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Targeted disruption of heat shock transcription factor 1 abolishes thermotolerance and protection against heat-inducible apoptosis. J Biol Chem 1998 Mar 27;273(13):7523-8

Date

04/29/1998

Pubmed ID

9516453

DOI

10.1074/jbc.273.13.7523

Scopus ID

2-s2.0-0032571397   406 Citations

Abstract

Heat shock transcription factor 1 (HSF1) is a member of the vertebrate HSF family that regulates stress-inducible synthesis of heat shock proteins (HSPs). Although the synthesis of the constitutively expressed and inducible members of the heat shock family of stress proteins correlates with increased cellular protection, their relative contributions in acquired cellular resistance or "thermotolerance" in mammalian cells is presently unknown. We report here that constitutive expression of multiple HSPs in cultured embryonic cells was unaffected by disruption of the murine HSF1 gene. In contrast, thermotolerance was not attainable in hsf1(-/-) cells, and this response was required for protection against heat-induced apoptosis. We conclude that 1) constitutive and inducibly expressed HSPs exhibit distinct physiological functions for cellular maintenance and adaptation, respectively, and 2) other mammalian HSFs or distinct evolutionarily conserved stress response pathways do not compensate for HSF1 in the physiological response to heat shock.

Author List

McMillan DR, Xiao X, Shao L, Graves K, Benjamin IJ

Author

Ivor J. Benjamin MD Center Director, Professor in the Medicine department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Alleles
Animals
Apoptosis
Base Sequence
Cells, Cultured
DNA-Binding Proteins
Fluorescence
Genotype
Heat Shock Transcription Factors
Heat-Shock Proteins
Hot Temperature
Mice
Mice, Inbred BALB C
Microscopy, Confocal
Molecular Sequence Data
RNA, Messenger
Transcription Factors
jenkins-FCD Prod-482 91ad8a360b6da540234915ea01ff80e38bfdb40a