Stress response is nearly universal. Living organisms respond to the changes in their chemical, physical, and biological environments by synthesizing a group of proteins called stress or heat-shock proteins (1 ). The preferential synthesis of these proteins appears to be involved in induced transient thermal resistance (2 ). It is well known that transcription of heat-shock genes is regulated by heat-shock transcription factors (HSFs), which bind to heat-shock elements (HSEs) located in the promoter region of genes encoding heat-shock proteins (3 ). Heat-shock protein gene promoter contains three heat-shock elements (HSE, 5′-GAAnnTTCnnGAA-3′) (4 ). The HSE is known as a conserved motif present in the promoters of many heat-inducible heat-shock protein genes. Many studies have demonstrated that stress-induced denatured, unfolded, or malfolded proteins trigger the activation of heat shock transcription factors (HSFs) (5 –7 ). In mammalian cells, the activated HSF binds to the HSE and then stimulates transcription.
