Abstract
The c-myc gene, the cellular counterpart of the oncogene of the avian retrovirus MC29 (Duesberg et al. 1980) appears to play an important role in normal cell proliferation. In response to exogenous stimuli like platelet-derived growth factor (PDGF) in fibroblasts and lectin or anti-IgM in lymphocytes, c-myc mRNA is accumulated in the cytoplasm about 2–3 h after induction, prior to the onset of cellular DNA synthesis (Armelin et al. 1984, Kelly et al. 1983, McCormack et al. 1984). The c-myc gene is composed of three exons, the first of which is noncoding (Battey et al. 1983, Bernard et al. 1983, Hamlyn and Rab-bitts 1983, Watt et al. 1983, Gazin et al. 1984). Transcription of the c-myc gene proceeds from two initiation sites 160 bp apart from each other at the beginning of the first exon. However, two proteins of 64 and 67 K, located in the nucleus were shown to be coded for by the c-myc gene. Their function is not yet understood (Hann and Eisenman 1984, Persson et al. 1984, Persson and Leder 1984).
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© 1986 Springer-Verlag Berlin Heidelberg
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Lipp, M., Schilling, R., Wiest, S., Hartl, P. (1986). Regulation of c-myc in Variant Chromosomal Translocations of Burkitt Lymphoma. In: Tanner, W., Gallwitz, D. (eds) Cell Cycle and Oncogenes. Colloquium der Gesellschaft für Biologische Chemie 10.–12. April 1986 in Mosbach/Baden, vol 37. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71686-7_11
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DOI: https://doi.org/10.1007/978-3-642-71686-7_11
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