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Membrane translocation and oligomerization of hBok are triggered in response to apoptotic stimuli and Bnip3

Gao, S. ; Fu, W. ; Dürrenberger, M. ; Geyter, C. ; Zhang, H.

In: Cellular and Molecular Life Sciences CMLS, 2005, vol. 62, no. 9, p. 1015-1024

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    Titre
    • Membrane translocation and oligomerization of hBok are triggered in response to apoptotic stimuli and Bnip3
    Auteur
    • Gao, S.. Department of Research and University Women's Hospital, University of Basel, Schanzenstrasse 46, 4031, Basel, Switzerland
    • Fu, W.. Center of Medical Research, University Hospital Zürich, 8091, Zürich, Switzerland
    • Dürrenberger, M.. Biocenter, University of Basel, 4031, Basel, Switzerland
    • Geyter, C.. Department of Research and University Women's Hospital, University of Basel, Schanzenstrasse 46, 4031, Basel, Switzerland
    • Zhang, H.. Department of Research and University Women's Hospital, University of Basel, Schanzenstrasse 46, 4031, Basel, Switzerland
    Type de document
    • Postprint
    Langue
    • Inglese
    Publié dans
    • Cellular and Molecular Life Sciences CMLS, 2005, vol. 62, no. 9, p. 1015-1024. Birkhäuser-Verlag; www.birkhauser.ch
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:314041
    Summary
    Abstract.: hBok is a human pro-apoptotic member of the Bcl-2 family. By fluorescence in situ hybridization and in silico analysis, hBok was found to be located on chromosome 2q37.3. Its expression was detected in various organs and several hormonally regulated cancer cells. Expression of hBok was shown to be upregulated in estrogen-dependent breast cancer by estrogen deprivation and in myocardial cells during hypoxia. Confocal laser scanning microscopy examinations and subcellular fractionation studies showed that hBok was distributed in both the cytosol and intracellular membranes of healthy cells. Upon overexpression of hBok or stimulation of apoptosis, hBok became integrated into the membrane. Furthermore, apoptosis and oligomerization were promoted by BH3-only proteins, such as Bid, Bnip3 and p53, but prevented by BFL-1. hBok was found to interact with Bnip3. Our findings suggest that functional BH3-only proteins facilite the oligomerization and insertion of hBok into the membrane to activate it