MITOCHONDRIAL MODULATION OF INTRACELLULAR CA++ SIGNALING

这个奖学金的长期目标是为我提供一个 深入了解线粒体对细胞内钙离子的影响 信号和数学建模方面的专业知识 建立实验与实验相结合的独立研究计划 模特儿。在未来，我有兴趣进行细胞生物学 以及对线粒体疾病影响的生物物理研究 神经系统。 异常的钙信号，尤其是线粒体的开放 过渡孔受到钙离子、自由基等多种调节剂的影响 在病理情况下与神经元和其他细胞的死亡有关。 该奖学金的具体研究目标是：1)延长Dr。 科泽S致力于通过以下方式将线粒体构建为钙信号模型 结合线粒体过渡孔和2)解决这些问题 两个和三维空间维度的系统。我们的目标是能够 对线粒体功能的影响做出可检验的预测 正常的Ca~(2+)信号和涉及Ca~(2+)和 细胞中的线粒体。

The long term objective of this fellowship is to provide me with a thorough knowledge of the effects of mitochondria on intracellular Ca2+ signaling and the expertise in mathematical modeling necessary to establish an independent research program that combines experiment and modeling. In the future I am interested in conducting cell biological and biophysical research on the effects of mitochondrial disorders on the nervous system. Aberrant Ca2+ signaling, and especially the opening of the mitochondrial transition pore by Ca2+, free radicals and other modulators, has been implicated in neuronal and other cell death in pathological situations. The specific research aims of this fellowship are 1) to extend Dr. Keizer s efforts to build mitochondria into Ca2+ signaling models by incorporating the mitochondrial transition pore and 2) to solve these systems in two and three spatial dimensions. The goal is to be able to make testable predictions about the effect of mitochondrial function on both normal Ca2+ signaling and pathological processes involving Ca2+ and mitochondria in cells.