Bcl-2 antiapoptotic protein mediates verotoxin II-induced cell death: possible association between bcl-2 and tissue failure by E. coli O157:H7.

نویسندگان

  • A Suzuki
  • H Doi
  • F Matsuzawa
  • S Aikawa
  • K Takiguchi
  • H Kawano
  • M Hayashida
  • S Ohno
چکیده

Verotoxin II (VTII: or Shiga-like toxin 2) is a key factor for Escherichia coli O157:H7-induced multiple tissue failure and contains a pentameric sequence (NWGRI) similar to the Bcl-2 homolog domain, BH1. In the current study, we demonstrate that VTII, but not VTI, interacts with Bcl-2 through each BH1 domain pentameric sequence (NWGRI) and that the VTII/Bcl-2 complex is necessary for cell-death induction in target cells. VTII translocates to mitochondria and induces cell death only when target cells are expressing Bcl-2. In addition, interruption of VTII-Bcl-2 complex formation by a pentameric BH1 synthetic peptide suppresses VTII-induced cell death. In the present article, we propose that Bcl-2 mediates VTII-induced target cell death by the interaction with each pentameric sequence of BH1 domain.

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عنوان ژورنال:
  • Genes & development

دوره 14 14  شماره 

صفحات  -

تاریخ انتشار 2000