Bcl‐2 protects from oxidative damage and apoptotic cell death without interfering with activation of NF‐κB by TNF
H Albrecht, J Tschopp, CV Jongeneel - FEBS letters, 1994 - Wiley Online Library
H Albrecht, J Tschopp, CV Jongeneel
FEBS letters, 1994•Wiley Online LibraryThe 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 H2O2.
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 …
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 H2O2.
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 …
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 H2O2. 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.
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