Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (19)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Zhang, H.
Right arrow Articles by De Geyter, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhang, H.
Right arrow Articles by De Geyter, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Human Molecular Genetics, 2001, Vol. 10, No. 21 2329-2339
© 2001 Oxford University Press

Bcl2-L-10, a novel anti-apoptotic member of the Bcl-2 family, blocks apoptosis in the mitochondria death pathway but not in the death receptor pathway

Hong Zhang+, Wolfgang Holzgreve and Christian De Geyter

University Women’s Hospital Basel, Schanzenstrasse 46, CH-4031 Basel, Switzerland

By GenBank database searches and PCR, we have identified a novel human Bcl2-like gene, Bcl2-L-10, which contains conserved BH4, BH1 and BH2 domains but lacks BH3 domain. The Bcl2-L-10 gene has been assigned to chromosome 15q21.2. Transfection experiments demonstrated that Bcl2-L-10 can block apoptosis induced by interleukin-3 withdrawal and Bax expression, by prevention of cytochrome C release, caspase-3 activation and mitochondrial membrane potential collapse. Bcl2-L-10 cannot block TNF{alpha}-induced apoptosis. Furthermore, both the BH4 domain and the transmembrane domain of Bcl2-L-10 are necessary for its suppressive action on cell death. Our results demonstrated that Bcl2-L-10 is a newly detected anti-apoptotic member of the Bcl-2 family and that it blocks apoptosis in the mitochondrial death pathway but not in the death receptor pathway.

+ To whom correspondence should be addressed. Tel: +41 61 3259354; Fax: +41 61 3259060; Email: hzhang@uhbs.ch


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Clin. Cancer Res.Home page
M. Krajewska, S. Kitada, J. N. Winter, D. Variakojis, A. Lichtenstein, D. Zhai, M. Cuddy, X. Huang, F. Luciano, C. H. Baker, et al.
Bcl-B Expression in Human Epithelial and Nonepithelial Malignancies
Clin. Cancer Res., May 15, 2008; 14(10): 3011 - 3021.
[Abstract] [Full Text] [PDF]

Home page
 Biol. Reprod.Home page
E. De La Chesnaye, B. Kerr, A. Paredes, H. Merchant-Larios, J. P. Mendez, and S. R. Ojeda
Fbxw15/Fbxo12J Is an F-Box Protein-Encoding Gene Selectively Expressed in Oocytes of the Mouse Ovary
Biol Reprod, April 1, 2008; 78(4): 714 - 725.
[Abstract] [Full Text] [PDF]

Home page
 Mol Biol EvolHome page
A. Aouacheria, F. Brunet, and M. Gouy
Phylogenomics of Life-Or-Death Switches in Multicellular Animals: Bcl-2, BH3-Only, and BNip Families of Apoptotic Regulators
Mol. Biol. Evol., December 1, 2005; 22(12): 2395 - 2416.
[Abstract] [Full Text] [PDF]

Home page
 GutHome page
H Ashktorab, S Frank, A R Khaled, S K Durum, B Kifle, and D T Smoot
Bax translocation and mitochondrial fragmentation induced by Helicobacter pylori
Gut, June 1, 2004; 53(6): 805 - 813.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
J. Lu, M. S. Caplan, A. P. Saraf, D. Li, L. Adler, X. Liu, and T. Jilling
Platelet-activating factor-induced apoptosis is blocked by Bcl-2 in rat intestinal epithelial cells
Am J Physiol Gastrointest Liver Physiol, February 1, 2004; 286(2): G340 - G350.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.