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Publication : Induction of apoptosis by the Bcl-2 homologue Bak.

First Author  Chittenden T Year  1995
Journal  Nature Volume  374
Issue  6524 Pages  733-6
PubMed ID  7715730 Mgi Jnum  J:43663
Mgi Id  MGI:1098206 Doi  10.1038/374733a0
Citation  Chittenden T, et al. (1995) Induction of apoptosis by the Bcl-2 homologue Bak. Nature 374(6524):733-6
abstractText  Cells are eliminated in a variety of physiological settings by apoptosis, a genetically encoded process of cellular suicide. Apoptosis comprises an intrinsic cellular defence against tumorigenesis, which, when suppressed, may contribute to the development of malignancies. The bcl-2 oncogene, which is activated in follicular lymphomas, functions as a potent suppressor of apoptosis under diverse conditions. 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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