Modulation of apoptosis by the widely distributed Bcl-2 homologue Bak

Nature. 1995 Apr 20;374(6524):736-9. doi: 10.1038/374736a0.


Members of the Bcl-2 family of proteins are characterized by their ability to modulate cell death. Bcl-2 and some of its homologues inhibit apoptosis, whereas other family members, such as Bax, will accelerate apoptosis under certain conditions. Here we describe the identification and characterization of a complementary DNA that encodes a previously unknown Bcl-2 homologue designated Bak. Like Bax, the bak gene product primarily enhances apoptotic cell death following an appropriate stimulus. Unlike Bax, however, Bak can inhibit cell death in an Epstein-Barr-virus-transformed cell line. The widespread tissue distribution of Bak messenger RNA, including those containing long-lived, terminally differentiated cell types, suggests that cell-death-inducing activity is broadly distributed, and that tissue-specific modulation of apoptosis is controlled primarily by regulation of molecules that inhibit apoptosis.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Apoptosis / physiology*
  • Base Sequence
  • Cell Line
  • Cell Line, Transformed
  • DNA, Complementary
  • Humans
  • Hybrid Cells
  • Membrane Proteins / genetics
  • Membrane Proteins / physiology*
  • Mice
  • Molecular Sequence Data
  • RNA, Messenger / analysis
  • Sequence Homology, Amino Acid
  • Tissue Distribution
  • bcl-2 Homologous Antagonist-Killer Protein


  • BAK1 protein, human
  • Bak1 protein, mouse
  • DNA, Complementary
  • Membrane Proteins
  • RNA, Messenger
  • bcl-2 Homologous Antagonist-Killer Protein

Associated data

  • GENBANK/U16811
  • GENBANK/U16812
  • GENBANK/U16813