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与对溴苯甲酰溴复合的BthA-I的结构:与缺乏药理活性的可能关联。

Structure of BthA-I complexed with p-bromophenacyl bromide: possible correlations with lack of pharmacological activity.

作者信息

Magro Angelo J, Takeda Agnes A S, Soares Andreimar M, Fontes Marcos R M

机构信息

Departamento de Física e Biofísica, Instituto de Biociências, UNESP, Distrito de Rubião Jr s/n, Botucatu-SP, Brazil.

出版信息

Acta Crystallogr D Biol Crystallogr. 2005 Dec;61(Pt 12):1670-7. doi: 10.1107/S0907444905029598. Epub 2005 Nov 19.

Abstract

The crystal structure of an acidic phospholipase A(2) isolated from Bothrops jararacussu venom (BthA-I) chemically modified with p-bromophenacyl bromide (BPB) has been determined at 1.85 Angstroms resolution. The catalytic, platelet-aggregation inhibition, anticoagulant and hypotensive activities of BthA-I are abolished by ligand binding. Electron-density maps permitted unambiguous identification of inhibitor covalently bound to His48 in the substrate-binding cleft. The BthA-I-BPB complex contains three structural regions that are modified after inhibitor binding: the Ca(2+)-binding loop, beta-wing and C-terminal regions. Comparison of BthA-I-BPB with two other BPB-inhibited PLA(2) structures suggests that in the absence of Na(+) ions at the Ca(2+)-binding loop, this loop and other regions of the PLA(2)s undergo structural changes. The BthA-I-BPB structure reveals a novel oligomeric conformation. This conformation is more energetically and conformationally stable than the native structure and the abolition of pharmacological activities by the ligand may be related to the oligomeric structural changes. A residue of the ;pancreatic' loop (Lys69), which is usually attributed as providing the anticoagulant effect, is in the dimeric interface of BthA-I-BPB, leading to a new hypothesis regarding the abolition of this activity by BPB.

摘要

已确定从具窍蝮蛇毒液中分离出的经对溴苯甲酰溴(BPB)化学修饰的酸性磷脂酶A(2)(BthA-I)的晶体结构,分辨率为1.85埃。配体结合使BthA-I的催化、血小板聚集抑制、抗凝和降压活性丧失。电子密度图明确鉴定出与底物结合裂隙中的His48共价结合的抑制剂。BthA-I-BPB复合物包含三个在抑制剂结合后发生修饰的结构区域:Ca(2+)结合环、β-翼和C末端区域。将BthA-I-BPB与另外两个受BPB抑制的PLA(2)结构进行比较表明,在Ca(2+)结合环处不存在Na(+)离子时,该环和PLA(2)的其他区域会发生结构变化。BthA-I-BPB结构揭示了一种新的寡聚构象。这种构象在能量和构象上比天然结构更稳定,配体导致药理活性丧失可能与寡聚结构变化有关。通常认为具有抗凝作用的“胰腺”环(Lys69)的一个残基位于BthA-I-BPB的二聚体界面,这导致了关于BPB消除该活性的新假说。

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