ABSTRACT
The activation of heat shock gene expression is a highly regulated response to diverse environmental and physiological conditions including heat shock, oxidative stress, heavy metals, various chemicals, bacterial and viral infection, and exposure to a number of acute and chronic disease states (Ritossa, 1962; Ashburner, 1970; Lindquist and Craig, 1988; Morimoto et al., 1990; 1994). These conditions (Figure 1) can be partitioned into three broad catergories: (1) environmental stress including heat shock, amino acid analogues, drugs, toxic chemicals, and heavy metals, (2) pathophysiologic and disease states including oxidative stress, fever, inflammation, infection, myocardial stress and ischemia, and neural degenerative diseases, and (3) non-stress conditions including the cell cycle, growth factors, serum stimulation, development, differentiation, and activation
1. Introduction 1.1 Inducible Transcription by a Family of Heat Shock Factors 2. The HSFI Cycle: Proposed Role for Heat Shock Proteins in Autoregulation of the Heat Shock Response
3. Activation of HSF2 is Linked to Proteolysis and the Activity of the Ubiquitin-Dependent Proteasome 4. HSF 3 and HSF4 5. Transcriptional Regulation of Endoplasmic Reticulum Stress Genes (GRP78): The Unfolded Protein Response 6. Conclusions 7. Acknowledgement 8. References
by certain oncogenes. The diverse nature of these conditions has led to questions on the identity and properties of the cellular machinery that detects “stress”. This chapter will address the stress-sensing mechanisms that operate in the cytosol and lumen of eukaryotic cells and that lead to the transcriptional activation of specific genes encoding compartment specific heat shock proteins and molecular chaperones.
