Analysis of the role of bcl-2 in apoptosis

Immunol Rev. 1994 Dec;142:127-39. doi: 10.1111/j.1600-065x.1994.tb00886.x.


Cells undergo apoptosis in response to a wide range of stimuli, and this response may represent an ancient defence mechanism against pathogens. Bcl-2 is able to prevent apoptosis in many cases. Although blocking cell suicide is not directly oncogenic, enforced bcl-2 expression can lead to cancer by lengthening the life-span of cells, during which time secondary changes, such as activation of additional oncogenes like c-myc, can occur. Bcl-2 cannot block apoptosis of target cells by cytotoxic T lymphocytes. Thus cytotoxic T cells are able to fight viruses that carry anti-apoptosis genes that resemble bcl-2. Genes involved in the regulation of mammalian apoptosis are similar to those that mediate programmed cell death in C. elegans. By studying cell death genes in viruses and worms as well as mammals, we will learn more about this fascinating process.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • B-Lymphocytes / immunology
  • Genes, myc / physiology
  • Humans
  • Proto-Oncogene Proteins / biosynthesis
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins / physiology
  • Proto-Oncogene Proteins c-bcl-2
  • T-Lymphocytes, Cytotoxic / immunology
  • Tumor Suppressor Protein p53 / physiology


  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53