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
04/29/1998Pubmed ID
9516453DOI
10.1074/jbc.273.13.7523Scopus ID
2-s2.0-0032571397 (requires institutional sign-in at Scopus site) 447 CitationsAbstract
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 IJAuthor
Ivor J. Benjamin MD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AllelesAnimals
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
