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May 2001, Volume 8, Number 5, Pages 486-494
Table of contents    Previous  Abstract  Next   Full text  PDF
Original Paper
Tissue expression and subcellular localization of the pro-survival molecule Bcl-w
L A O'Reilly, C Printa, G Hausmann, K Moriishib, S Cory, D C S Huang and A Strasser

The Walter and Eliza Hall Institute, Melbourne, Australia

Correspondence to: A Strasser, The Walter and Hall Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria 3050, Australia Tel: +61-3-9345-2555; Fax: +61-3-9347-0852; E-mail: strasser@wehi.edu.au

aCurrent address: Department of Pathology, University of Cambridge, Cambridge, UK

bCurrent address: Department of Veterinary Science, National Institute of Infectious Diseases, Tokyo, Japan

Edited by G Melino

Abstract

Anti-apoptotic members of the Bcl-2 family, such as Bcl-w, maintain cell viability by preventing the activation of the cell death effectors, the caspases. Gene targeting experiments in mice have demonstrated that Bcl-w is required for spermatogenesis and for survival of damaged epithelial cells in the gut. Bcl-w is, however, dispensable for physiological cell death in other tissues. Here we report on the analysis of Bcl-w protein expression using a panel of novel monoclonal antibodies. Bcl-w is found in a diverse range of tissues including colon, brain and testes. A survey of transformed cell lines and purified hematopoietic cells demonstrated that Bcl-w is expressed in cells of myeloid, lymphoid and epithelial origin. Subcellular fractionation and confocal laser scanning microscopy demonstrated that Bcl-w protein is associated with intracellular membranes. The implications of these results are discussed in the context of the phenotype of Bcl-w-null mice and recent data that suggest that Bcl-w may play a role in colon carcinogenesis. Cell Death and Differentiation (2001) 8, 486-494.

Keywords

apoptosis; Bcl-w; spermatogenesis; monoclonal antibody

Received 3 November 2000; revised 21 December 2000; accepted 21 December 2000
May 2001, Volume 8, Number 5, Pages 486-494
Table of contents    Previous  Abstract  Next   Full text  PDF
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