THE INVOLVEMENT OF TMC PROTEINS IN CELLULAR STRESS RESPONSES

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。 该项目的中心假设是，TPCN1钙释放通道部分负责调节细胞内钙浓度的关键瞬间增加，这是胞质分裂正确进行所需的。此外，假设这种调节是通过直接参与肌球蛋白轻链2-磷酸化、激活以及随后完成胞质分裂所必需的裂解沟形成的调节蛋白的参与来实现的。

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. The central hypothesis of this project is that the TPCN1 calcium release channel is in part responsible in regulating the key transient increases in intracellular calcium concentration needed for the correct progression of cytokinesis. In addition, it is hypothesized that this regulation is via direct involvement of the regulatory kinases responsible for myosin light chain 2-phosphorylation, activation, and the subsequent cleavage furrow formation necessary for completion of cytokinesis.