Pinkse Martijn W H, Rijkers Dirk T S, Dostmann Wolfgang R, Heck Albert J R
From the Biomolecular Mass Spectrometry and Proteomics Group, Bijvoet Center for Biomolecular Research and Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Sorbonnnelaan 16, Utrecht 3584 CA, The Netherlands; Department of Biotechnology, Delft, University of Technology, Delft 2628 BC, The Netherlands.
Medicinal Chemistry and Chemical Biology, Utrecht Institute for Pharmaceutical Sciences, Department of Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht 3584 CA, The Netherlands.
J Biol Chem. 2009 Jun 12;284(24):16354-16368. doi: 10.1074/jbc.M808521200. Epub 2009 Apr 15.
The inhibitor peptide DT-2 (YGRKKRRQRRRPPLRKKKKKH) is the most potent and selective inhibitor of the cGMP-dependent protein kinase (PKG) known today. DT-2 is a construct of a PKG tight binding sequence (W45, LRKKKKKH, KI=0.8 microM) and a membrane translocating sequence (DT-6, YGRKKRRQRRRPP, KI=1.1 microM), that combined strongly inhibits PKG catalyzed phosphorylation (KI=12.5 nM) with approximately 1000-fold selectivity toward PKG over protein kinase A, the closest relative of PKG. However, the molecular mechanism behind this inhibition is not entirely understood. Using a combination of photoaffinity labeling, stable isotope labeling, and mass spectrometry, we have located the binding sites of PKG-specific substrate and inhibitor peptides. Covalent linkage of a PKG-specific substrate analogue was localized in the catalytic core on residues 356-372, also known as the glycine-rich loop, essential for ATP binding. By analogy, the individual inhibitor peptides W45 and DT-6 were also found to cross-link near the glycine-rich loop, suggesting these are both substrate competitive inhibitors. A bifunctional photoreactive analogue of DT-2 was found to generate dimers of PKG. This cross-linking induced covalent PKG dimerization was not observed for an N-terminal deletion mutant of PKG, which lacks the dimerization domain. In addition, non-covalent mass spectrometry was used to determine binding stoichiometry and binding order of the inhibitor peptides. Dimeric PKG binds two W45 and DT-6 peptides, whereas only one DT-2 molecule was observed to bind to the dimeric PKG. Taken together, these findings imply that (i) the two individual components making up DT-2 are both targeted against the substrate-binding site and (ii) binding of a single DT-2 molecule inactivates both PKG monomers simultaneously, which is an indication that (iii) in cGMP-activated PKG the catalytic centers of both subunits may be in each other's proximity.
抑制肽DT-2(YGRKKRRQRRRPPLRKKKKKH)是目前已知的对环磷酸鸟苷依赖性蛋白激酶(PKG)最有效且最具选择性的抑制剂。DT-2由PKG紧密结合序列(W45,LRKKKKKH,抑制常数KI = 0.8微摩尔)和膜转运序列(DT-6,YGRKKRRQRRRPP,抑制常数KI = 1.1微摩尔)构建而成,二者结合后能强烈抑制PKG催化的磷酸化反应(抑制常数KI = 12.5纳摩尔),对PKG的选择性比对其亲缘关系最近的蛋白激酶A高约1000倍。然而,这种抑制作用背后的分子机制尚未完全明确。通过结合光亲和标记、稳定同位素标记和质谱分析,我们确定了PKG特异性底物和抑制剂肽的结合位点。一种PKG特异性底物类似物的共价连接定位于催化核心中356 - 372位的残基上,该区域也被称为富含甘氨酸环,对ATP结合至关重要。以此类推,还发现单个抑制剂肽W45和DT-6也在富含甘氨酸环附近发生交联,表明它们都是底物竞争性抑制剂。一种DT-2的双功能光反应类似物被发现能产生PKG的二聚体。对于缺乏二聚化结构域的PKG N端缺失突变体,未观察到这种交联诱导的共价PKG二聚化现象。此外,非共价质谱分析用于确定抑制剂肽的结合化学计量和结合顺序。二聚体PKG结合两个W45和DT-6肽,而仅观察到一个DT-2分子与二聚体PKG结合。综上所述,这些发现表明:(i)构成DT-2的两个单独组分均靶向底物结合位点;(ii)单个DT-2分子的结合同时使两个PKG单体失活,这表明(iii)在环磷酸鸟苷激活的PKG中,两个亚基的催化中心可能彼此靠近。