Rel-dependent induction of A1 transcription is required to protect B cells from antigen receptor ligation-induced apoptosis (original) (raw)
- Raelene J. Grumont,
- Ian J. Rourke, and
- Steve Gerondakis
- The Walter and Eliza Hall Institute of Medical Research, Post Office, The Royal Melbourne Hospital, Parkville, Victoria 3050 Australia
Abstract
In response to different extracellular signals, Rel/NF-κB transcription factors are critical regulators of apoptosis in a variety of cell types. Here we show that in normal B and T cells, expression of the Bcl-2 prosurvival homolog, A1, is rapidly induced in a Rel-dependent manner by mitogens. In B-cell lines derived from c-rel−/− mice, which like primary cells lacking Rel undergo apoptosis in response to antigen receptor ligation, constitutive expression of an _A1_transgene inhibits this pathway to cell death. These findings are the first to show that Rel/NF-κB regulates physiologically the expression of a Bcl-2-like protein that is critical for the control of cell survival during lymphocyte activation.
Footnotes
↵Corresponding author.
E-MAIL gerondakis{at}wehi.edu.au; FAX 61-3-93470852.
- Received November 12, 1998.
- Accepted December 30, 1998.
Cold Spring Harbor Laboratory Press