Activation of heat shock transcription factor 3 by c-Myb in the absence of cellular stress
Activation of heat shock transcription factor 3 by c-Myb in the absence of cellular stress
复制标题
DOI：
10.1126/science.277.5323.246
复制
发表时间：
1997-07-11
期刊：
影响因子：
56.9
通讯作者：
Ishii, S
中科院分区：
文献类型：
--
作者：
KaneiIshii, C;Tanikawa, J;Ishii, S
在脊椎动物中，多种热休克转录因子（HSFs）的存在表明这些因子可能受到不同的应激信号的调节。HSF 3在未应激的增殖细胞中通过直接结合c-myb原癌基因产物（c-Myb）而特异性活化。这些因子通过它们的DNA结合结构域形成复合物，该复合物刺激核进入和转录活性的HSF 3三聚体的形成。由于c-Myb参与细胞增殖，因此这种调节途径可能提供细胞增殖和应激反应之间的联系。
In vertebrates, the presence of multiple heat shock transcription factors (HSFs) indicates that these factors may be regulated by distinct stress signals. HSF3 was specifically activated in unstressed proliferating cells by direct binding to the c-myb proto-oncogene product (c-Myb). These factors formed a complex through their DNA binding domains that stimulated the nuclear entry and formation of the transcriptionally active trimer of HSF3. Because c-Myb participates in cellular proliferation, this regulatory pathway may provide a link between cellular proliferation and the stress response.