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Bcl‐2 protects from oxidative damage and apoptotic cell death without interfering with activation of NF‐κB by TNF
Author(s) -
Albrecht Hugo,
Tschopp Jürg,
Jongeneel C.Victor
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)00817-5
Subject(s) - pyrrolidine dithiocarbamate , apoptosis , nfkb1 , reactive oxygen species , nf κb , programmed cell death , tumor necrosis factor alpha , chemistry , transcription factor , microbiology and biotechnology , cancer research , biology , biochemistry , gene , immunology
The recent demonstration of the anti‐oxidant properties of the Bcl‐2 gene product suggested that expression of Bcl‐2 may interfere with the nuclear migration of the NF‐κB transcription factor, which is thought to depend on the presence of reactive oxygen intermediates. In mouse L cells, overexpression of Bcl‐2 interfered with the activation of NF‐κB by H 2 O 2 . However, Bcl‐2 had no effect on the activation of NF‐κB by TNF, even though it protected cells from TNF‐induced apoptosis. The effects of exogenous pyrrolidine dithiocarbamate were very similar to those of Bcl‐2 overexpression. We conclude that the protective effects of anti‐oxidants against induced apoptotic cell death are unrelated to their ability to interfere with NF‐κB activation.