The transcriptional corepressor NAB2 blocks Egr-1-mediated growth factor activation and angiogenesis
The transcriptional corepressor NAB2 blocks Egr-1-mediated growth factor activation and angiogenesis
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DOI：
10.1006/bbrc.2001.4810
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发表时间：
2001-05-04
影响因子：
3.1
通讯作者：
Braddock, M
中科院分区：
文献类型：
--
作者：
Houston, P;Campbell, CJ;Braddock, M
有效的组织修复是由一系列快速的、时间上协调的事件产生的。在局部组织损伤部位，许多生长因子和细胞因子的产生部分地受到早期生长反应转录因子如Egr-1的刺激，Egr-1蛋白与称为NAB的辅阻遏蛋白家族结合，其功能是阻断或限制Egr-1对同源靶基因的反式激活。NABS阻断Egr-1对组织因子（TF）启动子的激活，Egr-1刺激PDGF-AB、HGF、TGF β（1）和VEGF的产生，以及PDGF-AB和TGF β（1）的内源性表达。在体外血管生成模型中，野生型NABS而非显性负性NABS突变体的表达消除了Egr-1驱动的TF启动子活性和小管形成。这些发现可能对急性或慢性损伤后形成瘢痕的任何组织具有重要意义。(C)北京：科学出版社.
Effective tissue repair results from a rapid, temporally orchestrated series of events. At the site of local tissue injury, the production of many growth factors and cytokines is, in part, stimulated by the early growth response transcription factors such as Egr-1, Egr-1 protein binds to a family of corepressor proteins called NAB which function to block or limit Egr-1 trans-activation of cognate target genes. NABS blocks Egr-1 activation of the tissue factor (TF) promoter, Egr-1 stimulated production of PDGF-AB, HGF, TGF beta (1), and VEGF and the endogenous expression of PDGF-AB and TGF beta (1). Expression of a wild-type NABS hut not a dominant negative NABS mutant abrogates Egr-1 driven TF promoter activity and tubule formation in an in vitro model of angiogenesis. These findings may have importance in any tissue that is subject to scarring after acute or chronic injury. (C) 2001 Academic Press.