A study on the HSF2-mediated suppression mechanism of neurodegenerative diseases based on mouse models.

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The heat shock transcription factor (heat shock factor) HSF2 is an important HSF for cortical development and highly-expressed in CNS, however, whether it can suppress cellular stress and denatured protein-mediated toxicity causing neurodegenerative diseases or not. By the support of this grand-in-aid, the principal investigator revealed that HSF2 can suppress the intracellular aggregation caused by denatured or unfolded protein. We also analyzed the novel mechanism of HSF2-mediated cytoprotection. Although only HSF1 has chromatin opening and transcription activating ability among four HSFs, some of these novel HSF2 target genes were activated by HSF2 alone in the HSF1-deficient cells. These results suggest that HSF2 has the chromatin opening activity as well as HSF1, and that the induction of novel HSF2 regulated genes involved in toxic protein degradation can lead to the suppression of neurodegenerative diseases.