Zanela Tania M Palhano, Zangiabadi Milad, Zhao Yan, Underbakke Eric S
Roy J. Carver Department of Biochemistry, Biophysics, and Molecular Biology, Iowa State University Ames IA 50011 USA
Department of Chemistry, Iowa State University Ames Iowa 50011 USA.
RSC Chem Biol. 2024 Mar 13;5(5):447-453. doi: 10.1039/d3cb00228d. eCollection 2024 May 8.
Pyk2 is a multi-domain non-receptor tyrosine kinase that serves dual roles as a signaling enzyme and scaffold. Pyk2 activation involves a multi-stage cascade of conformational rearrangements and protein interactions initiated by autophosphorylation of a linker site. Linker phosphorylation recruits Src kinase, and Src-mediated phosphorylation of the Pyk2 activation loop confers full activation. The regulation and accessibility of the initial Pyk2 autophosphorylation site remains unclear. We employed peptide-binding molecularly imprinted nanoparticles (MINPs) to probe the regulatory conformations controlling Pyk2 activation. MINPs differentiating local structure and phosphorylation state revealed that the Pyk2 autophosphorylation site is protected in the autoinhibited state. Activity profiling of Pyk2 variants implicated FERM and linker residues responsible for constraining the autophosphorylation site. MINPs targeting each Src docking site disrupt the higher-order kinase interactions critical for activation complex maturation. Ultimately, MINPs targeting key regulatory motifs establish a useful toolkit for probing successive activational stages in the higher-order Pyk2 signaling complex.
Pyk2是一种多结构域非受体酪氨酸激酶,兼具信号酶和支架双重作用。Pyk2的激活涉及由连接位点的自磷酸化引发的多阶段构象重排和蛋白质相互作用级联反应。连接区磷酸化招募Src激酶,Src介导的Pyk2激活环磷酸化赋予其完全激活状态。最初的Pyk2自磷酸化位点的调控和可及性仍不清楚。我们采用肽结合分子印迹纳米颗粒(MINP)来探测控制Pyk2激活的调控构象。区分局部结构和磷酸化状态的MINP显示,Pyk2自磷酸化位点在自抑制状态下受到保护。Pyk2变体的活性分析表明,FERM和连接区残基负责限制自磷酸化位点。靶向每个Src对接位点的MINP破坏了对激活复合物成熟至关重要的高阶激酶相互作用。最终,靶向关键调控基序的MINP建立了一个有用的工具包,用于探测高阶Pyk2信号复合物中的连续激活阶段。