Abstract
CELLS are eliminated in a variety of physiological settings by apoptosis, a genetically encoded process of cellular suicide1,2. Apoptosis comprises an intrinsic cellular defence against tumorigenesis, which, when suppressed, may contribute to the development of malignancies3. The bcl-2oncogene, which is activated in follicular lymphomas, functions as a potent suppressor of apoptosis under diverse conditions4. Here we describe the complementary DNA cloning and functional analysis of a new Bcl-2 homologue, Bak, which promotes cell death and counteracts the protection from apoptosis provided by Bcl-2. Moreover, enforced expression of Bak induces rapid and extensive apoptosis of serum-deprived fibroblasts. This raises the possibility that Bak is directly involved in activating the cell death machinery.
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Chittenden, T., Harrington, E., O'Connor, R. et al. Induction of apoptosis by the Bcl-2 homologue Bak. Nature 374, 733–736 (1995). https://doi.org/10.1038/374733a0
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DOI: https://doi.org/10.1038/374733a0
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