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金黄色葡萄球菌纤连蛋白受体的纤连蛋白结合决定簇

Fibronectin binding determinants of the Staphylococcus aureus fibronectin receptor.

作者信息

McGavin M J, Raucci G, Gurusiddappa S, Höök M

机构信息

Department of Biochemistry, University of Alabama, Birmingham 35294.

出版信息

J Biol Chem. 1991 May 5;266(13):8343-7.

PMID:1827119
Abstract

Synthetic peptide analogs mimicking a repeated motif within the Staphylococcus aureus fibronectin receptor inhibit binding of the bacteria to fibronectin (Signäs, C., Raucci, G., Jonsson, K., Lindgren, P. E., Anantharamaiah, G. M., Höök, M., and Lindberg, M. (1989) Proc. Natl. Acad. Sci. U.S.A. 86, 699-703). In this study, we have further localized the fibronectin-binding determinant within the 37 amino acid D3 peptide. Chemical modification of the carboxyl side chains of the glutamic and aspartic residues in D3 abolished fibronectin-binding activity, whereas modifications of lysine or tyrosine residues had little effect. An active peptide encompassing residues 15-36 was isolated from a trypsin digest of D3, and a synthetic peptide S16-36 had activity comparable with that of intact D3. Scrambling the amino acid sequence of S16-36 or replacing the aspartic and glutamic residues with asparagine and glutamine resulted in loss of activity. Therefore, one or more of the acidic residues are essential for activity. However, additional sequence is required. Reduction in the size of S16-36 from either the N- or C-terminal end resulted in peptides with greatly diminished activity. These data suggest that the amino acids essential for binding fibronectin are contained within residues 21-33 of the D3 peptide and that the flanking N- and C-terminal amino acids are necessary for the peptide to acquire a conformation that is favorable for fibronectin binding.

摘要

模拟金黄色葡萄球菌纤连蛋白受体中重复基序的合成肽类似物可抑制细菌与纤连蛋白的结合(西纳斯,C.,劳奇,G.,琼森,K.,林德格伦,P.E.,阿南塔拉马亚,G.M.,胡克,M.,和林德伯格,M.(1989年)《美国国家科学院院刊》86,699 - 703)。在本研究中,我们进一步将纤连蛋白结合决定簇定位在37个氨基酸的D3肽内。D3中谷氨酸和天冬氨酸残基羧基侧链的化学修饰消除了纤连蛋白结合活性,而赖氨酸或酪氨酸残基的修饰影响很小。从D3的胰蛋白酶消化物中分离出一个包含15 - 36位残基的活性肽,合成肽S16 - 36具有与完整D3相当的活性。打乱S16 - 36的氨基酸序列或用天冬酰胺和谷氨酰胺取代天冬氨酸和谷氨酸残基导致活性丧失。因此,一个或多个酸性残基对活性至关重要。然而,还需要额外的序列。从N端或C端减小S16 - 36的大小会导致活性大大降低的肽。这些数据表明,结合纤连蛋白所必需的氨基酸包含在D3肽的21 - 33位残基内,并且侧翼的N端和C端氨基酸对于肽获得有利于纤连蛋白结合的构象是必要的。

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