Role of HSP70 in the regulation of miRNA biogenesis in heat stressed cells

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Environmental stress or disease can result in protein damage, which is toxic to cells and can lead to inappropriate cell death. Cells respond to stressful stimuli by activating an evolutionarily conserved ‘heat shock response’ that results in the increased production of heat shock proteins. These proteins function as molecular chaperones and are part of a defense mechanism that acts to limit the extent of protein damage and thereby allow cells and organisms to survive proteotoxic stresses. Stress-induced cell death occurs through a regulated process of cell elimination known as apoptosis, which is controlled by pro- and anti-apoptotic members of the BCL2 family. A fundamental question in cell biology is how cells regulate the decision to initiate the process of apoptotic cell destruction. The overarching focus of my research program has been to examine the role of heat-shock proteins in this decision-making process.