Centre for Biomolecular Sciences, School of Pharmacy, University of Nottingham, Nottingham, UK.
Aflac Cancer and Blood Disorders Center, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
J Thromb Haemost. 2019 May;17(5):759-770. doi: 10.1111/jth.14418. Epub 2019 Mar 19.
Essentials Zymogen PK is activated to PKa and cleaves substrates kininogen and FXII contributing to bradykinin generation. Monomeric PKa and dimeric homologue FXI utilize the N-terminal apple domains to recruit substrates. A high-resolution 1.3 Å structure of full-length PKa reveals an active conformation of the protease and apple domains. The PKa protease and four-apple domain disc organization is 180° rotated compared to FXI. SUMMARY: Background Plasma prekallikrein (PK) and factor XI (FXI) are apple domain-containing serine proteases that when activated to PKa and FXIa cleave substrates kininogen, factor XII, and factor IX, respectively, directing plasma coagulation, bradykinin release, inflammation, and thrombosis pathways. Objective To investigate the three-dimensional structure of full-length PKa and perform a comparison with FXI. Methods A series of recombinant full-length PKa and FXI constructs and variants were developed and the crystal structures determined. Results and conclusions A 1.3 Å structure of full-length PKa reveals the protease domain positioned above a disc-shaped assemblage of four apple domains in an active conformation. A comparison with the homologous FXI structure reveals the intramolecular disulfide and structural differences in the apple 4 domain that prevents dimer formation in PK as opposed to FXI. Two latchlike loops (LL1 and LL2) extend from the PKa protease domain to form interactions with the apple 1 and apple 3 domains, respectively. A major unexpected difference in the PKa structure compared to FXI is the 180° disc rotation of the apple domains relative to the protease domain. This results in a switched configuration of the latch loops such that LL2 interacts and buries portions of the apple 3 domain in the FXI zymogen whereas in PKa LL2 interacts with the apple 1 domain. Hydrogen-deuterium exchange mass spectrometry on plasma purified human PK and PKa determined that regions of the apple 3 domain have increased surface exposure in PKa compared to the zymogen PK, suggesting conformational change upon activation.
酶原激肽释放酶(PK)被激活为 PKa,裂解激肽原和 FXII,从而生成缓激肽。单体 PKa 和二聚体同源物 FXI 利用 N 端苹果结构域募集底物。全长 PKa 的高分辨率 1.3Å 结构揭示了蛋白酶和苹果结构域的活性构象。与 FXI 相比,PKa 蛋白酶和四苹果域盘结构旋转了 180°。
背景 血浆激肽原(PK)和因子 XI(FXI)是含有苹果结构域的丝氨酸蛋白酶,当被激活为 PKa 和 FXIa 时,分别裂解激肽原、因子 XII 和因子 IX,从而引导血浆凝固、缓激肽释放、炎症和血栓形成途径。目的 研究全长 PKa 的三维结构并与 FXI 进行比较。
方法 开发了一系列重组全长 PKa 和 FXI 构建体和变体,并确定了晶体结构。
结果和结论 全长 PKa 的 1.3Å 结构揭示了位于一个圆盘状四苹果结构域组装体上方的蛋白酶域,处于活性构象。与同源 FXI 结构的比较揭示了苹果 4 结构域中的分子内二硫键和结构差异,这阻止了 PK 中的二聚体形成,而不是 FXI。两个类似闩锁的环(LL1 和 LL2)从 PKa 蛋白酶域延伸,分别与苹果 1 和苹果 3 结构域形成相互作用。与 FXI 相比,PKa 结构的一个主要意外差异是苹果结构域相对于蛋白酶域的 180°盘旋转。这导致了闩锁环的切换构型,使得 LL2 与苹果 3 结构域相互作用并掩埋其部分,而在 PKa 中,LL2 与苹果 1 结构域相互作用。对从血浆中纯化的人 PK 和 PKa 进行的氢氘交换质谱分析表明,与酶原 PK 相比,苹果 3 结构域的某些区域在 PKa 中表面暴露增加,这表明在激活时发生了构象变化。