The heat shock response (HSR) is an essential cellular and organismal protective mechanism against acute forms of physiological and environmental stress. Induction of the HSR by exposure to acute stress conditions such as elevated temperature, oxidants, and heavy metals involves activation of heat shock transcription factors (HSFs) and elevated expression of genes encoding heat shock proteins and molecular chaperones that restore proteostasis and prevent the further accumulation of misfolded and aggregated proteins. Here, we examine the stress-sensing mechanisms that regulate HSFs and the role of post-translational modifications that regulate HSF activity. In addition to its role in acute stress, the expression of molecular chaperones and heat shock genes is important for development and is protective when challenged by chronic proteostasis imbalance during aging and diseases of protein conformation.
|Original language||English (US)|
|Title of host publication||Protein Quality Control in Neurodegenerative Diseases|
|Editors||Richard Morimoto, Yves Christen|
|Publisher||Springer Berlin Heidelberg|
|Number of pages||18|
|State||Published - 2012|