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Rel-dependent induction of A1 transcription is required to protect B cells from antigen receptor ligation-induced apoptosis

Rel-dependent induction of A1 transcription is required to protect B cells from antigen receptor... Downloaded from genesdev.cshlp.org on November 4, 2021 - Published by Cold Spring Harbor Laboratory Press Rel-dependent induction of A1 transcription is required to protect B cells from antigen receptor ligation-induced apoptosis 1 1 1,2 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 In response to different extracellular signals, Rel/NF-kB 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-kB regulates physiologically the expression of a Bcl-2-like protein that is critical for the control of cell survival during lymphocyte activation. [Key Words:Rel/NF-kB; A1; apoptosis; lymphocyte; mitogenesis] Received November 12, 1998; revised version accepted December 30, 1998. Multicellular organisms eliminate unwanted cells that CED4; and the caspase CED-3. CED9 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genes & Development Unpaywall

Rel-dependent induction of A1 transcription is required to protect B cells from antigen receptor ligation-induced apoptosis

Grumont, R. J.; Rourke, I. J.; Gerondakis, S.
Genes & Development – Feb 15, 1999
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Unpaywall
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0890-9369
DOI
10.1101/gad.13.4.400
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Abstract

Downloaded from genesdev.cshlp.org on November 4, 2021 - Published by Cold Spring Harbor Laboratory Press Rel-dependent induction of A1 transcription is required to protect B cells from antigen receptor ligation-induced apoptosis 1 1 1,2 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 In response to different extracellular signals, Rel/NF-kB 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-kB regulates physiologically the expression of a Bcl-2-like protein that is critical for the control of cell survival during lymphocyte activation. [Key Words:Rel/NF-kB; A1; apoptosis; lymphocyte; mitogenesis] Received November 12, 1998; revised version accepted December 30, 1998. Multicellular organisms eliminate unwanted cells that CED4; and the caspase CED-3. CED9

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Genes & Development – Unpaywall

Published: Feb 15, 1999

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