The bcl-2 major breakpoint region (mbr) possesses transcriptional regulatory function.
The bcl-2 major breakpoint region (mbr) possesses transcriptional regulatory function.
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DOI：
10.1016/j.gene.2006.05.002
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发表时间：
2006-09
期刊：
影响因子：
3.5
通讯作者：
Jingjing Zhang;Changyan Ma;Xiao Han;L. Durrin;Yujie Sun
中科院分区：
文献类型：
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作者：
Jingjing Zhang;Changyan Ma;Xiao Han;L. Durrin;Yujie Sun
bcl-2主要断裂点区域（mbr）位于bcl-2基因的3′-UTR内，是滤泡性淋巴瘤中最常见的染色体易位t（14;18）（q32;q21）的位点。mbr在生理条件下形成三链体DNA结构，并且转录因子特异性富含AT的序列结合蛋白1（SATB 1）紧接着mbr的下游结合。这些观察结果提出了mbr可能参与调节bcl-2基因表达的可能性。我们研究了bcl-2 mbr对报告基因活性的作用，以及SATB 1在多种细胞系中与此功能的相关性。我们发现mbr能上调报告基因的表达。删除37 bp的AT-丰富的SATB 1结合位点废除bcl-2 mbr的报告基因表达的调节。SATB 1的过表达增强了bcl-2 mbr对报告基因活性的上调。我们的数据有力地证明了bcl-2 mbr具有与SATB 1相关的调节功能。
The bcl-2 major breakpoint region (mbr), located within the 3′-UTR of the bcl-2 gene, is the site of the most common chromosomal translocation, t(14;18) (q32;q21), which occurs in follicular lymphoma. The mbr forms a triplex DNA structure under physiological conditions and the transcription factor special AT-rich sequence-binding protein 1 (SATB1) binds immediately downstream of the mbr. These observations raise the possibility that the mbr may be involved in regulation of bcl-2 gene expression. We investigated the role of the bcl-2 mbr on reporter gene activity and the relevance of SATB1 to this function in a variety of cell lines. We found that the mbr up-regulated reporter gene expression. Deletion of the 37-bp AT-rich SATB1 binding site abolished the bcl-2 mbr regulation of reporter gene expression. Overexpression of SATB1 enhanced bcl-2 mbr up-regulation of the reporter gene activity. Our data strongly demonstrated that the bcl-2 mbr possessed regulatory function that was related to SATB1.