Sue Shih-Che, Cervantes Carla, Komives Elizabeth A, Dyson H Jane
Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
J Mol Biol. 2008 Jul 25;380(5):917-31. doi: 10.1016/j.jmb.2008.05.048. Epub 2008 May 29.
The mechanism of inhibition of the transcriptional activator nuclear factor kappaB (NF-kappaB) by the inhibitor IkappaB* is central to the understanding of the control of transcriptional activity via this widely employed pathway. Previous studies suggested that IkappaB* , a modular protein with an NF-kappaB binding domain consisting of six ankyrin repeat domains (ANKs), shows differential flexibility, with ANK 1-4 apparently more rigid in solution in the absence of NF-kappaB than ANK 5 and 6. Here we report NMR studies that confirm the enhanced flexibility of ANK 5 and 6 in free IkappaB* . Upon binding of NF-kappaB, ANK 5 and 6 become well structured and rigid, but, somewhat surprisingly, other domains of the IkappaB* , which were relatively rigid in the free protein, become significantly more flexible. Due to the high molecular masses of the component proteins and the complexes, we employ a hierarchical experimental plan to maximize the available information on local flexibility in the ankyrin repeat domains. Backbone resonances of the 221-residue IkappaB* protein were assigned firstly in a smaller construct consisting of ankyrin repeats 1-4. These assignments could be readily transferred to the spectra of the construct containing six repeats, both free and complexed with various combinations of the NF-kappaB p50 and p65 domains. Transverse relaxation optimized spectroscopy-type NMR experiments on differentially labeled proteins enabled information on backbone structure and dynamics to be obtained, even in complexes with molecular masses approaching 100 kDa. Changes in the flexibility and stability of the various ankyrin repeat domains of IkappaB* complex formation take a variety of forms depending on the position of the domain in the complex, providing a variety of examples of the structural and functional utility of intrinsically unstructured or partly folded protein domains.
抑制蛋白IkappaB对转录激活因子核因子κB(NF-κB)的抑制机制,是理解通过这一广泛应用的途径控制转录活性的核心。先前的研究表明,IkappaB是一种模块化蛋白,其NF-κB结合结构域由六个锚蛋白重复结构域(ANKs)组成,具有不同的灵活性,在没有NF-κB的情况下,ANK 1-4在溶液中明显比ANK 5和6更刚性。在此我们报告核磁共振研究结果,证实了游离IkappaB中ANK 5和6的灵活性增强。在与NF-κB结合后,ANK 5和6变得结构良好且刚性增强,但令人惊讶的是,IkappaB的其他结构域在游离蛋白中相对刚性,在结合后变得明显更灵活。由于组成蛋白和复合物的分子量较大,我们采用分层实验方案,以最大限度地获取有关锚蛋白重复结构域局部灵活性的可用信息。首先在由锚蛋白重复结构域1-4组成的较小构建体中对221个残基的IkappaB蛋白的主链共振进行了归属。这些归属可以很容易地转移到包含六个重复结构域的构建体的光谱中,该构建体无论是游离状态还是与NF-κB p50和p65结构域的各种组合形成复合物。对不同标记的蛋白进行横向弛豫优化光谱型核磁共振实验,即使在分子量接近100 kDa的复合物中,也能获得有关主链结构和动力学的信息。IkappaB复合物形成过程中各种锚蛋白重复结构域的灵活性和稳定性变化呈现出多种形式,这取决于该结构域在复合物中的位置,为内在无序或部分折叠的蛋白结构域的结构和功能效用提供了多种实例。