Rel依赖的A1转录诱导是保护B细胞免受抗原受体连接诱导的凋亡所必需的。
Rel-dependent induction of A1 transcription is required to protect B cells from antigen receptor ligation-induced apoptosis.
作者信息
Grumont R J, Rourke I J, Gerondakis S
机构信息
The Walter and Eliza Hall Institute of Medical Research, Post Office, The Royal Melbourne Hospital, Parkville, Victoria 3050 Australia.
出版信息
Genes Dev. 1999 Feb 15;13(4):400-11. doi: 10.1101/gad.13.4.400.
Abstract
In response to different extracellular signals, Rel/NF-kappaB 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-kappaB regulates physiologically the expression of a Bcl-2-like protein that is critical for the control of cell survival during lymphocyte activation.
摘要
作为对不同细胞外信号的响应，Rel/NF-κB转录因子是多种细胞类型中凋亡的关键调节因子。我们在此表明，在正常B细胞和T细胞中，有丝分裂原以Rel依赖的方式快速诱导抗凋亡同源物Bcl-2的表达。在源自c-rel-/-小鼠的B细胞系中，如同缺乏Rel的原代细胞在抗原受体连接时会发生凋亡一样，A1转基因的组成型表达可抑制这条细胞死亡途径。这些发现首次表明，Rel/NF-κB在生理上调节一种Bcl-2样蛋白的表达，该蛋白对于淋巴细胞激活过程中细胞存活的控制至关重要。
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