Division of Bioorganic Chemistry and Molecular Pharmacology, Washington University School of Medicine , St. Louis, Missouri 63110, USA.
Biochemistry. 2013 Jun 18;52(24):4250-63. doi: 10.1021/bi4004233. Epub 2013 Jun 10.
The multifaceted roles of calcium-independent phospholipase A2β (iPLA2β) in numerous cellular processes have been extensively examined through utilization of the iPLA2-selective inhibitor (E)-6-(bromomethylene)-3-(1-naphthalenyl)-2H-tetrahydropyran-2-one (BEL). Herein, we employed accurate mass/high resolution mass spectrometry to demonstrate that the active site serine (S465) and C651 of iPLA2β are covalently cross-linked during incubations with BEL demonstrating their close spatial proximity. This cross-link results in macroscopic alterations in enzyme molecular geometry evidenced by anomalous migration of the cross-linked enzyme by SDS-PAGE. Molecular models of iPLA2β constructed from the crystal structure of iPLA2α (patatin) indicate that the distance between S465 and C651 is approximately 10 Å within the active site of iPLA2β. Kinetic analysis of the formation of the 75 kDa iPLA2β-BEL species with the (R) and (S) enantiomers of BEL demonstrated that the reaction of (S)-BEL with iPLA2β was more rapid than for (R)-BEL paralleling the enantioselectivity for the inhibition of catalysis by each inhibitor with iPLA2β. Moreover, we demonstrate that the previously identified selective acylation of iPLA2β by oleoyl-CoA occurs at C651 thereby indicating the importance of active site architecture for acylation of this enzyme. Collectively, these results identify C651 as a highly reactive nucleophilic residue within the active site of iPLA2β which is thioesterified by BEL, acylated by oleoyl-CoA, and located in close spatial proximity to the catalytic serine thereby providing important chemical insights on the mechanisms through which BEL inhibits iPLA2β and the topology of the active site.
钙非依赖性磷脂酶 A2β(iPLA2β)在许多细胞过程中的多方面作用已通过使用 iPLA2 选择性抑制剂(E)-6-(溴亚甲基)-3-(1-萘基)-2H-四氢吡喃-2-酮(BEL)进行了广泛研究。在这里,我们采用精确质量/高分辨率质谱法证明 iPLA2β 的活性位点丝氨酸(S465)和 C651 在与 BEL 孵育过程中发生共价交联,表明它们的空间接近度。这种交联导致酶分子几何形状发生宏观变化,这一变化由 SDS-PAGE 中交联酶的异常迁移证明。基于 iPLA2α(patatin)晶体结构构建的 iPLA2β 分子模型表明,在 iPLA2β 的活性位点内,S465 和 C651 之间的距离约为 10 Å。用 BEL 的(R)和(S)对映异构体对形成 75 kDa iPLA2β-BEL 物种的动力学分析表明,(S)-BEL 与 iPLA2β 的反应比(R)-BEL 更快,与每种抑制剂对 iPLA2β 催化抑制的对映选择性一致。此外,我们证明先前鉴定的 iPLA2β 的油酸酰基-CoA 选择性酰化作用发生在 C651,从而表明活性位点结构对于该酶的酰化的重要性。总之,这些结果确定 C651 是 iPLA2β 活性位点内的一个高反应性亲核残基,该残基被 BEL 硫酯化,被油酸酰基-CoA 酰化,并且与催化丝氨酸空间接近,从而为 BEL 抑制 iPLA2β 的机制和活性位点的拓扑结构提供了重要的化学见解。