Journal article
Rac1 Regulates Stress-induced, Redox-dependent Heat Shock Factor Activation
The Journal of biological chemistry, Vol.275(45), pp.35377-35383
11/2000
DOI: 10.1074/jbc.M005287200
PMID: 10952983
Abstract
The signaling pathway by which environmental stresses activate heat shock factors (HSFs) is not completely understood. We show that the small GTPase rac1, and Rac1-regulated reactive oxygen species (ROS) play an important role in stress-stimulated heat shock response. A dominant-negative allele of Rac1 (Rac1N17) inhibits the hypoxia/reoxygenation and sodium arsenite-induced transcriptional activity of HSF-1 and the transcription of heat shock protein 70. Rac1N17 also suppresses the production of intracellular ROS induced by hypoxia/reoxygenation or sodium arsenite. Moreover, direct suppression of intracellular ROS levels by antioxidants decreases stress-stimulated HSF activity. However, expression of a constitutively active mutant of Rac1 (Rac1V12) in the absence of extracellular stresses does not increase intracellular ROS levels or induce the heat shock response. These results show that Rac1 is a necessary but insufficient component of the stress-induced signaling pathway that leads to ROS production, activation of HSFs, and transcription of heat shock proteins.
Details
- Title: Subtitle
- Rac1 Regulates Stress-induced, Redox-dependent Heat Shock Factor Activation
- Creators
- Michitaka OzakiShailesh S DeshpandePiamsook AngkeowSeiichi SuzukiKaikobad Irani
- Resource Type
- Journal article
- Publication Details
- The Journal of biological chemistry, Vol.275(45), pp.35377-35383
- DOI
- 10.1074/jbc.M005287200
- PMID
- 10952983
- NLM abbreviation
- J Biol Chem
- ISSN
- 0021-9258
- eISSN
- 1083-351X
- Language
- English
- Date published
- 11/2000
- Academic Unit
- Cardiovascular Medicine; Radiation Oncology; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
- Record Identifier
- 9984046920502771
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