Nickel Sequestration by the Host-Defense Protein Human Calprotectin.

The human innate immune protein calprotectin (CP, S100A8/S100A9 oligomer, calgranulin A/calgranulin B oligomer, MRP-8/MRP-14 oligomer) chelates a number of first-row transition metals, including Mn(II), Fe(II), and Zn(II), and can withhold these essential nutrients from microbes. Here we elucidate t...

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Publicado en:Journal of the American Chemical Society Vol. 139; no. 26; pp. 8828 - 8837
Autores principales: Nakashige, Toshiki G., Zygiel, Emily M., Drennan, Catherine L., Nolan, Elizabeth M.
Formato: Artículo
Publicado: American Chemical Society 7/5/2017
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Acceso en línea:Ver este registro en EBSCOhost
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      dt: 7/5/2017
      vid: 139
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      pub: American Chemical Society
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        10.1021/jacs.7b01212
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        atl: Nickel Sequestration by the Host-Defense Protein Human Calprotectin.
      aug:
        au:
          Nakashige, Toshiki G.
          Zygiel, Emily M.
          Drennan, Catherine L.
          Nolan, Elizabeth M.
        affil:
          Department of Chemistry, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, United States
          Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, United States
          Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, United States
      su:
        Sequestration (Chemistry)
        Lectins
        Coordinate covalent bond
        Chelation
        Staphylococcus aureus
        Enzyme inhibitors
        Urease
      sug:
        subj:
          Sequestration (Chemistry)
          Lectins
          Coordinate covalent bond
          Chelation
          Staphylococcus aureus
          Enzyme inhibitors
          Urease
      ab: The human innate immune protein calprotectin (CP, S100A8/S100A9 oligomer, calgranulin A/calgranulin B oligomer, MRP-8/MRP-14 oligomer) chelates a number of first-row transition metals, including Mn(II), Fe(II), and Zn(II), and can withhold these essential nutrients from microbes. Here we elucidate the Ni(II) coordination chemistry of human CP. We present a 2.6-Šcrystal structure of Ni(II)- and Ca(II)-bound CP, which reveals that CP binds Ni(II) ions at both its transition-metal-binding sites: the HisAsp motif (site 1) and the His motif (site 2). Further biochemical studies establish that coordination of Ni(II) at the hexahistidine site is thermodynamically preferred over Zn(II). We also demonstrate that CP can sequester Ni(II) from two human pathogens, Staphylococcus aureus and Klebsiella pneumoniae, that utilize this metal nutrient during infection, and inhibit the activity of the Ni(II)-dependent enzyme urease in bacterial cultures. In total, our findings expand the biological coordination chemistry of Ni(II)-chelating proteins in nature and provide a foundation for evaluating putative roles of CP in Ni(II) homeostasis at the host-microbe interface and beyond.
      pubtype: Academic Journal
      doctype: Article
      src: R
    language: English
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          year: 2017
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