来自B19细小病毒的11千道尔顿小蛋白在体外以Src同源3结构域/配体依赖的方式与生长因子受体结合蛋白2结合。

The small 11-kDa protein from B19 parvovirus binds growth factor receptor-binding protein 2 in vitro in a Src homology 3 domain/ligand-dependent manner.

作者信息

Fan M M, Tamburic L, Shippam-Brett C, Zagrodney D B, Astell C R

机构信息

Graduate Program in Neuroscience, Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada.

出版信息

Virology. 2001 Dec 20;291(2):285-91. doi: 10.1006/viro.2001.1217.

DOI:10.1006/viro.2001.1217

PMID:11878897

Abstract

The small 11-kDa proteins of B19 parvovirus contain three proline-rich regions which conform to consensus Src homology 3 (SH3) ligand sequences present in signaling molecules within the cell. We have shown that the B19 11-kDa proteins specifically interact with the growth factor receptor-binding protein 2 (Grb2) in vitro. Mutation of prolines within one of the three SH3 ligand-like sequences decreases the binding of B19 11-kDa proteins to Grb2, suggesting that the proline-rich region is involved in the B19 11-kDa/Grb2 interaction. Therefore, the B19 11-kDa proteins may function to alter Grb2-mediated signaling by disrupting SH3 domain/ligand interactions. These results implicate the 11-kDa proteins in B19 pathogenesis through perturbation of normal cellular signaling pathways.

摘要

B19细小病毒的11-kDa小蛋白包含三个富含脯氨酸的区域，这些区域与细胞内信号分子中存在的共有Src同源3（SH3）配体序列相符。我们已经表明，B19 11-kDa蛋白在体外与生长因子受体结合蛋白2（Grb2）特异性相互作用。三个SH3配体样序列之一内的脯氨酸突变会降低B19 11-kDa蛋白与Grb2的结合，这表明富含脯氨酸的区域参与了B19 11-kDa/Grb2相互作用。因此，B19 11-kDa蛋白可能通过破坏SH3结构域/配体相互作用来改变Grb2介导的信号传导。这些结果表明11-kDa蛋白通过干扰正常细胞信号通路参与B19发病机制。