Penn L J, Laufer E M, Land H
Imperial Cancer Research Fund, Lincoln's Inn Fields, London, UK.
Semin Cancer Biol. 1990 Feb;1(1):69-80.
The nuclear c-myc proto-oncogene promotes cell proliferation and can inhibit terminal differentiation as well as induce immortalisation in its oncogenic form. There is increasing evidence that c-myc exerts these biological activities by modulating transcription and by directly affecting the initiation of DNA replication. The regulation of these disparate activities may involve the carboxyl end of the c-myc protein, which is essential for transformation and autosuppression of c-myc transcription. Conserved motifs in this region of the c-myc protein may mediate complex formation and sequence-specific nucleic acid binding.
核原癌基因c-myc可促进细胞增殖，以其致癌形式抑制终末分化并诱导永生化。越来越多的证据表明，c-myc通过调节转录和直接影响DNA复制的起始发挥这些生物学活性。这些不同活性的调节可能涉及c-myc蛋白的羧基末端，这对c-myc转录的转化和自身抑制至关重要。c-myc蛋白这一区域的保守基序可能介导复合物形成和序列特异性核酸结合。
