THE INVOLVEMENT OF TMC PROTEINS IN CELLULAR STRESS RESPONSES

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 该项目的中心假设是TPCN 1钙释放通道部分负责调节胞质分裂正确进展所需的细胞内钙浓度的关键瞬时增加。此外，据推测，这种调节是通过直接参与的调节激酶负责肌球蛋白轻链2-磷酸化，激活，并随后的分裂沟的形成所必需的胞质分裂的完成。

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.