In 1963, Jandl and Katz1 showed that the binding of serum transferrin to immature red cells was a specific and saturable process and postulated that the iron required for heme synthesis was delivered from transferrin to these cells via specific cell surface receptors. In the next two decades, as the requirements for the growth of mammalian cells in tissue culture were defined, it was found that transferrin was an essential growth factor for virtually all cells.2 This latter observation stimulated interest in the role of transferrin in cell growth, and transferrin binding studies carried out in the late 1970s showed that transferrin receptors could be detected on a wide variety of cultured cell lines and that their expression on the cell surface was coordinately regulated with cell growth.3–6 At about this time, in studies aimed at defining changes in the cell surface of human hematopoietic cells during differentiation and malignant transformation, an immunodominant proliferation-associated cell surface antigen was detected on cultured human tumor cells by means of a murine monoclonal antibody (MAb).7 Further characterization of this molecule showed that it was the human transferrin receptor.8–10
KeywordsIron Uptake Transferrin Receptor Vesicular Stomatitis Virus Cell Surface Antigen Cell Surface Glycoprotein
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