An Artificial Copper Complex Incorporating a Cell-Penetrating Peptide Inhibits Nuclear Factor-κB (NF-κB) Activation

  • Kanemaru Yosuke
    Department of Bioorganic Medicinal Chemistry, Faculty of Life Sciences, Kumamoto University
  • Momiki Yumi
    Department of Bioorganic Medicinal Chemistry, Faculty of Life Sciences, Kumamoto University
  • Matsuura Saori
    Department of Bioorganic Medicinal Chemistry, Faculty of Life Sciences, Kumamoto University
  • Horikawa Tatsufumi
    Department of Bioorganic Medicinal Chemistry, Faculty of Life Sciences, Kumamoto University
  • Gohda Jin
    Research Institute for Drug Discovery, School of Pharmacy, Kumamoto University
  • Inoue Jun-ichiro
    Research Institute for Drug Discovery, School of Pharmacy, Kumamoto University
  • Okamoto Yoshinari
    Department of Bioorganic Medicinal Chemistry, Faculty of Life Sciences, Kumamoto University
  • Fujita Mikako
    Division of Cellular and Molecular Biology, Institute of Medical Science, University of Tokyo
  • Otsuka Masami
    Department of Bioorganic Medicinal Chemistry, Faculty of Life Sciences, Kumamoto University

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タイトル別名
  • An Artificial Copper Complex Incorporating a Cell-Penetrating Peptide Inhibits Nuclear Factor-.KAPPA.B (NF-.KAPPA.B) Activation

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Nuclear factor-κB (NF-κB) is an inducible transcription factor activated by a variety of cytokines, and promotes the transcription of genes involved in cancer, inflammation, autoimmune disease, and viral infection, among others. Because of its involvement in numerous disease processes, considerable research has focused on NF-κB as a potential drug target. We previously reported that cupric ion (Cu2+) blocks NF-κB activation. However, Cu2+ is unsuitable for drug applications. The copper complex of an artificial peptide HPH-Pep (HPH-Pep-Cu2+) was a promising alternative, but it did not easily cross the cell membrane. We report the development of a NF-κB inhibiting Cu2+ complex with improved cell-penetrating activity arising from the coupling of a Tat peptide to HPH-Pep-Cu2+.

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