Trojanowsky Michelle, Vidovic Dusica, Simanski Scott, Penas Clara, Schurer Stephan, Ayad Nagi G
a From the Center for Therapeutic Innovation; Department of Psychiatry and Behavioral Sciences ; University of Miami ; Miami , FL USA.
Cell Cycle. 2015;14(8):1274-81. doi: 10.1080/15384101.2015.1006987.
Kinase signaling networks are well-established mediators of cell cycle transitions. However, how kinases interact with the ubiquitin proteasome system (UPS) to elicit protein turnover is not fully understood. We sought a means of identifying kinase-substrate interactions to better understand signaling pathways controlling protein degradation. Our prior studies used a luciferase fusion protein to uncover kinase networks controlling protein turnover. In this study, we utilized a similar approach to identify pathways controlling the cell cycle protein p27(Kip1). We generated a p27(Kip1)-luciferase fusion and expressed it in cells incubated with compounds from a library of pharmacologically active compounds. We then compared the relative effects of the compounds on p27(Kip1)-luciferase fusion stabilization. This was combined with in silico kinome profiling to identify potential kinases inhibited by each compound. This approach effectively uncovered known kinases regulating p27(Kip1) turnover. Collectively, our studies suggest that this parallel screening approach is robust and can be applied to fully understand kinase-ubiquitin pathway interactions.
激酶信号网络是细胞周期转换中公认的介质。然而,激酶如何与泛素蛋白酶体系统(UPS)相互作用以引发蛋白质周转尚未完全了解。我们寻求一种识别激酶-底物相互作用的方法,以更好地理解控制蛋白质降解的信号通路。我们之前的研究使用荧光素酶融合蛋白来揭示控制蛋白质周转的激酶网络。在本研究中,我们采用类似的方法来识别控制细胞周期蛋白p27(Kip1)的途径。我们构建了一个p27(Kip1)-荧光素酶融合蛋白,并将其在与来自药理活性化合物库的化合物孵育的细胞中表达。然后,我们比较了这些化合物对p27(Kip1)-荧光素酶融合蛋白稳定性的相对影响。这与计算机激酶组分析相结合,以识别每种化合物抑制的潜在激酶。这种方法有效地发现了调节p27(Kip)周转的已知激酶。总的来说,我们的研究表明,这种平行筛选方法是可靠的,可用于全面了解激酶-泛素途径的相互作用。