DIACYLGLYCEROL KINASE IOTA LINKS HEAT SHOCK GENE EXPRESSION TO THE SUPPRESSION O

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 据报道，自噬中断在几种疾病中存在，包括神经退行性变和某些类型的癌症。尽管受到相似条件的调控，但热休克和自噬之间的相互作用尚不清楚。该项目的目标是研究热休克反应对自噬的影响，并确定负责任的信号传递过程。我们的初步发现确定脂蛋白激酶DGK是一种潜在的串扰介体。DGK的产物磷脂酸(PA)通过mTOR蛋白激酶抑制自噬。我们INBRE项目的具体目标是：1.评估依赖于HSF1的基因表达与自噬的关系；2.探讨热休克对DGK和PA水平的调节；3.评估DGK与自噬的关系。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Disruptions in autophagy have been reported in several diseases, including neurodegeneration and some types of cancers. Despite being regulated by similar conditions, the interplay between heat shock and autophagy is unclear. The goals of this project are to examine the impact of the heat shock response on autophagy and the define the responsible signaling processes. Our preliminary findings identified the lipid kinase DGK as a potential cross-talk mediator. The product of DGK, phosphatidic acid (PA) inhibits autophagy through the mTOR protein kinase. The Specific Aims of our INBRE project are: 1. Evaluate the relationship between HSF1-dependent gene expression and autophagy; 2. Explore the regulation of DGK and PA levels by heat shock; and 3. Evaluate the relationship between DGK and autophagy.