ACTIVATION OF HEAT-SHOCK TRANSCRIPTION FACTOR-3 BY C-MYB IN THE ABSENCE OF CELLULAR STRESS

In vertebrates, the presence of multiple heat shock transcription fact ors (HSFs) indicates that these factors may be regulated by distinct s tress signals. HSF3 was specifically activated in unstressed prolifera ting cells by direct binding to the c-myb proto-oncogene product (c-My b). These factors formed a complex through their DNA binding domains t hat stimulated the nuclear entry and formation of the transcriptionall y active trimer of HSF3. Because c-Myb participates in cellular prolif eration, this regulatory pathway may provide a link between cellular p roliferation and the stress response.