Abstract
Ever since the demonstration that acutely transforming viruses carry oncogenes derived from cellular genes, the basis for the functional differences between the products of these cellular proto-oncogenes (c-onc genes) and their viral counterparts (v-onc genes) has been an important issue. Comparison of the c-src gene product to that of the v-src gene encoded by the Rous sarcoma virus (RSV) indicated that the two proteins are similar in size and enzyme activity, but quite different in relative abundance. This finding raised the basic question of whether transformation by RSV is due to the mere overproduction of the c-src gene product (as a consequence of placing the gene under the control of viral regulatory elements) or whether qualitative alteration of the coding sequences is involved in “activating” the transformation potential of c-src. Early biological studies demonstrated the rescue of transforming sarcoma viruses from chickens infected with RSV mutants which contained deletions in the src gene, indicating that c-src sequences can replace v-src sequences in RSV to restore transforming activity (Hanafusa et al. 1977). However, since this rescue occurred via homologous recombination between the residual v-src sequences in the deletion mutants and the c-src sequences, these results did not provide a definitive answer to the above question.
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Hanafusa, H. (1986). Activation of the c-src Gene. In: Kahn, P., Graf, T. (eds) Oncogenes and Growth Control. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73325-3_14
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DOI: https://doi.org/10.1007/978-3-642-73325-3_14
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