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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 细胞增殖研究中的一个核心问题是控制细胞周期转变的原因。尽管有丝分裂细胞周期蛋白的积累驱动了从G2期到胚胎细胞中M相的过渡，但在体细胞中有丝分裂进入的触发因素仍然未知。我们报告说，Bora和激酶Aurora A（AUR-A）的协同作用控制G2-M转变。 BORA在G2相中积累，并促进了类似polo样激酶1（PLK1）的AUR-A介导的激活，从而导致Cyclin依赖性激酶1（CDK1）和有丝分裂输入的激活。从机械上讲，Bora与PLK1相互作用，并控制其激活环的可访问性，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，它为细胞周期中最重要，但定义不明的事件提供了一种机制。