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The Regulation of IGF-I Receptor Gene Expression by Positive and Negative Zinc-Finger Transcription Factors

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Current Directions in Insulin-Like Growth Factor Research

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 343))

Abstract

The insulin-like growth factor-I receptor (IGF-I-R) is a trans-membrane tyrosine kinase which mediates the trophic, metabolic, and differentiative effects of IGF-I and IGF-II1,2. Beginning at early organogenesis, the IGF-I-R gene is constitutively expressed by most body tissues, consistent with the putative role of IGF-I as a progression factor in the cell cycle3. Recent studies have shown that overexpression of the IGF-I-R in a fibroblast cell line abrogates all requirements for exogenous growth factors, suggesting that this receptor does, in fact, mediate a central mechanism in the cell cycle4.

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Author information

Authors and Affiliations

  1. Section on Molecular and Cellular Physiology, Diabetes Branch, NIDDK, National Institutes of Health, Building 10, Room 8S-239, Bethesda, Maryland, 20892, USA

    Haim Werner, Charles T. Roberts Jr. & Derek LeRoith

Authors
  1. Haim Werner
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  2. Charles T. Roberts Jr.
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  3. Derek LeRoith
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Editor information

Editors and Affiliations

  1. National Institutes of Health, Bethesda, Maryland, USA

    Derek Le Roith M.D., Ph.D.

  2. University of Florida, Gainesville, Florida, USA

    Mohan K. Raizada Ph.D.

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© 1994 Springer Science+Business Media New York

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Werner, H., Roberts, C.T., LeRoith, D. (1994). The Regulation of IGF-I Receptor Gene Expression by Positive and Negative Zinc-Finger Transcription Factors. In: Le Roith, D., Raizada, M.K. (eds) Current Directions in Insulin-Like Growth Factor Research. Advances in Experimental Medicine and Biology, vol 343. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2988-0_10

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  • DOI: https://doi.org/10.1007/978-1-4615-2988-0_10

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-6301-9

  • Online ISBN: 978-1-4615-2988-0

  • eBook Packages: Springer Book Archive

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