Sabatier J M, Fremont V, Mabrouk K, Crest M, Darbon H, Rochat H, Van Rietschoten J, Martin-Eauclaire M F
Biochemistry Laboratory, CNRS URA 1455, Faculty of Medicine North, Marseille, France.
Int J Pept Protein Res. 1994 May;43(5):486-95. doi: 10.1111/j.1399-3011.1994.tb00548.x.
Recently, we reported a structure-activity relationship study on P05, a novel leiurotoxin I-like scorpion toxin which is selective for the apamin-sensitive Ca(2+)-activated K+ channel [Sabatier et al. (1993) Biochemistry 32, 2763-2770]. Arg6, Arg7 and C-terminal His31 appeared to be key residues for P05 biological activity. Owing to the high sequence identity between P05 and leiurotoxin I (87%), several analogs of leiurotoxin I (Lei-NH2) with point mutations at these positions were designed and chemically synthesized using an optimized solid-phase technique. The synthesized peptides were [L6]Lei-NH2, [R7]Lei-NH2, Lei-OH and [R7]Lei-OH, as well as fragment [R7,Abu8]N4-S11-NH2. A chimeric analog ([M22,K24,R27]Lei-NH2), which possesses part of the iberiotoxin C-terminus, was also constructed. Circular dichroism analyses of these analogs, in agreement with their structural models obtained by molecular dynamics, showed that the point mutations did not significantly affect the overall secondary structures, as compared to natural Lei-NH2. All the peptides and natural toxins were compared in vitro for their capacity to inhibit binding of [125I]-apamin to rat brain synaptosomes, and in vivo for their specific neurotoxicity in mice. The Arg6 residue was essential for high biological activity of leiurotoxin I. Further, substitution of Met7 in the natural toxin by Arg7, or C-terminal amidation of His31, greatly increased affinity for the apamin receptor but did not significantly affect toxin neurotoxicity. Remarkably, the chimeric analog [M22,K24,R27]Lei-NH2 was found to retain leiurotoxin I-like activity, thus indicating that the negatively charged residues Asp24 and Glu27 (and Ile22) are not directly involved in the high toxin bioactivity. However, the chimeric molecule had no iberiotoxin-like effect on rat muscular maxi-K+ channels incorporated in lipid bilayers.
最近,我们报道了对P05的构效关系研究,P05是一种新型的类leurotoxin I蝎毒素,对蜂毒明肽敏感的Ca(2+)激活的K+通道具有选择性[Sabatier等人(1993年)《生物化学》32卷,2763 - 2770页]。Arg6、Arg7和C末端的His31似乎是P05生物活性的关键残基。由于P05与leurotoxin I之间具有高度的序列同一性(87%),设计了在这些位置具有点突变的几种leurotoxin I(Lei - NH2)类似物,并使用优化的固相技术进行化学合成。合成的肽有[L6]Lei - NH2、[R7]Lei - NH2、Lei - OH和[R7]Lei - OH,以及片段[R7,Abu8]N4 - S11 - NH2。还构建了一种嵌合类似物([M22,K24,R27]Lei - NH2),它具有部分iberiotoxin C末端。对这些类似物的圆二色性分析与其通过分子动力学获得的结构模型一致,表明与天然Lei - NH2相比,点突变并未显著影响整体二级结构。在体外比较了所有肽和天然毒素抑制[125I] - 蜂毒明肽与大鼠脑突触体结合的能力,在体内比较了它们对小鼠的特异性神经毒性。Arg6残基对leurotoxin I的高生物活性至关重要。此外,将天然毒素中的Met7替换为Arg7,或对His31进行C末端酰胺化,极大地增加了对蜂毒明肽受体的亲和力,但并未显著影响毒素的神经毒性。值得注意的是,发现嵌合类似物[M22,K24,R27]Lei - NH2保留了类leurotoxin I的活性,因此表明带负电荷的残基Asp24和Glu27(以及Ile22)不直接参与高毒素生物活性。然而,该嵌合分子对掺入脂质双层的大鼠肌肉大电导K+通道没有iberiotoxin样作用。