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

环境压力或疾病会导致蛋白质损伤，这对细胞是有毒的，并可能导致不适当的细胞死亡。细胞对应激刺激的反应是激活一种进化上保守的‘热休克反应’，导致热休克蛋白的产生增加。这些蛋白质作为分子伴侣发挥作用，是防御机制的一部分，该机制可以限制蛋白质损伤的程度，从而允许细胞和有机体在蛋白毒性压力下生存下来。应激诱导的细胞死亡是通过一种被称为细胞凋亡的受调控的细胞清除过程发生的，该过程由BCL2家族中支持和反对凋亡的成员控制。细胞生物学中的一个基本问题是，细胞如何调控启动细胞凋亡破坏过程的决定。我的研究计划的主要重点一直是研究热休克蛋白在这一决策过程中的作用。

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.