BORA AND THE KINASE AURORA A COOPERATIVELY ACTIVATE THE KINASE PLK1

BORA 和激酶 AURORA A 协同激活激酶 PLK1

• 批准号: 7957749
• 负责人: GUOWEI FANG
• 金额: $ 0.33万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-01 至 2010-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7957749
• 关键词: Biology; CDC2 Protein Kinase; Cell Cycle; Cell Cycle Regulation; Cell Proliferation; Computer Retrieval of Information on Scientific Projects Database; Cyclins; Event; Funding; Fungal Genome; G2 Phase; G2/M Transition; Grant; Institution; Mediating; Mitosis; Mitotic; PLK1 gene; Phosphorylation; Phosphotransferases; Reporting; Research; Research Personnel; Resources; Somatic Cell; Source; United States National Institutes of Health; aurora-A kinase; blastomere structure; human PLK1 protein

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. A central question in the study of cell proliferation is, what controls cell- cycle transitions. Although the accumulation of mitotic cyclins drives the transition from the G2 phase to the M phase in embryonic cells, the trigger for mitotic entry in somatic cells remains unknown. We report that the synergistic action of Bora and the kinase Aurora A (Aur-A) controls the G2-M transition. Bora accumulates in the G2 phase and promotes Aur-A-mediated activation of the Polo-like kinase 1 (Plk1), leading to the activation of the cyclin-dependent kinase 1 (Cdk1) and mitotic entry. Mechanistically, Bora interacts with Plk1 and controls the accessibility of its activation loop for phosphorylation and activation by Aur-A. Thus, Bora and Aur-A control mitotic entry, which provides a mechanism for one of the most important, and yet ill-defined events in the cell cycle.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 细胞增殖研究中的一个中心问题是，是什么控制着细胞周期的转换.虽然有丝分裂细胞周期蛋白的积累驱动了胚胎细胞从G2期到M期的转变，但体细胞有丝分裂进入的触发因素仍然未知。我们报告说，协同作用的Bora和激酶极光A（Aur-A）控制G2-M过渡。Bora在G2期积累并促进Aur-A介导的Polo样激酶1（Plk 1）的激活，导致细胞周期蛋白依赖性激酶1（Cdk 1）的激活和有丝分裂进入。从机制上讲，Bora与Plk 1相互作用，并控制其激活环的可及性，以通过Aur-A进行磷酸化和激活。因此，Bora和Aur-A控制有丝分裂进入，这为细胞周期中最重要但尚未明确的事件之一提供了机制。