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Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19K

Nature volume 374, pages 731–733 (1995)Cite this article

An Erratum to this article was published on 01 June 1995

Abstract

A NUMBER of DNA viruses carry apoptosis-inhibiting genes which enable the virus to escape from the host reponse1–5. The adenovirus E1B 19K protein can inhibit apoptosis induced by El A, tumour-necrosis factor-α, FAS antigen and nerve growth factor deprivation6–9. The molecular basis of this inhibition remains poorly understood, but the fact that protection is seen in the absence of other viral proteins suggests that E1B 19K targets cellular proteins. We report here the identification of three cellular proteins that bind El B 19K. One of these is a new member of the bcl-2 family10–16, which we have called bak (for bcl-2 homologous antagonist/killer). This protein, which is expressed in a wide variety of cell types, binds to E1B 19K and to the Bcl-2 homologue Bcl-xL, (ref. 17) in yeast. In addition, overexpression of bak in sympathetic neurons deprived of nerve growth factor accelerates apoptosis and blocks the protective effect of co-injected E1B 19K.

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Authors and Affiliations

  1. Molecular Science Department, Glaxo Research and Development Ltd, Greenford, Middlesex, UB6 OHE, UK

    Stuart N. Farrow, Julia H. M. White, Thomas Raven, Kwok-Tao Pun, Christine J. Grinham & Robin Brown

  2. Glaxo institute of Molecular biology, Chemin des Aulx 14, CH-1228, Plan les Ouates, Switzerland

    Isabelle Martinou & Jean-Claude Martinou

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  1. Stuart N. Farrow
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  2. Julia H. M. White
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Farrow, S., White, J., Martinou, I. et al. Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19K. Nature 374, 731–733 (1995). https://doi.org/10.1038/374731a0

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