Interplay of Bcl-2 Proteins Decides the Life or Death Fate
Grant Dewson*
Abstract
Ever since the discovery that the founding member of the Bcl-2 family of proteins contributes to tumour development by inhibiting cell survival rather than encouraging proliferation [1], interest (and controversy) in these functionally diverse homologues has raged. The Bcl-2 family of proteins participate in multiple protein-protein interactions that govern whether a cell dies in response to toxic stress. This review summarises the current knowledge of how a death stimulus culminates in the activation of Bax and Bak, the pivotal effectors of the apoptotic program, and how these critical proteins cause damage to mitochondria and the consequent demise of a cell.
Keywords: Apoptosis, Bcl-2 family, Bak, Bax, mitochondria.
Article Information
Article History:
Received Date: 2/3/2010
Revision Received Date: 21/8/2010
Acceptance Date: 22/10/2010
Electronic publication date: 14/4/2011
Collection year: 2011
© Grant Dewson; Licensee Bentham Open
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (
http: //creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
* Address correspondence to this author at the Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3052, Australia; Tel: +61 3 93452335; E-mail: dewson@wehi.edu.au
Open Peer Review Details |
Manuscript submitted on 2-3-2010 |
Original Manuscript |
Interplay of Bcl-2 Proteins Decides the Life or Death Fate |