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Blood, Vol. 93 No. 1 (January 1), 1999: pp. 363-369

Protein Replacement by Receptor-Mediated Endocytosis Corrects the Sensitivity of Fanconi Anemia Group C Cells to Mitomycin C

Hagop Youssoufian, Frank A.E. Kruyt, and Xiaotong Li

From the Department of Molecular and Human Genetics and the Department of Medicine, Baylor College of Medicine, Houston, TX.

Current methods for direct gene transfer into hematopoietic cells are inefficient. Here we show that functional complementation of Fanconi anemia (FA) group C cells by protein replacement can be as efficacious as by transfection with wild-type FAC cDNA. We expressed a chimeric protein (called His-ILFAC) consisting of the mature coding portion of gibbon interleukin-3 (IL-3) and full-length FAC in Escherichia coli. The purified bacterial protein is internalized by hematopoietic cells via IL-3 receptors. The intracellular half-life of His-ILFAC is approximately 60 minutes, which is comparable to that of the transgene-encoded FAC protein. In this cell-culture model His-ILFAC completely corrects the sensitivity of FA group C cells to mitomycin C, but it has no effect on FA cells that belong to complementation groups A and B. We suggest that receptor-mediated endocytosis of cytokine-fusion proteins may be of general use to deliver macromolecules into hematopoietic progenitor cells.


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R. K. Holmes, K. Harutyunyan, M. Shah, H. Joenje, and H. Youssoufian
Correction of cross-linker sensitivity of Fanconi anemia group F cells by CD33-mediated protein transfer
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