Blanes-Mira Clara, Pastor Maria T, Valera Elvira, Fernández-Ballester Gregorio, Merino Jaime M, Gutierrez Luis M, Perez-Payá Enrique, Ferrer-Montiel Antonio
Instituto de Biología Molecular y Celular, Universidad Miguel Hernández, Av. De la Universidad s/n, 03202 Elche, Alicante, Spain.
Biochem J. 2003 Oct 1;375(Pt 1):159-66. doi: 10.1042/BJ20030509.
Synthetic peptides patterned after the proteins involved in vesicle fusion [the so-called SNARE (soluble N -ethylmaleimide-sensitive fusion protein attachment protein receptor) proteins] are potent inhibitors of SNARE complex assembly and neuronal exocytosis. It is noteworthy that the identification of peptide sequences not related to the SNARE proteins has not been accomplished yet; this is due, in part, to the structural constraints and the specificity of the protein interactions that govern the formation of the SNARE complex. Here we have addressed this question and used a combinatorial approach to identify peptides that modulate the assembly of the SNARE core complex and inhibit neuronal exocytosis. An alpha-helix-constrained, mixture-based, 17-mer combinatorial peptide library composed of 137180 sequences was synthesized in a positional scanning format. Peptide mixtures were assayed for their ability to prevent the formation of the in vitro -reconstituted SDS-resistant SNARE core complex. Library deconvolution identified eight peptides that inhibited the assembly of the SNARE core complex. Notably, the most potent 17-mer peptide (acetyl-SAAEAFAKLYAEAFAKG-NH2) abolished both Ca2+-evoked catecholamine secretion from detergent-permeabilized chromaffin cells and L-glutamate release from intact hippocampal primary cultures. Collectively, these findings indicate that amino acid sequences that prevent SNARE complex formation are not restricted to those that mimic domains of SNARE proteins, thus expanding the diversity of molecules that target neuronal exocytosis. Because of the implication of neurosecretion in the aetiology of several human neurological disorders, these newly identified peptides may be considered hits for the development of novel anti-spasmodic drugs.
模仿囊泡融合相关蛋白(即所谓的SNARE蛋白,可溶性N - 乙基马来酰亚胺敏感融合蛋白附着蛋白受体)构建的合成肽是SNARE复合体组装和神经元胞吐作用的有效抑制剂。值得注意的是,与SNARE蛋白无关的肽序列的鉴定尚未完成;部分原因在于控制SNARE复合体形成的蛋白质相互作用的结构限制和特异性。在此,我们解决了这个问题,并采用组合方法来鉴定可调节SNARE核心复合体组装并抑制神经元胞吐作用的肽。合成了一个基于混合物的、由137180个序列组成的α - 螺旋受限17肽组合文库,采用位置扫描形式。检测肽混合物阻止体外重构的抗SDS的SNARE核心复合体形成的能力。文库解卷积鉴定出8种抑制SNARE核心复合体组装的肽。值得注意的是,最有效的17肽(乙酰基 - SAAEAFAKLYAEAFAKG - NH2)消除了去污剂通透的嗜铬细胞中Ca2 + 引发的儿茶酚胺分泌以及完整海马原代培养物中L - 谷氨酸的释放。总体而言,这些发现表明,阻止SNARE复合体形成的氨基酸序列并不局限于那些模仿SNARE蛋白结构域的序列,从而扩大了靶向神经元胞吐作用的分子多样性。由于神经分泌在几种人类神经系统疾病的病因学中有重要作用,这些新鉴定的肽可能被视为开发新型抗痉挛药物的有效成分。