Document Detail

A novel HSF1-mediated death pathway that is suppressed by heat shock proteins.
MedLine Citation:
PMID:  17024176     Owner:  NLM     Status:  MEDLINE    
Heat shock response is an adoptive response to proteotoxic stress, and a major heat shock transcription factor 1 (HSF1) has been believed to protect cells from cell death by inducing heat shock proteins (Hsps) that assist protein folding and prevent protein denaturation. However, it is revealed recently that HSF1 also promotes cell death of male germ cells. Here, we found a proapoptotic Tdag51 (T-cell death associated gene 51) gene as a direct target gene of HSF1. Heat shock and other stresses induced different levels of Hsps and Tdag51, which depend on cell types. Hsps bound directly to the N-terminal pleckstrin-homology like (PHL) domain of Tdag51, and suppressed death activity of the C-terminal proline/glutamine/histidine-rich domain. Tdag51, but not major Hsps, were induced in male germ cells exposed to high temperatures. Analysis of Tdag51-null testes showed that Tdag51 played substantial roles in promoting heat shock-induced cell death in vivo. These data suggest that cell fate on proteotoxic condition is determined at least by balance between Hsp and Tdag51 levels, which are differently regulated by HSF1.
Naoki Hayashida; Sachiye Inouye; Mitsuaki Fujimoto; Yasunori Tanaka; Hanae Izu; Eiichi Takaki; Hitoshi Ichikawa; Jaerang Rho; Akira Nakai
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-10-05
Journal Detail:
Title:  The EMBO journal     Volume:  25     ISSN:  0261-4189     ISO Abbreviation:  EMBO J.     Publication Date:  2006 Oct 
Date Detail:
Created Date:  2006-10-18     Completed Date:  2006-12-04     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  8208664     Medline TA:  EMBO J     Country:  England    
Other Details:
Languages:  eng     Pagination:  4773-83     Citation Subset:  IM    
Department of Biochemistry and Molecular Biology, Yamaguchi University School of Medicine, Ube, Japan.
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MeSH Terms
Cell Death / genetics
DNA-Binding Proteins / deficiency,  metabolism*
Heat-Shock Proteins / genetics,  metabolism
Hela Cells
Hot Temperature
Mice, Mutant Strains
Protein Binding
Protein Structure, Tertiary / genetics
Signal Transduction* / genetics
Spermatozoa / metabolism*
Stress, Physiological / genetics,  metabolism
Testis / metabolism*
Transcription Factors / deficiency,  genetics,  metabolism*
Reg. No./Substance:
0/DNA-Binding Proteins; 0/Heat-Shock Proteins; 0/Hsf1 protein, mouse; 0/Phlda1 protein, mouse; 0/Transcription Factors

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