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Hollenberg, and P. Cua­ trecasas, unpublished observations, 1973; Hollenberg and Cua­ trecasas, 1974a) and for growth hormone (R. S. Bockman and M. Sonenberg, personal communication, 1973) can also b e detected on lectin-transformed lymphocytes. However, no binding sites either for glucagon or for epidermal growth factor can be detected in either 58 Hollenberg and Cuatrecasas co 60 10 20 INSULIN, ng/ml FlG. 7. Insulin binding by transformed human peripheral lymphocytes. (Above) Cells transformed by ConA (O) and by PHA ( · ) .

Since various combinations of human chromosomes are main­ tained by the rat-human hybrids, it becomes possible to determine if the presence of a specific human chromosome results in the suppres­ sion of the differentiated phenotype. As shown in Figs. 1 and 2, it is possible by the Giemsa banding technique (Seabright, 1971) to identify each single mouse, rat, and human chromosome. Figure 3 is a karyotype of a rat-human hybrid clone between Fu5AH rat hepatoma cells and human KOP cells, which contain a translocation of the long arm of the X chromosome to D-14.

1971) appears to be responsible for the unresponsiveness of the cells of the urogenital tract to testosterone. The mechanism in­ volved in Tfm is clearly different from that involved in the suppres­ sion of TAT inducibility in rat-human and rat-mouse hybrids, since these hybrids had the same or higher dexamethasone receptor activ­ ity as the rat hepatoma parental cells. In addition, studies on the nuclear transfer of the dexa­ methasone-receptor complex in the parental and in the hybrid cells indicate that the nuclear transfer takes place to a higher extent in the suppressed hybrid cells than in the parental rat hepatoma cells.

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