene Expression in Normal and Pathological States. In: Raizada, M.K., LeRoith, D. (eds) Molecular Biology and Physiology of Insulin and Insulin-Like Growth Factors. Advances in Experimental Medicine and Biology, vol 293. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5949-4_24
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DOI: https://doi.org/10.1007/978-1-4684-5949-4_24
Publisher Name: Springer, Boston, MA
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