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Science 11 July 1997:
Vol. 277. no. 5323, pp. 246 - 248
DOI: 10.1126/science.277.5323.246
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Reports

Activation of Heat Shock Transcription Factor 3 by c-Myb in the Absence of Cellular Stress

Chie Kanei-Ishii, Jun Tanikawa, * Akira Nakai, Richard I. Morimoto, Shunsuke Ishii dagger

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.

C. Kanei-Ishii, J. Tanikawa, S. Ishii, Laboratory of Molecular Genetics, Tsukuba Life Science Center, RIKEN, Tsukuba, Ibaraki 305, Japan.
A. Nakai, Department of Cell Biology, Chest Disease Research Institute, Kyoto University, Kyoto 606, Japan.
R. I. Morimoto, Department of Biochemistry, Molecular Biology and Cell Biology, Rice Institute for Biomedical Research, Northwestern University, Evanston, IL 60208, USA.
*   Permanent address: Research Institute for Microbial Diseases, Osaka University, Yamada-oka, Suita, Osaka 565, Japan.

dagger    To whom correspondence should be addressed. E-mail: sishii{at}rtc.riken.go.jp

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p53 Suppresses the c-Myb-induced Activation of Heat Shock Transcription Factor 3.
J. Tanikawa, E. Ichikawa-Iwata, C. Kanei-Ishii, A. Nakai, S.-i. Matsuzawa, J. C. Reed, and S. Ishii (2000)
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