Further Characterization of Galloyl Pedunculagin as an Effective Autophosphorylation Inhibitor of C-Kinase in Vitro.

DOI 機関リポジトリ HANDLE Web Site Web Site ほか1件をすべて表示 一部だけ表示 被引用文献2件 参考文献33件
  • Ueno Takashi
    Genetical Biochemistry, Graduate School of Medical Sciences, Kitasato University
  • Miyanaga Takahiro
    Genetical Biochemistry, Graduate School of Medical Sciences, Kitasato University
  • Kawakami Fumitaka
    Genetical Biochemistry, Graduate School of Medical Sciences, Kitasato University
  • Okano Maiko
    Genetical Biochemistry, Graduate School of Medical Sciences, Kitasato University
  • Tanaka Takashi
    Department of Molecular Medicinal Sciences, Graduate School of Biomedical Sciences, Nagasaki University
  • Ohtsuki Kenzo
    Genetical Biochemistry, Graduate School of Medical Sciences, Kitasato University

この論文をさがす

説明

The inhibitory effect of galloyl pedunculagin (GP) isolated from Platycarya strobilacea on the activity and autophosphorylation of Ca2+- and phospholipid-dependent protein kinase (C-kinase) was examined in vitro. It was found that (i) GP inhibited the activity (phosphorylation of complement C3 from guinea pig) of C-kinaseα (rat brain) in a dose-dependent manner with an ID50 of approx. 0.12 μM; (ii) GP at lower doses (ID50=approx. 6 nM) inhibited autophosphorylation of C-kinaseα; and (iii) the GP-induced inhibition of autophosphorylation of C-kinaseα and its enzyme activity was a manner non-competitive to ATP. Similar inhibitory effect of GP on autophosphorylation of recombinant human C-kinaseη (rhC-kinaseη) and its phosphorylating activity was observed. These results suggest that GP is an effective autophosphorylation inhibitor of these two C-kinase isoforms (α and η) in vitro. In addition, the CD analysis suggests that the proline-containing six amino acid residues (PVLTPP) including a threonine residue (autophosphorylation site) at the C-terminal region (positions 635—640) of C-kinaseα may be one of the GP-binding sites.

収録刊行物

被引用文献 (2)*注記

もっと見る

参考文献 (33)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ