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血管紧张素Ⅱ对Smad2/3的活化及对Smad3相互作用蛋白质组的影响
发表时间：2008-08-15 浏览量：2266 下载量：872
| 全部作者： | 花芳，周军兰，杨红振，胡卓伟 |
| 作者单位： | 中国医学科学院药物研究所 |
| 摘 要： | 血管紧张素Ⅱ（Angiotensin Ⅱ, Ang Ⅱ）在心血管纤维化中发挥了十分重要的作用。Ang Ⅱ作为一种细胞外信号，经过细胞膜AT1受体和细胞内信号传导通道，激活核转录因子进而调控相关基因表达。了解Ang Ⅱ信号途径中重要的转录因子及其相互作用的辅因子，可以从整体角度更全面地认识Ang Ⅱ对心血管系统的生长调节机制。通过细胞核转录因子微阵列研究发现：血管平滑肌细胞中多种核转录因子在Ang Ⅱ的作用下活性发生变化，其中转录因子Smad3/4活性明显增强。通过对Ang Ⅱ作用前后，Smad3相互作用蛋白的蛋白质组学研究，鉴定到两种新的Smad3相互作用蛋白，这为研究Smad3在Ang Ⅱ信号通路中的调控机制提供了新的线索。 |
| 关 键 词： | 分子生物学；Smad3；相互作用蛋白；蛋白质组学；血管紧张素Ⅱ |
| Title： | Angiotensin Ⅱ mediating the activation of Smad2/3 and its efficacy for proteomic alteration of Smad3 binding proteins |
| Author： | HUA Fang, ZHOU Junlan, YANG Hongzhen, HU Zhuowei |
| Organization： | Institute of Meteria Medica, Chinese Academy of Medical Sciences |
| Abstract： | Angiotensin Ⅱ (Ang Ⅱ) has recently emerged as a key mediator of cardiovascular fibrosis. It is recognized as a cytokine and signal through its Ang Ⅱ receptor 1 (AT1) to exert most of its biological functions. Through multiple downstream intracellular signaling pathways, Ang Ⅱ activates transcription factors and regulates target gene expression. Studying for the transcription factors and its interacting co-factors in Ang Ⅱ signaling can provide comprehensive insights for understanding the regulatory mechanism of Ang Ⅱ in cardiovascular system. In the transcription factor-DNA array study, the authors found that Ang Ⅱ can activate Smad3/4 in vascular cells, and it can induce the phosphorylation of Smad2/3. Through proteomic analysis, the authors confirmed that the binding affinity of two Smad3 interacting proteins can be altered by Ang Ⅱ stimulation. These results suggested that Smad3 activation might be involved in Ang Ⅱ-induced fibrosis, and provided new clues for studying the regulatory mechanism of Smad3 in the Ang Ⅱ signaling pathway. |
| Key words： | molecular biology; Smad3; interacting proteins; proteomics; Angiotensin Ⅱ |
| 发表期数： | 2008年12月第15期 |
| 引用格式： | 花芳，周军兰，杨红振，等. 血管紧张素Ⅱ对Smad2/3的活化及对Smad3相互作用蛋白质组的影响[J]. 中国科技论文在线精品论文，2008，1（15）：1690-1694. |
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