Induction of apoptosis by the Bcl-2 homologue Bak

Nature. 1995 Apr 20;374(6524):733-6. doi: 10.1038/374733a0.


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.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Apoptosis / physiology*
  • Base Sequence
  • Cell Line
  • Cloning, Molecular
  • Humans
  • Membrane Proteins / biosynthesis
  • Membrane Proteins / genetics
  • Membrane Proteins / physiology*
  • Mice
  • Molecular Sequence Data
  • Proto-Oncogene Proteins / antagonists & inhibitors
  • Proto-Oncogene Proteins c-bcl-2
  • Rats
  • Recombinant Fusion Proteins / biosynthesis
  • Sequence Homology, Amino Acid
  • bcl-2 Homologous Antagonist-Killer Protein


  • BAK1 protein, human
  • Bak1 protein, mouse
  • Bak1 protein, rat
  • Membrane Proteins
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Recombinant Fusion Proteins
  • bcl-2 Homologous Antagonist-Killer Protein

Associated data

  • GENBANK/U23765