MYB and MYC in the cell cycle.
MYB and MYC in the cell cycle.
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DOI:
10.1101/sqb.1991.056.01.014
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发表时间:
1991
期刊:
影响因子:
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通讯作者:
J. Bishop;Martin Eilers;A. Katzen;Thomas B. Kornberg;G. Ramsay;S. Schirm
中科院分区:
文献类型:
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作者:
J. Bishop;Martin Eilers;A. Katzen;Thomas B. Kornberg;G. Ramsay;S. Schirm
The engine that drives mammalian cell division is governed in at least three ways. First, there are signaling pathways that serve as accelerators to activate the engine when it is idling and keep it running as long as cell division is required. The proteins encoded by proto-oncogenes represent components of these pathways, ranging from growth factors and their receptors to transcription factors that are activated in response to mitogenic stimuli (Bishop 1991a). Second, multiple governors retard or arrest the engine when the cell should cease division. The products of tumor suppressor genes are likely candidates for governors, although their mechanisms of action are presently obscure (Marshall 1991). Third, the engine runs according to a strict schedule that is maintained by a biochemical clock or oscillator, constructed around the cdc2 kinase and the cyclins (Nurse 1990).The proto-oncogenes MYB and MYC exemplify potential accelerators for the cell cycle (L/ischer and Eisenman 1990a, b). Both genes were encountered first as oncogenes in retroviruses. Both are prototypes for small gene families whose sizes are not yet certain and most of whose members remain poorly studied. Both encode nuclear phosphoproteins that have short halflives, bind specific sites in DNA, and probably function as components of transcription factors. Both have been implicated by diverse forms of evidence as positive effectors of cellular proliferation (for review, see Liischer and Eisenman 1990a, b; see also Mucenski et al. 1991). Here we summarize our efforts to characterize the biochemical properties of the MYB and MYC proteins and to explore the role of these proteins in the cell cycle.