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A. Proteau, S. Blier, A. L. Albert, S. B. Lavoie, A. M. Traish and M. Vincent, “The Multifunctional Nuclear Protein p54nrb Is Multiphosphorylated in Mitosis and Interacts with the Mitotic Regulator Pin1,” Journal of Molecular Biology, Vol. 436, No. 4, 2005, pp. 1163-1172. doi:10.1016/j.jmb.2004.12.034

has been cited by the following article:

  • TITLE: p54nrb, a PSF Protein Partner, Contributes to Meningitic Escherichia coli K1-Mediated Pathogenicities

    AUTHORS: Lina He, Feng Chi, Tao Bo, Lin Wang, Chunhua Wu, Ambrose Jong, Shenghe Huang

    KEYWORDS: Meningitis; Escherichia coli; BMEC; IbeA; p54nrb; Invasion Protein; Receptor; Protein Interaction

    JOURNAL NAME: Open Journal of Applied Sciences, Vol.2 No.1, March 29, 2012

    ABSTRACT: IbeA is an important invasion determinant contributing to Escherichia coli K1 entry into brain microvascular endothelial cells (BMEC) that is a key step in the pathogenesis of E. coli meningitis. Our previous studies have shown that IbeA-induced signaling and E. coli K1 invasion is mediated by two IbeA-binding proteins, vimentin, which is constitutively present in the surface of human BMECs (HBMECs), and PSF, which is inducibly expressed in both mesenchymal (endothelium) and non-mesenchymal (epithelium) cells. However, it is unknown whether p54nrb, a PSF partner protein, could contribute to the pathogenesis of E. coli K1 meningitis. Here, we reported that a 54-kDa protein was identified by copurification with PSF through IbeA-affinity chromatography as an IbeA-binding protein, which is identical to p54nrb. Both p54nrb and PSF are RNA-binding proteins and share significant sequence homology. The specific interaction between IbeA and p54nrb was confirmed by Western blot and ligand overlay assays. Recombinant p54nrb blocked E. coli K1 invasion of human BMEC very effectively. Overexpressed p54nrb as a GFP fusion protein in the transfected 293T cells significantly enhanced E. coli K1 invasion. Furthermore, higher levels of surface p54nrb in the transfected 293T cells were detected by flow cytometry. These results suggest that the IbeA invasion protein of E. coli K1 interacts with p54nrb for bacterial invasion of human BMEC.