Oncogenic transformation by Jun: role of transactivation and homodimerization.

Oncogenic transformation by Jun: role of transactivation and homodimerization.
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DOI：
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发表时间：
1992-12
期刊：
Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
影响因子：
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通讯作者：
M. Hartl;P. Vogt
M. Hartl;P. Vogt
中科院分区：
其他
文献类型：
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作者：
M. Hartl;P. Vogt

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Jun/JunD和Jun/GCN4嵌合体转化了鸡胚成纤维细胞，并激活了这些细胞中的胶原酶启动子。个体构念在两种活动中差异很大，并且在转换和交互之间没有相关性。这些结果表明，Jun的致癌转化不仅仅是由AP-1活性的上调引起的。Jun构建的修饰二聚化结构域只允许同型二聚化，在鸡胚成纤维细胞培养中的转化和转激活是活跃的。因此，Jun的同型二聚体可以转化和反激活。
Jun/JunD and Jun/GCN4 chimeras transform chicken embryo fibroblasts and activate the collagenase promoter in these same cells. Individual constructs differ widely in the two activities, and there is no correlation between transformation and transactivation. These results suggest that oncogenic transformation by Jun is not caused merely by an upregulation of AP-1 activity. Jun constructs with a modified dimerization domain allowing only homodimerization are active in transformation and transactivation in chicken embryo fibroblast cultures. Homodimers of Jun therefore transform and transactivate.