Abstract
p53, a transformation-related protein located in the nucleus, shares several properties with the product of the nuclear proto-oncogene c- myc. The latter is transiently induced after different membrane-originating stimuli. A similar observation has been made with c- fos, a gene that also belongs to the ‘nuclear’ class of oncogenes. Here we show that p53, unlike the products of the c- myc and c- fos genes, is not induced by the signal generated by the interaction between epidermal growth factor (EGF) and its receptor. Hence, p53 does not appear to be involved in EGF signal transduction. In order to draw this conclusion we have used an EGF receptor gene-amplified human breast tumor cell line that is growth-inhibited by EGF, and exponentially growing normal human fibroblasts.
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