Wyke A W, Cushley W, Wyke J A
Beatson Institute for Cancer Research, CRC Beatson Laboratories, Wolfson Laboratory for Molecular Pathology, Bearsden, Glasgow, United Kingdom.
Cell Growth Differ. 1993 Aug;4(8):671-8.
Activation of the tyrosine kinase of a temperature sensitive v-Src mutant of Rous sarcoma virus in quiescent Rat-1 cells leads to passage through the cell cycle. This is accompanied by a transient increase of the DNA binding activity of the transcription factor AP-1 which is not sufficient for the v-Src mediated cell cycle traverse. There is another need for v-Src later in the G1 phase of the cycle, and after completion of that event, cells are able to progress through DNA synthesis and division in the absence of either v-Src or other growth factors. When cells are exposed to v-Src activity for periods insufficient for it to behave as a complete mitogen, it can act as either a competence or progression factor in conjunction with appropriate purified growth factors.
在静止的大鼠-1细胞中,劳氏肉瘤病毒温度敏感型v-Src突变体的酪氨酸激酶激活会导致细胞通过细胞周期。这伴随着转录因子AP-1的DNA结合活性短暂增加,但这不足以介导v-Src诱导的细胞周期进程。在细胞周期的G1期后期对v-Src还有其他需求,完成该事件后,细胞能够在没有v-Src或其他生长因子的情况下进行DNA合成和分裂。当细胞暴露于v-Src活性的时间不足以使其表现为完全有丝分裂原时,它可以与适当的纯化生长因子一起作为感受态或促细胞增殖因子发挥作用。