| First Author | Fujimoto M | Year | 2010 |
| Journal | Mol Biol Cell | Volume | 21 |
| Issue | 1 | Pages | 106-16 |
| PubMed ID | 19864465 | Mgi Jnum | J:159048 |
| Mgi Id | MGI:4441107 | Doi | 10.1091/mbc.E09-07-0639 |
| Citation | Fujimoto M, et al. (2010) A novel mouse HSF3 has the potential to activate nonclassical heat-shock genes during heat shock. Mol Biol Cell 21(1):106-16 |
| abstractText | The heat-shock response is characterized by the expression of a set of classical heat-shock genes, and is regulated by heat-shock transcription factor 1 (HSF1) in mammals. However, comprehensive analyses of gene expression have revealed very large numbers of inducible genes in cells exposed to heat shock. It is believed that HSF1 is required for the heat-inducible expression of these genes although HSF2 and HSF4 modulate some of the gene expression. Here, we identified a novel mouse HSF3 (mHSF3) translocated into the nucleus during heat shock. However, mHSF3 did not activate classical heat-shock genes such as Hsp70. Remarkably, overexpression of mHSF3 restored the expression of nonclassical heat-shock genes such as PDZK3 and PROM2 in HSF1-null mouse embryonic fibroblasts (MEFs). Although down-regulation of mHSF3 expression had no effect on gene expression or cell survival in wild-type MEF cells, it abolished the moderate expression of PDZK3 mRNA and reduced cell survival in HSF1-null MEF cells during heat shock. We propose that mHSF3 represents a unique HSF that has the potential to activate only nonclassical heat-shock genes to protect cells from detrimental stresses. |
