c-Myb对T细胞受体δ基因重排的调控
Regulation of T cell receptor delta gene rearrangement by c-Myb.
作者信息
Hernández-Munain C, Lauzurica P, Krangel M S
机构信息
Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA.
出版信息
J Exp Med. 1996 Jan 1;183(1):289-93. doi: 10.1084/jem.183.1.289.
Abstract
Developmental activation of VDJ recombination at the T cell receptor (TCR) delta locus is controlled by an intronic transcriptional enhancer (E delta). Transcriptional activation by E delta is dependent on c-Myb. To determine whether c-Myb plays a role in the activation of TCR-delta gene rearrangement, we compared VDJ recombination in transgenic mice carrying two versions of a human TCR-delta gene minilocus recombination substrate. One includes a wild-type E delta, whereas the other carries an E delta with a mutation that abrogates c-Myb binding. We demonstrate that an intact Myb binding site is necessary for efficient rearrangement of the minilocus substrate, suggesting that c-Myb plays a crucial role in activating VDJ recombination at the endogenous TCR-delta locus.
摘要
T细胞受体（TCR）δ基因座处VDJ重组的发育激活受一个内含子转录增强子（Eδ）调控。Eδ介导的转录激活依赖于c-Myb。为确定c-Myb是否在TCR-δ基因重排的激活中发挥作用，我们比较了携带两种人TCR-δ基因小基因座重组底物的转基因小鼠中的VDJ重组。一种包含野生型Eδ，而另一种携带的Eδ带有一个消除c-Myb结合的突变。我们证明完整的Myb结合位点对于小基因座底物的有效重排是必需的，这表明c-Myb在内源性TCR-δ基因座激活VDJ重组中起关键作用。
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