Bcl-2 family member Bcl-G is not a proapoptotic protein
- Author(s)
- Giam, M; Okamoto, T; Mintern, JD; Strasser, A; Bouillet, P;
- Journal Title
- CELL DEATH & DISEASE
- Publication Type
- Journal Article
- Abstract
- The three major subgroups of the Bcl-2 family, including the prosurvival Bcl-2-like proteins, the proapoptotic Bcl-2 homology (BH) 3-only proteins and Bax/Bak proteins, regulate the mitochondrial apoptotic pathway. In addition, some outliers within the Bcl-2 family do not fit into these subgroups. One of them, Bcl-G, has a BH2 and a BH3 region, and was proposed to trigger apoptosis. To investigate the physiological role of Bcl-G, we have inactivated the gene in the mouse and generated monoclonal antibodies to determine its expression. Although two isoforms of Bcl-G exist in human, only one is found in mice. mBcl-G is expressed in a range of epithelial as well as in dendritic cells. Loss of Bcl-G did not appear to affect any of these cell types. mBcl-G only binds weakly to prosurvival members of the Bcl-2 family, and in a manner that is independent of its BH3 domain. To understand what the physiological role of Bcl-G might be, we searched for Bcl-G-binding partners through immunoprecipitation/mass spectroscopy and yeast-two-hybrid screening. Although we did not uncover any Bcl-2 family member in these screens, we found that Bcl-G interacts specifically with proteins of the transport particle protein complex. We conclude that Bcl-G most probably does not function in the classical stress-induced apoptosis pathway, but rather has a role in protein trafficking inside the cell. Cell Death and Disease (2012) 3, e404; doi:10.1038/cddis.2012.130; published online 11 October 2012
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- PRO-APOPTOTIC MEMBER; ACUTE LYMPHOBLASTIC-LEUKEMIA; PROGRAMMED CELL-DEATH; DENDRITIC CELLS; BH3-ONLY PROTEINS; GENE-EXPRESSION; LIFE-SPAN; IN-VIVO; LIGANDS; CANCER
- Research Division(s)
- Molecular Genetics Of Cancer
- Link To PubMed Central Version
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481120/
- Publisher's Version
- https://doi.org/10.1038/cddis.2012.130
- Open Access at Publisher's Site
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481120/- Terms of Use/Rights Notice
- Copyright © 2012 Macmillan Publishers Limited This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
Creation Date: 2012-10-01 12:00:00